Histopathological and Histochemical Assessment of the Protective Effects of Zinc on Ethanol-Induced Acute Hepatotoxicity in Adult Albino Rats
- *Corresponding Author:
- Elshennawy TMA
Department of Histology,Faculty of Medicine
Omar Al-Mukhtar University
Tobruk Branch, Libya
E-mail: [email protected]
Received date: February 23, 2015; Accepted date: April 06, 2015; Published date: April 08, 2015.
Citation: Elshennawy ATM, Sayed SR, Saber EA, Rifaai RA (2015) Histopathological and Histochemical Assessment of the Protective Effects of Zinc on Ethanol-Induced Acute Hepatotoxicity in Adult Albino Rats. J Cytol Histol 6:321. doi:10.4172/2157-7099.1000321
Copyright: © 2015 Elshennawy ATM, 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.
Alcoholic hepatotoxicity is a worldwide major cause of death. The objectives of the present study are to evaluate qualitatively as well as to a less extent quantitatively the protective effects of zinc on acute alcoholic hepatotoxicity. Forty five adult male albino rats were equally divided into three groups. Group I, the ‘control’ one while group II, ‘ethanol-treated’ was received ethanol with a total accumulative dosage of 15 g/kg/36 hours (10 g/kg/day) by three equally divided gavages of 5 g/kg/12 hours each, to simulate acute alcohol intoxication or quadruple bingedrinking among humans. Group III, ‘zinc/ethanol-treated’ was received an intraperitoneal injection of zinc sulfate as 5 mg/kg/day for three days before ethanol administration. Qualitative histological and histochemical parameters were undertaken by using hematoxylin and eosin, iron hematoxylin, periodic acid-Schiff and detectors for the activity of succinic dehydrogenase and ATPase. Also some quantitative morphometric parameters were utilized. Ethanol-treated animals showed loss of normal architecture of hepatic lobules, high cellular degeneration and fatty changes, increased apoptosis, marked mitochondrial affection, inflammatory infiltration in portal space and sinusoids, depletion of glycogen content and decrease in the activity of succinic dehydrogenase and ATPase. Zinctreated animals showed ameliorative changes as mild cellular degeneration, proportionally less apoptosis, mild mitochondrial affection, almost no inflammatory infiltration, mild decrease of glycogen content and mild decrease of succinic dehydrogenase activity while ATPase activity was rendered normal. These results conclude that Zinc is an essential hepatoprotective agent against alcoholic hepatotoxicity. Zinc is qualified to be the first essential and the modest trace element in the map of prophylaxis and management of liver diseases. Finally, the classical histological, histochemical and morphometric techniques are fair enough to explore the big picture of these effects.