Abstract
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.
Highlights
Alcohol abuse and alcoholism are major worldwide health problems since ancient times and first coined medically at 1852 A.C. by Magnus Huss - Swedish professor of medicine - till recorded as the fourth most common cause of death among adults of USA at 1983 [15]
The aim of the present study is to evaluate the protective effects of zinc against acute alcoholic hepatotoxicity as regard histopathological and histochemical parameters
Statistical analysis of the present study showed that acute alcohol administration caused significant wide spread hepatocytic apoptosis which was in agreement with some previous studies [19,28,29,30,31]
Summary
Alcohol abuse and alcoholism are major worldwide health problems since ancient times and first coined medically at 1852 A.C. by Magnus Huss - Swedish professor of medicine - till recorded as the fourth most common cause of death among adults of USA at 1983 [15]. Zinc importance comes the second after iron among essential trace metals. It is directly or indirectly involved in the action of >300 known enzymes and >1000 transcription factors. Zinc is a cytoprotective element as had been reported six decades ago [14], making the cell more resistant and less vulnerable to apoptotic induction agents. It stabilizes and protects macromolecules (e.g. proteins, DNA and microtubules) from oxidation and proteolysis through inhibiting caspases and interfering the activation of endonucleases [15,16]. Zinc is needed at a daily amount between 2 mg for newborn and increasing with growth to be 12 mg (upper limit is 40 mg/ day) for adults and being available in rich amount among oysters, red meat, poultry and sea food (e.g. crab and lobsters) and to a moderate
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