alexa Use of Fish as Bio-indicator of the Effects of Heavy Metals Pollution | OMICS International
ISSN: 2155-9546
Journal of Aquaculture Research & Development

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Use of Fish as Bio-indicator of the Effects of Heavy Metals Pollution

Authman MMN1*, Zaki MS1, Khallaf EA2 and Abbas HH1

1Hydrobiology Department, National Research Centre, 33 EL Bohouth St. (Former EL Tahrir St.), Dokki, Giza, Egypt, P.O. 12622

2Zoology Department, Faculty of Science, Minufiya University, Shebeen Alkoom, Egypt

*Corresponding Author:
Authman MMN
Hydrobiology Department
National Research Centre
33 EL Bohouth St. (Former EL Tahrir St.)
Dokki, Giza, Egypt
Tel: 002-01005591998
E-mail: [email protected]

Received Date: January 26, 2015; Accepted Date: February 16, 2015; Published Date: March 15, 2015

Citation: Authman MMN, Zaki MS, Khallaf EA, Abbas HH (2015) Use of Fish as Bio-indicator of the Effects of Heavy Metals Pollution. J Aquac Res Development 6:328. doi:10.4172/2155-9546.1000328

Copyright: © 2015 Authman MMN, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Abstract

The present review gives a brief account of the toxic effects of heavy metals on fish. In aquatic ecosystem, heavy metals are considered as the most important pollutants, since they are present throughout the ecosystem and are detectable in critical amounts. Heavy metals, such as mercury, cadmium, copper, lead and zinc are of the most important pollutants which effect aquatic environment and fish. They are extremely dangerous for the health of fish. Most of these metals are characterized by being accumulated in tissues, and lead to the poisoning of fish. These metals can effectively influence the vital operations and reproduction of fish; weaken the immune system, and induce pathological changes. As such, fish are used as bio-indictors, playing an important role in monitoring heavy metals pollution. Finally, some recommendations are given to treatment of different kinds of wastewaters, sewage and agricultural wastes before discharge into the aquatic systems. Also, enforcement of laws and legislations regarding the protection of aquatic environments must be taken into consideration.

Keywords

Fish; Bio-indicators; Heavy metals; Bioaccumulation; Alterations; Aquatic pollution

Introduction

Due to feeding and living in the aquatic environments fish are particularly vulnerable and heavily exposed to pollution because they cannot escape from the detrimental effects of pollutants [1-3]. Fish, in comparison with invertebrates, are more sensitive to many toxicants and are a convenient test subject for indication of ecosystem health [4-17]. Heavy metals are produced from a variety of natural and anthropogenic sources [18]. In aquatic environments, heavy metal pollution results from direct atmospheric deposition, geologic weathering or through the discharge of agricultural, municipal, residential or industrial waste products, also via wastewater treatment plants (WWTPs) [19-22]. Coal combustion is one of the most important anthropogenic emission sources of trace elements and an important source of a number of metals [23]. The contamination of heavy metals and metalloids in water and sediment, when occurring in higher concentrations, is a serious threat because of their toxicity, long persistence, and bioaccumulation and bio magnification in the food chain [24,25]. Fishes are considered to be most significant biomonitors in aquatic systems for the estimation of metal pollution level [26,27], they offer several specific advantages in describing the natural characteristics of aquatic systems and in assessing changes to habitats [28]. In addition, fish are located at the end of the aquatic food chain and may accumulate metals and pass them to human beings through food causing chronic or acute diseases [29]. Studies from the field and laboratory works showed that accumulation of heavy metals in a tissue is mainly dependent on water concentrations of metals and exposure period; although some other environmental factors such as water temperature, oxygen concentration, pH, hardness, salinity, alkalinity and dissolved organic carbon may affect and play significant roles in metal's accumulation and toxicity to fish [30-35]. Ecological needs, size and age of individuals, their life cycle, feeding habits, and the season of capture were also found to affect experimental results from the tissues [36-38]. Fish have the ability to uptake and concentrate metals directly from the surrounding water or indirectly from other organisms such as small fish, invertebrates, and aquatic vegetation [39]. Fish accumulate pollutants preferentially in their fatty tissues like liver and the effects become apparent when concentrations in such tissues attain a threshold level [40]. However, this accumulation depends upon their intake, storage and elimination from the body [41]. This means that metals which have high uptake and low elimination rates in tissues of fish are expected to be accumulated to higher levels [42,43]. Heavy metals can be taken up into fish either from ingestion of contaminated food via the alimentary tract or through the gills and skin [44,45]. Effectively, after the absorption, metals in fish are then transported through blood stream to the organs and tissues where they are accumulated [46, 47]. The heavy metal concentration in fish tissues reflects past exposure via water and/or food and it can demonstrate the current situation of the animals before toxicity affects the ecological balance of populations in the aquatic environment [48]. The obvious sign of highly polluted water, dead fish, is readily apparent, but the sublethal pollution might result only in unhealthy fish. Dupuy et al. [49] reported that the fish health status in some polluted systems (estimated by the condition factor) indicated that the fish have a lower condition. Very low-levels of pollution may have no apparent impact on the fish itself, which would show no obvious signs of illness, but it may decrease the fecundity of fish populations, leading to a longterm decline and eventual extinction of this important natural resource [34,50]. Also, heavy metals are known to induce oxidative stress and/ or carcinogenesis by mediating free radicals/reactive oxygen species [51]. In general, metals can be categorized as biologically essential and non-essential. The nonessential metals (e.g., aluminum (Al), cadmium (Cd), mercury (Hg), tin (Sn) and lead (Pb)) have no proven biological function (also called xenobiotics or foreign elements), and their toxicity rises with increasing concentrations [45]. Essential metals (e.g., copper (Cu), zinc (Zn), chromium (Cr), nickel (Ni), cobalt (Co), molybdenum (Mo) and iron (Fe)) on the other hand, have a known important biological roles [52], and toxicity occurs either at metabolic deficiencies or at high concentrations [53]. The deficiency of an essential metal can therefore cause an adverse health effect, whereas its high concentration can also result in negative impacts which are equivalent to or worse than those caused by non-essential metals [54]. Moreover, the toxicity of metals to fish is significantly affected by the form in which they occur in water. The ionic forms of metals or simple inorganic compounds are more toxic than complex inorganic or organic compounds. The toxic action of metals is particularly pronounced in the early stages of fish development [55] and adversely affects various metabolic processes in developing fish (embryos in particular), resulting in developmental retardation, morphological and functional deformities, or death of the most sensitive individuals [45]. Heavy metals produce toxic effects at high concentrations, and thus could be considered as risk factors for several diseases [56-58]. Heavy metals are able to disturb the integrity of the physiological and biochemical mechanisms in fish that are not only an important ecosystem component, but also used as a food source [59-65]. Previous studies have shown that marine and farmed fish and shellfish are significant contributors to consumer intake of some contaminants due to their presence in the aquatic environment and their accumulation in the flesh of fish and shellfish [66,67].The objective of the present review article is to briefly describe the toxicity and effects of different heavy metals on the fish health and the consequent use as bioindicators. The heavy metals: Aluminum, Arsenic, Cadmium, Chromium, Copper, Iron, Lead, Manganese, Mercury, Nickel, Vanadium and Zinc, are going to be investigated in this review.

Aluminum (Al)

Aluminum (Al) is the third most common and abundant metal on earth after oxygen and silicon [10]. It is similar to many other metals in that it is generally considered most toxic in its soluble ionic form [68]. It is found in the atmospheric air of the big cities and industrialized areas, and is used as a flocculation agent in water treatment [69, 70]. The toxicity of aluminum to fish depends to a large extent on the physicochemical properties of the water and particularly on its pH. Aluminum is soluble at pH values below 6.0 [71]. The mechanism of toxicity in fish seems to be related to interference with ionic and osmotic balance and with respiratory problems resulting from coagulation of mucous on the gills of fish and has been found to cause severe fusion of lamellae and filaments in the gills [72]. Al is considered to be an endocrine disrupting chemical in mature Oreochromis niloticus females [73]. Fish exposed to Al showed significantly higher total erythrocyte counts; haematocrit (Hct); mean corpuscular haemoglobin concentration (MCHC) and mean corpuscular haemoglobin (MCH) while mean corpuscular volume (MCV) was significantly lower [74]. Using concentrations as low as 0.52 mg/l aluminum led to markedly reduction in fish growth [75]. Physiological alterations frequently observed in different fish species exposed to Al are mainly related to cardiovascular [76], haematologic [77], respiratory, ionoregulatory [78], reproductive [79], metabolic [80], and endocrine [81] disturbances, beyond structural gill damage [82].

Arsenic (As)

Arsenic reach aquatic ecosystems by a variety of sources including manufacturing companies, mineral or strip mines, smelting operations, and electric generating stations (power plants). One major agricultural source of as is the manufacture and use of arsenical defoliants and pesticides. It also has been used to kill aquatic plants to reduce the difficulty encountered during hook-and-line fishing of areas overgrown with aquatic vegetation [83]. Arsenic is able to accumulate in large quantities in the sediments on the bed of water courses and reservoirs, and in aquatic organisms [71]. Arsenic compounds in the third (III) oxidation state (arsenites) are absorbed fairly rapidly into fish and are more toxic than arsenic compounds in the oxidation state V (arsenates) [84]. Arsenic is actively metabolized in the tissue of fish especially in organs such as the liver and has the tendency to accumulate as reported in different teleosts such as green sunfish [85], rainbow trout [86], Japanese medaka and Tilapia mossambica [87,88]. Donohue and Abernathy [89] reported that total arsenic in marine fish, shellfish, and freshwater fish tissues ranged from 0.19 to 65, 0.2 to 125.9, and 0.007 to 1.46 μg g−1 dw, respectively. Koch et al. [90] demonstrated that total arsenic in freshwater fish ranged from 0.28 to 3.1 for whitefish (Coregonus clupeaformis), 0.98 to 1.24 for sucker (Catostomus commersoni), 0.46 to 0.85 for walleye (Stizostedion vitreum), and 1.30 to 1.40 μg g−1 dry wt for pike (Esox lucius). Acute exposures can result in immediate death because of As-induced increases in mucus production, causing suffocation, or direct detrimental effects on the gill epithelium. Chronic exposures can result in the accumulation of the metalloid to toxic levels and is responsible for several disease conditions [91]. Hemosiderin granules probably represent an alternate storage site for arsenicals in teleosts [83].Fish are continually exposed to arsenic through their gills and intake of As-contaminated food [92]. Arsenic has been found to cause the head kidney cells to be swollen with intercellular oedema in Clarias batrachus [93] while vacuolation has also been found in Clarias batrachus exposed to As [94]. On the other hand, renal histopathological changes in freshwater teleosts were significant in various fish species such as arsenic-exposed rainbow trout [95], lake white fish and lake trout [96]. Arsenic was also found to cause a depletion of lymphocytes and melano-macrophage centres in Clarias batrachus [94]. Hepatic degenerative changes in fish exposed to as include submassive necrosis, focal necrosis, bile duct proliferation, bile plug's, and acidophilic bodies. Other changes include the formation of necrotic bodies, fibrous bodies, and cytoplasmic and intra nuclear Asinclusions within the parenchymal hepatocytes [83].

It has been observed that, although arsenic accumulates primarily in retina, liver and kidney of fish, it can interfere with the fish immune system by suppressing antibody [93]. It has also been reported that short-term exposure of fish to non-lethal concentration of arsenic can induce time-dependent and tissue-specific changes in B and T-lymphocytes cells functioning, making them susceptible to infections [84,97]. Arsenicals are also known to induce a number of major stress protein families, including heat shock proteins (hsps) both in vitro and in vivo in several organs and systems with a rapid dose dependent response to acute exposure to arsenite [98,99]. Studies on zebrafish revealed that arsenic inhibited synthesis of macrophage-derived cytokines like TNFα and IFN-γ thereby compromising the antiviral responses [100]. Exposure of fish to various concentrations of arsenic also affected the phagocytic potential of macrophages and helped in the dissemination and persistence of viral and bacterial pathogens into distant host tissues [101].

Cadmium (Cd)

Cadmium is a naturally occurring nonessential trace element and its' tendency to bio accumulate in living organisms often in hazardous levels, raises environmental concern [45,102,103]. Cadmium production, consumption and emissions to the environment have increased dramatically during the 20th century, due to its industrial use (batteries, electroplating, plastic stabilizers, pigment), and consequently lead to contamination of aquatic habitats [104]. The use of cadmium containing fertilizer, agricultural chemicals, pesticides and sewage sludge in farm land, might also contribute to the contamination of water [105]. As a nondegradable cumulative pollutant, Cd is considered capable of altering aquatic trophic levels for centuries [83]. This heavy metal has been shown to accumulate mainly (about 75 %) in kidney, liver and gills of freshwater fish [106], but it can also be deposited in the hearts [107] and other tissues [108] and cause pathological changes of varying severity in above mentioned organs [109]. Morphological and histological alterations in liver of fishes exposed to cadmium have been documented [110]. Higher doses of cadmium caused visible external lesions such as discoloration and necrosis on livers of Cyprinus carpio, Carassius auratus and Corydoras paleatus [111]. Oreochromis mossambicus exposed to Cd showed liver alterations in the form of hyalinisation, hepatocyte vacuolation, cellular swelling and congestion of blood vessels [112]. Epithelial swelling of the renal tubules and mitochondrial and endoplasmic reticulum (ER) swelling (cloudy swelling) were observed in kidney of Dicentrarchus labrax exposed to cadmium [113]. Chloride cells proliferation has been observed in gills of specimens of D. labrax exposed to cadmium [113]. Moreover, cadmium inhibits calcium uptake in gills [114] and may alter the metabolism of essential trace element by affecting normal tissue distribution of trace elements as Zn and Cu [115]. Omer et al. [116] reported histopathological alterations in liver, intestine and kidneys of tilapia fish (Oreochromis niloticus) exposed to cadmium. Fish exposed to cadmium revealed disturbances in blood constituents and differential blood count. Cadmium causes the destruction of erythrocytes, decreases the hematocrit value and hemoglobin concentration and leads to anemia [117]. Cadmium in plasma of goldfish significantly increased the activities of plasma glutamic acidoxaloacetic acid-transaminase (GOT) and glutamic acid-pyruvic acidtransaminase (GPT) [118]. Also, cadmium altered the metabolism of carbohydrates, causing hyperglycemia in some marine [119] and freshwater fish species [120,121]. Cadmium is considered as endocrine disrupter and has been shown to interfere with the formation of steroids, eggs and sperm in rainbow trout (Oncorynchus mykiss) where it alters hormone synthesis in testes [122]. In carp (Cyprinus carpio) it inhibits steroid formation and ovarian function [123]. Also, adverse influence of long exposure to cadmium upon the maturation, hatchability and development of larvae was recorded [113]. Fish exposed to cadmium revealed a negative effect on the growth rate, meat quality and blood physiology of Nile tilapia [124]. Exposure of Anabas testudineus, to cadmium also showed a significant decline in carbohydrate content in body tissues [125]. Shukla et al. [126] showed toxic effects of cadmium individually and in combination with other metals on the nutritive value of freshwater fish Channa punctatus. About the genotoxicity of cadmium in fish species, Sanchez-Galan et al. [127] reported that the cadmium chloride injection induced the formation of micronuclei in erythrocytes of Anguilla anguilla. Bolognesi et al. [128] reported that cadmium yielded negative results with the micronucleus test. Induction of micronuclei in polychromatic erythrocytes of Cyprinus carpio by cadmium treatment was demonstrated by [129]. Exposures to low levels of Cd can cause DNA damage and stress in common carp (Cyprinus carpio) [130].

Effects of accumulation of Cd on indicators of oxidative stress in several tissues of Sparus aurata were investigated by Souid et al. [131]. After exposure to 0.5 mg Cd/L for 24 h, concentration in intestine was 0.4 while that in liver was 0.13 mg/kg wet mass (wm). Witeska et al. [132] studied the effects of Cd (100 μg/L) on the embryonic, larval or both stages of the ide, Leuciscus idus. Their results showed that metal toxication affected mortality, body size, various body morphometrics and deformities (vertebral curvatures and yolk sac deformities). Low and Higgs [133] exposed fathead minnows (Pimephales promelas) for 96 h to a range of cadmium concentrations and found that cadmium caused an increase in auditory threshold and a decrease in response latency.

Chromium (Cr)

Chromium is an essential nutrient metal, necessary for metabolism of carbohydrates [134]. Chromium enter the aquatic ecosystem through effluents discharged from leather tanneries, textiles, electroplating, metal finishing, mining, dyeing and printing industries, ceramic, photographic and pharmaceutical industries etc. [135,136]. Poor treatment of these effluents can lead to the presence of Cr (VI) in the surrounding water bodies, where it is commonly found at potentially harmful levels to fish [45,137,138]. In surface waters, depending on physicochemical characteristics, the most stable forms of chromium are the oxidation states trivalent Cr (III) or (Cr3+) and the hexavalent Cr(VI) or (Cr6+). Hexavalent chromium (Cr6+) is considered to be toxic (i.e. carcinogenic) because of its powerful oxidative potential and ability to cross cell membranes [139-141]. Fish assimilate Cr by ingestion or by the gill uptake tract and accumulation in fish tissues, mainly liver, occurs at higher concentrations than those found in the environment [138,142]. The overall toxic impact on organs like gill, kidney and liver may seriously affect the metabolic, physiologic activities and could impair the growth and behavior of fish [55]. Toxic effects of Cr in fish include: hematological, histological and morphological alterations, inhibition/reduction of growth, production of reactive oxygen species (ROS) and impaired immune function [143, 144]. Oreochromis mossambicus exposed to sublethal Cr showed histological alterations in the liver (congestion of blood vessels; fat accumulation; increase in melano-macrophage centres and necrosis), gills (hyperplasia of primary lamellar epithelium), ovaries (deposits in interstitial tissue) and testes (hypertrophy and vacuolation of spermatocytes) [145]. Acute poisoning by chromium compounds causes excess mucous secretion, damage in the gill respiratory epithelium and the fish may die with symptoms of suffocation [146]. Palaniappan and Karthikeyan [147] reported that the kidney is a target organ for chromium accumulation, which implies that it is also the “critical” organ for toxic symptoms. On chronic exposures, hexavalent chromium severely affected the renal tubules causing hypertrophy of epithelial cells, reduction of tubular lumen, contraction of glomeruli and epithelial and glomerular necrosis [148]. Necrosis and fibrosis of tubular lumen was reported in chronic chromium-exposed chinook salmon [134]. Chromium compounds also cause renal failure leading to the loss of osmoregulatory ability and respiration in fish [149].Sublethal effects of chromium in fish were directly related to the inhibition of various metabolic processes [150]. The hexavalent chromium induced depletion in the profiles of liver glycogen, total protein and total lipid has been reported [151]. Nguyen and Janssen [152] studied the effect of chromium on the African catfish (Clarias gariepinus). The exposure took place right after fertilization and lasted for 5 days. Concentrations used varied from 11 to 114 mg/L (K2Cr2O7). They found that the main deformity reported was abnormal body axis. Virk and Sharma [153] assessed the effects of acute toxicity of chromium on fingerlings of the C. mrigala. After 45 days of exposure significant decline in the protein and carbohydrate content of gills was observed. Reduced locomotor activity has been reported in chronic chromium-exposed Gambusia affinis [154].

Copper (Cu)

Copper (Cu) is an essential trace metal and micronutrient for cellular metabolism in living organisms on account of being a key constituent of metabolic enzymes [155]. However it can be extremely toxic to intracellular mechanisms in aquatic animals at high concentrations which exceed normal levels [156, 157]. It is an abundant element which occurs as a natural mineral with a wide spread use [45]. Copper pollution is through extensive use of fungicides, algaecides, molluscicides, insecticides and discharge of wastes [158]. Copper sulfate (CuSO4) is often used as an algaecide in commercial and recreational fish ponds to control the growth of phytoplankton and filamentous algae and to control certain fish disease [159]. Fish can accumulate copper via diet or ambient exposure [45]. Even at low environmental concentrations, copper shows distinct affinity to accumulate in the fish liver [160]. The typical patho-anatomical appearance includes a large amount of mucus on body surface, under the gill covers and in between gill filaments [71]. Copper-induced histological alterations are found in the gill, kidney hematopoietic tissue, mechanoreceptoes, chemoreceptors, and other tissues [83]. Morphological and histological alterations in liver of fishes exposed to copper have been documented [161]. Higher doses of copper caused visible external lesions such as discoloration and necrosis on livers of Cyprinus carpio, Carassius auratus and Corydoras paleatus [111]. Arellano et al. [162] reported vacuolization of endothelial cells in fish liver by after copper exposure. Hepatocyte vacuolization, necrosis, shrinkage, nuclear pyknosis and increase of sinusoidal spaces were the distinct changes observed in the liver of copper-exposed fish [163]. Exposure of Nile tilapia (Oreochromis niloticus) to sublethal levels of Cu has been shown to cause histopathological alterations in gills (edema; vasodilation of the lamellar vascular axis) and livers (vacuolation and necrosis) [163]. Oreochromis mossambicus exposed to Cu showed histopathological alterations in the testes (testicular hemorrhage necrosis; pyknosis; disintegration of primary spermatogonia and interstitial tissue) [164].In copper exposed fish; Esomus danricus, decreased oxygen consumption and increased opercular activity have been reported due to gill damage [165]. Chloride cell dystrophies were observed by Arellano et al. [162] in S. senegalensis exposed to waterborne copper. It was demonstrated that the gill Na,K-ATPase activity appeared to be more sensitive to the chronic waterborne Cu exposure in Oncorhynchus mykiss compared to intestinal tissue [166]. Grosell et al. [167] observed that Na+/K+-ATPase enzyme activity elevated as Cu exposure progressed in the intestine of Opsanus beta and this was associated with a compensatory elevation of intestinal fluid absorption. High concentrations of copper have been reported to inhibit catalase (CAT) enzyme in liver, gill and muscle after 24 hr of exposure in carp (Cyprinus carpio L.) [168]. Radhakrishnaiah et al. [169] have recorded stimulation of glycogenolysis in fish L. rohita on exposure to a sub lethal concentration of copper. Sanchez et al. [170] showed that Cu is able to induce oxidative stress in fish (Gasterosteus aculeatus) even before significant metal accumulation occurs in the liver. Cyriac et al. [171] showed that fish acutely exposed to copper showed an increase in both hematocrit as well as hemoglobin content in blood, possibly due to changes in blood parameters which result in erythrocyte swelling or by release of large red blood cells from the spleen. Nussey et al. [172] reported that; during copper poisoning; the release of erythroblasts usually results from an increased rate of red blood cells (RBCs) catabolism. Reproductive effects are noted at low levels of Cu and include blockage of spawning, reduced egg production per female, abnormalities in newly-hatched fry, reduced survival of young, and other effects [83]. Gainey and Kenyon [173] mentioned that exposure of fishes to sublethal concentrations of copper leads to cardiac activity and reduction in heart rate. Dietary Cu level of 20 mg/Kg significantly reduced the weight gain of growing tilapia [174]. Chronic toxic effects may induce poor growth, decreased immune response, shortened life span, reproductive problems, low fertility and changes in appearance and behavior [175]. An increased superoxide dismutase activity in gills of rainbow trout after three days of exposure to 20 mg/L copper was found by Eyckmans et al. [176]. Barjhoux et al. [177] studied the effect of Cu spiked sediment on the Japanese medaka during the entire embryonic stage (concentrations varied between 6.95 and 23.1 μg/g d.w.). They observed deformed larvae up to 52% in the populations. Specimens were examined at hatching and the deformities found were mostly spinal (mainly kyphosis, lordosis and C-shaped larvae) and cardiovascular (mainly abnormal positioning and heart looping).

Iron (Fe)

Iron is prevalent component of industrial and mining effluents that are often discharged into aquatic environments. Ferrous iron (Fe2+) is considered to be more toxic to fish than the ferric (Fe3+) form [178]. The highest bioconcentration of iron in fish tissues was found in the liver and gonads, decreasing in brain, muscle and heart [179,180]. Recently, Omar et al. [40], in their study, proofed that the fish liver is the target organ for iron. Respiratory disruption due to physical clogging of the gills is suggested as a possible mechanism for iron toxicity [181]. Because the gill surface of the fish tends to be alkaline, soluble ferrous iron can be oxidized to insoluble ferric compounds which then cover the gill lamellae and inhibit respiration [182]. The precipitated iron compounds has serious effect starting from reduce the gill area available for respiration, damage the respiratory epithelium and ending with suffocate the fish and death. In banded tilapia (Tilapia sparrmanii), iron caused hyperplasia and necrosis of the secondary lamellae [183]. Gonzalez et al. [184] suggested that respiratory distress was a significant factor in the mortality of brook charr Salvelinus fontinalis (Mitchill) on exposure to iron, and Grobler et al. [180] observed a decrease in activity, coughing, yawning, spasmodic movements and an increase in opercular movements in iron exposed Tilapia sparrmanii (Smith). Peuranen et al. [185] agreed with earlier research, observing iron deposits on the surface of gill epithelia in brown trout Salmo trutta L., exposed to iron. They reported gill damage during exposure to 0.8–1.7 mg l−1 iron at pH 5 and 6. They suggested that as iron had been detected only on the surface, and not inside gill epithelia, it exerted its toxicity through action on the gill surface. A scanning electron micrograph study on the gills of T. sparrmanii after exposure to sublethal iron concentrations for 72 hrs in a continuous flow system, revealed collapse of the gills as well as increased amounts of mucus cells [179]. Gill collapse reduces the diffusion distance between the water and blood, and benefits the oxygen consumption of fish. Also, iron compounds can precipitate on the surface of fish eggs causing death due to a lack of oxygen [71]. Clarias gariepinus showed restricted growth when fed a Fe-rich diet [186].

Lead (Pb)

Lead (Pb) is a persistent heavy metal which has been characterized as a priority hazardous substance [45]. Although Pb is a naturally occurring substance, its environmental concentrations are significantly increased by anthropogenic sources which include base metal mining, battery manufacturing, Pb-based paints and leaded gasoline [187,188]. Lead in water may come from industrial and smelter discharges; from the dissolution of old lead plumbing, lead containing pesticides, through precipitation, fallout of lead dust, street runoff, and municipal wastewater [83,189]. The concentration and bioavailability of Pb is mainly dependent on the absorption into the sediments and the natural organic matter content of the water as well as the pH, alkalinity and hardness [187,189]. Aquatic organisms bio accumulate Pb from water and diet, although there is evidence that Pb accumulation in fish, is most probably originated from contaminated water rather than diet [190]. Lead deposits in various fish organs: liver, kidneys and spleen, but also digestive tract and gills [160]. Accumulation of lead in different fish species has been determined in several works [191], leading to disorders in fish body. When C. batrachus exposed to 5 ppm of lead nitrate for 150 days, it exhibited marked inhibition of gonadal growth and showed decrease in cholesterol and lipid levels in brain, testis and ovary whereas the liver showed an elevation of both [192]. Iger and Abraham [193] observed a very high number of rodlet cells (RCs) in the epidermis of common carp and rainbow trout kept in lead polluted water. Hepatocyte vacuolization, hepatic cirrhosis, necrosis, shrinkage, parenchyma degeneration, nuclear pyknosis and increase of sinusoidal spaces were the distinct changes observed in the liver of lead-exposed fish [194]. Acute lead toxicity is initially characterized by damaging gill epithelium and ultimately suffocation. Two types of structural alterations of gill, defense/ compensatory responses and direct deleterious effects were observed in chronic lead exposed fish [195]. The necrosis and desquamation of gill epithelium as well as lamellar curling and aneurisms were the direct deleterious effects reported in chronic lead exposed Clarias gariepinus [194]. The characteristic symptoms of chronic lead toxicity include changes in the blood parameters with severe damage to erythrocytes and leucocytes and damage in the nervous system [196]. Lead deplete major antioxidants in the cell, especially thiol-containing antioxidants and enzymes, and can cause significant increases in an reactive oxygen species (ROS) production, followed by a situation known as ‘‘oxidative stress’’ leading to various dysfunctions in lipids, proteins and DNA [197]. Low levels of Pb pollution could cause some adverse effects on fish health and reproduction [198]. Also, lead was found to inhibit the impulse conductivity by inhibiting the activities of mono aminooxidase and acetylcholine esterase, to cause pathological changes in tissue and organs [199] and to impair the embryonic and larval development of fish species [200]. Hou et al. [201] monitored the effect of lead on the Chinese sturgeon, Acipenser sinensis. They observed deformities as body (spinal) curvatures. The authors also reported reduced ability of locomotion and foraging by deformed juveniles. Shah and Altindağ [202] reported significant increase in immunological metrics following Pb exposure, which suggests that Pb may weaken the immune system, resulting in increased susceptibility to infections.

Mercury (Hg)

Unpolluted water contains trace amounts which do not exceed than 0.1 μg/l of mercury [203]. The main source of mercury in environment is the fungicides, especially in the organic fungicides as mercurial materials which are organic compounds of mercury. The chronic data about mercury toxicity indicated that the organic form of Hg, methylmercury (MeHg+) is the most chronically toxic of the mercury compounds [204-206], and it is estimated that 70 to 100% of the Hg in fish is present as MeHg+ [207,208]. Methylmercury is generated by methylation of inorganic Hg by microorganisms such as anaerobic sulfate-reducing bacteria (SRB), iron reducers (FeRP), and methanogens (MPA) [209,210]. The rise in water temperatures attributed to climate change may stimulate methylation of Hg. Simulations of ocean warming rates of 0.4°C and 1°C predicted increases in the mean MeHg+ concentration of 1.7% (range, 1.6– 1.8%) and 4.4% (range, 4.1–4.7%), respectively, resulting in elevated MeHg+ concentrations in fish [210,211]. The LC50 of MeHg for fish is reported to be in the range of 0.004–0.125 mg/L, depending on the species, which is far lower than the LC50 of inorganic Hg [212]. The adverse effects of methylmercury (MeHg) were first recognized in the early 1970s following the pollution of Minamata Bay, Japan [213] and shortly thereafter a massive human poising that occurred in Iraq [214]. This organometallic compound is a highly lipophilic environmental contaminant derived from inorganic mercury by bacterial activity which easily crosses the blood barrier. The primary route of exposure for fish is through ingestion of contaminated food [44, 215]. The liver plays a central role in the binding, storage, and redistribution of mercurials which enter peripheral circulation [83].Fish tissues are sensitive indicators of aquatic pollution and have a high mercury bioaccumulation capacity for both organic and inorganic forms [216]. Although damages have been observed in the gill arches, liver, kidney, blood parameters, olfactory epithelium and nervous system [217-219], some reports showed that mercury compounds could be retained in the tissues of animals for long periods, resulting in irreversible damages, such as neurological impairment and lesions, behavioral and cognitive changes, ataxia, as well as convulsions, in addition to its harmful effect on reproduction [220, 221]. Necrosis and fibrosis of renal tubular lumen was reported earlier in chronic mercury exposed Clarias batrachus kidney [222]. At very low concentrations mercury reduces the viability of spermatozoa, reduce egg production and affect the survival rate of developing eggs and fry [223]. Zaki et al. [224] observed a significant increase in cholesterol, alkaline phosphatase, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and cortisol levels and a significant decrease in haemoglobin (Hb), haematocrite (Ht), mean total protein values in serum and body weight of Clarias gariepinus fish fed with 15 mg/kg diet mercuric oxide for 4 weeks.

Nickel (Ni)

Nickel is a ubiquitous trace metal and occurs in soil, water, air, and in the biosphere. It is emitted into the environment from both natural and man-made sources. Nickel is released during nickel mining and by industries that convert scrap or new nickel into alloys or nickel compounds or by industries that use nickel and its compounds. These industries may also discharge nickel in wastewater. Nickel is also released by oil-burning power plants, coal-burning power plants and trash incinerators [225]. Once released to the environment, nickel readily forms complexes with many ligands, making it more mobile than most heavy metals [147].While nickel is an essential element at low concentrations for many organisms, it is toxic at higher concentrations [226]. Exposure to nickel may lead to various adverse health effects, such as nickel allergy, contact dermatitis, and organ system-toxicity. According to the Institute of Medicine [227], nickel can cause respiratory problems and is carcinogenic [228]. Numerous studies have confirmed the carcinogenic potency of nickel compounds in experimental animals [147]. Friedrich and Filice [229] studied the intake and accumulation pattern of nickel in Mytules edulis over a period of 4 weeks. The accumulation pattern was found to be varying with time. As with the toxicity of other metals, the toxicity of nickel compounds to aquatic organisms is markedly influenced by the physicochemical properties of water [71]. The toxicity of nickel may be due to nickel being in contact with the skin (body surface), penetrating the epidermis and combining with body protein [230]. Sreedevi et al. [231] studied the effect of nickel on freshwater fish Cyprinus carpio treated to various concentrations. The study indicates that nickel accumulation is more in lethal than in sub-lethal concentrations. After toxic exposure to nickel compounds, the gill chambers of the fish are filled with mucus and the lamellae appeared dark red in colour [232]. Nickel, for instance, induces histopathological changes in the different tissues of the silver carp (Hypophthalmichthys molitrix) including fusion of the gill lamellae and tissue hypertrophy [233]. Al- Attar [225] studied the effect of nickel on freshwater fish Oreochromis niloticus treated with sublethal concentration of nickel and found decreased values of serum sodium, chloride and osmolality, whereas levels of serum glucose, cholesterol, total protein, albumin, amylase, lipase, alanine aminotransferase and aspartate aminotransferase were significantly elevated. Also, he reported some histological changes in fish gill structure which included hyperplasia, hypertrophy, shortening of secondary lamellae and fusion of adjacent lamellae. Cyprinus carpio fingerlings exposed to nickel showed decreased blood parameters (erythrocyte, leucocytes, hematocrit and hemoglobin count) and lowered values of mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH) and mean corpuscular hemoglobin concentration (MCHC) when compared with the control [234].

Selenium (Se)

Selenium is an essential trace element required in the diet for normal growth and physiological function of animal, including fish [235-237]. This element is required for normal development, growth and maintenance of homeostatic functions at trace concentrations [238]. It is a part of the antioxidant defense system and is involved in thyroid hormone metabolism, in spermatogenesis, and probably in other processes unidentified to date [239]. Se is involved in many functions such as moderation of the immune system and prevention of cancer, acting directly as a support for the organismal health [240]. It is widely distributed throughout the environment and is found in most ground and surface waters at concentrations between 0.1 and 0.4 μg/L of Se [241,242]. Agricultural drain water, sewage sludge, fly ash from coal-fired power plants, oil refineries, and mining of phosphates and metal ores are all sources of selenium contamination of the aquatic environment [243,244]. Sorensen [83] documents the tendency of selenium to concentrate more highly in the liver, gonads, and kidneys of fish than in muscle. Se is a suspected carcinogen and teratogen [245] and becomes very toxic to fish when it is elevated above a threshold concentration [246]. The difference between nutritional requirement and toxic levels is very narrow for Se. For most fish, the requirement range is 0.25–0.70 μg Se/g diet [247,248] and the toxic levels with prolonged exposure can be as low as 3 μg Se/g diet [235]. The U.S. Environmental Protection Agency (USEPA) proposed a chronic criterion for selenium at a whole body fish concentration of 7.91 μg/g dry weight [241,242]. Excess selenium, even as low as 3-8 ppb, in the water can cause numerous life-threatening changes in feral freshwater fish [83]. However, there is still controversy regarding the proposed selenium threshold for the protection of fish populations [249]. The most significant effect of excess Se in fish is growth inhibition, tissue damage, damage on most biomolecules (namely lipids, proteins and DNA), reproductive impairment, larval deformities and mortality [250]. Other documented effects in fish include skin lesions, cataracts, swollen gill filament lamellae, myocarditis, and liver and kidney necrosis [244].

Vanadium (V)

The emission of vanadium into the environment is mostly associated with industrial sources, especially oil refineries and power plants using V-rich fuel oil and coal [251]. Such sources can release appreciable amounts of V and combine to increase natural background levels associated to rock weathering and sediment leaching [189]. Vanadium is essential for normal growth where it has been found to regulate the activity of various enzymes that induce pronounced changes in metabolic functions. At higher concentrations (>1–10 nM), vanadium becomes toxic to the cells inducing several injury effects at specific target organs, such as liver and kidney, inducing oxidative damage, lipid peroxidation and changes in haematological, reproductive and respiratory systems [252-256]. Earlier studies indicated that in vivo exposure to 5 mM vanadate or cadmium solutions intra peritoneally injected affect differently subcellular metal distribution and antioxidant enzymes activities (catalase, CAT; superoxide dismutase, SOD; and glutathione peroxidases, GPx), induce lipid peroxidation, methaemoglobinemia and tissue damage in several organs, namely kidney, liver and heart of the H. didactylus [257-259].Vanadium toxicity to Clarias lazera fish caused a significant decrease in body weight, haemoglobin (Hb), haematocrite (Ht) and protein levels, and increase in cholesterol, alkaline phosphate, cortisol, aspartate aminotransferase (AST) enzyme, alanine aminotransferase (ALT) enzyme, urea and creatinine levels. Also, abnormal swimming, lighting of the skin and hemorrhages were seen on the external body surface [260].

Zinc (Zn)

Zinc (Zn) is the second most abundant trace element after Fe and is an essential trace element and micronutrient in living organisms, found almost in every cell and being involved in nucleic acid synthesis and occurs in many enzymes [45]. Additionally, Zn is involved in more complicated functions, such as the immune system, neurotransmission and cell signaling [261,262]. It may occur in water as a free cation as soluble zinc complexes, or can be adsorbed on suspended matter. Zinc and its compounds are extensively used in commerce and in medicine. The common sources of it are galvanized ironwork, zinc chloride used in plumbing and paints containing zinc [263]. Zinc wastes can have a direct toxicity to fish at increased waterborne levels [264], and fisheries can be affected by either zinc alone or more often together with copper and other metals [83,265]. The main target of waterborne Zn toxicity are the gills [262], where the Ca2+ uptake is disrupted, leading to hypocalcemia and eventual death [264]. The other endpoints of toxicity vary amongst freshwater and marine fish with the most common being survival, growth, reproduction, and hatching [262]. Also, fish kidney is considered as a target organ for Zn accumulation [40]. The clinical symptoms and patho-anatomical picture of zinc poisoning in fish are similar to those found for copper [71, 266]. Zinc causes mortality, growth retardation, respiratory and cardiac changes, inhibition of spawning, and a multitude of additional detrimental effects which threaten survival of fish. Gill, liver, kidney, and skeletal muscle are damaged [83]. In fish, zinc significantly increases the activity of serum transaminases in some freshwater fishes [267]. Gill proliferation and stimulation of mucous cells and an increase in mucus production generally occur in response to zinc exposure [268]. The first sign of gill damage is detachment of chloride cells from underlying epithelium. The sub epithelial space enlarges because of detachment of epithelial cells from basal lamina. Water to blood distance can more than double, making gaseous exchange more difficult [83]. Abd El-Gawad [269] mentioned that, Oreochromis niloticus fish exposed to zinc sulphate, showed pale and congested gills. The epithelial covering of the gill filaments was hyperplastic and edematous with vacuolated epithelial covering of the gill rakers. The lamellar blood spaces showed telangiectasis. Zinc exposure has been shown to induce histopathological alterations in ovarian tissue of Tilapia nilotica (degeneration and hyperaemia) [270] and liver tissue of Oreochromis mossambicus (hyalinisation; hepatocyte vacuolation; cellular swelling and congestion of blood vessels) [112]. Finally, for the protection of aquatic systems and fish from heavy metals pollution, new methods of eliminating pollutants, including heavy metals, from wastewater must be applied. Among these are treatments with powdered or granular activated carbon, ozonation, ultraviolet light, and reverse osmosis [271]. For wastewater treatment plants (WWTPs), powdered or granular activated carbon and/or ozonation in combination with different types of sand filters are currently the most common advanced wastewater treatment technologies [20, 272]. In addition, new technologies such as environmental flow diagram (EFD) must be considered [273-275].

Conclusion and recommendations

In conclusion, the toxic effects of heavy metals in fish have been demonstrated in the present study. It is abundantly clear that metals induce an early response in the fish as evidenced by alterations both at structural and functional levels of different organs include enzymatic and genetic effects, thereby affecting the innate immune system of exposed fish and/or increasing susceptibility to multiple types of disease.

Biomarkers can offer additional biologically and ecologically relevant information – a valuable tool for the establishment of guidelines for effective environmental management. So, it can be stated that fish biomarkers are necessary for monitoring environmentally induced alterations to assess the impact of xenobiotic compounds (i.e. heavy metals) on fish. Also, it is recommended that treatment of all kinds of wastewaters, sewage and agricultural wastes must be conducted before discharge into the aquatic systems. Also, enforcement of all articles of laws and legislations regarding the protection of aquatic environments must be taken into considerations.

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