alexa Impact of low dose of organophosphate, monocrotophos on the epithelial cells of gills of Cyprinuscarpiocommunis Linn.--SEM study


Toxicology: Open Access

Author(s): Johal MS, Sharma ML, Ravneet

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The paper deals with the deleterious changes at ultrastructural level of the epithelial cells of gills of Cyprinus carpio communis Linn. upon exposure to 1/10th of LC50 of monocrotophos which is considered to be insignificant concentration from toxicological point of view. The gills of the fish are the primary corridor formolecularexchange between the internal milieu of a fish and its environment. Gills perform numerous functions such as oxygen uptake and CO2 excretion, osmoregulation, acid-basic balance, excretion of nitrogenous compounds and taste. Hazardous chemicals present in water may alter the morphology of the epithelial cells of gills of the fish, which may affect the process of diffusion of gases and ultimately the overall health of the fish. To prove this fact Cyprinus carpio communis Linn. was kept in water for 30 days having low concentration of 0.038 ppm (1\10th of LC50) of monocrotophos and an attempt was made to study the different types of degenerations produced in the epithelial cells of gills as compared to the normal epithelial cells of gills of this culturable fish using Scanning Electron Microscope (SEM) technique. The ultrastructural changes due to the toxic exposure at finer scale were thinning of microridges, upliftment of epithelial cells, development of hyperplasia, decrease in the density of mucous cells which are considered to be the first line of defence and total dystrophy of epithelial tissue. Thus, it is opined that a low concentration of monocrotophos has the potential to bring different type of degenerations at finer scale hence affecting the fish's health drastically and altering the fitness of the fish in water even having insignificant amount of this toxicant in the ambient water

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This article was published in Journal of Environmental Biology and referenced in Toxicology: Open Access

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