Effect of Vitamin E on Ethanol Induced Exocrine Pancreatic Injury in Adult Male Albino Rat: Light, Electron microscopic and Biochemical Study.

Document Type : Original Article

Authors

Human Anatomy and Embryology Department, Faculty of Medicine, Cairo University, Egypt

Abstract

Background: Excessive alcohol intake is a leading factor of chronic pancreatitis. Chronic administration of ethanol causes marked pancreatic oedema, inflammatory cellular infiltration, acinar necrosis, and fibrosis. Vitamin E is a fat-soluble vitamin that helps in formation of red blood cells and prevention of oxidation in the body. The current study aimed to compare between the protective effect of vitamin E and withdrawal from ethanol in ethanol induced injury of exocrine pancreas. Methods: Fifty adult male albino rats were divided into five equal groups: (control, sham control, ethanol-treated group, ethanol and vitamin E-treated group, withdrawal group). Light microscopic examination was done using hematoxylin and eosin and Masson’s trichrome stains. Electron microscopic examination was carried out using transmission electron microscopy. Serum level of lipase and alpha amylase was measured in blood samples. Measurements of malondialdehyde (MDA) and superoxide dismutase (SOD) activity in pancreatic tissue homogenates were performed.
Results: Examination of specimens of ethanol treated rats revealed markedly disturbed pancreatic architecture, pancreatic acini, widening of spaces, dilated interlobular ducts, pyknotic nuclei, destruction of mitochondria with loss of cristae and extensive fibrosis. These morphological changes were associated with significant increase in serum lipase, alpha amylase, MDA and decrease in SOD activity. Ethanol and vitamin E co-administration markedly ameliorated these histological alterations, but withdrawal from ethanol could not improve its harmful effects. Conclusion: this study revealed that concomitant administration of vitamin E with ethanol could significantly improve ethanol induced exocrine pancreatic damage, possibly due to its antioxidant property.

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