Chronic Aluminium Oral Administration Induces Reversible Preventable Biochemical and Histological Hepatic Alterations in Rats
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Objectives: The present study aimed to evaluate the biochemical and histological findings of chronic oral administration of aluminium (Al) in rats and if concomitant administration of vitamin C or vitamin E could ameliorate these effects. Materials & Methods: The study comprised 110 normal healthy growing male albino rats assigned to control group (n=10): did not receive medications, ALUM Group (n=40): received aqueous solution of aluminium chloride (AlC13) orally in a daily dose of 330 mg/kg for 3 months, ALUM+E Group (n=30): received similar solution of AlC13 with vitamin E in a daily dose of 300 mg/kg and ALUM+C Group (n=30): received similar solution of A103 with vitamin C in a daily dose of 100 mg/kg; 10 animals in each group were sacrificed monthly. Blood samples were drawn for estimation of serum levels of liver function parameters and animals were sacrificed and liver was dissected for histological examination. Results: Liver function parameters showed steadily progressive increase with the duration of exposure that was significant in ALUM compared to control group. Combined treatment with antioxidants ameliorated Al-induced hepatotoxi city, however, vitamin C treatment was more beneficial as serum levels of ALT and ALP were non-significantly higher compared to control levels throughout the study period and serum bilirubin levels started to be significantly higher only at 3" month of treatment On contrary, vitamin E treated rats had significantly elevated serum levels of estimated parameters compared to control levels with significantly higher serum levels of AST and ALP compared to ALUIVI+C group. In ALUM group histological examination revealed progressive harmful effect manifested as marked cellular infiltration with lymphocytes and plasma cells around the portal tracts, dilated congested portal vein with bile duct proliferation after 1st month of administration, later on the liver showed dilated congested portal vein with marked cellular infiltration around the portal area and bile duct proliferation and after three months of treatment, the liver showed ballooning of hepatocytes due to marked hydropic degeneration of hepatocytes and dilated congested central vein with and severe hydropic degeneration of hepatocytes. In ALUM+E group, there was mild cellular infiltration and bile duct proliferation with some degree of congestion progressed to marked cellular infiltration and severe dilatation and congestion of central veins with mild dilatation of blood sinusoids, and the hepatocytes showed mild degree of hydropic degeneration at the end of the 3^1 month. However, in ALUIVI+C group there was only mild cellular infiltration around the portal tracts that became marked at the end of the 2=, month and later on rats showed mild degree of dilatation and congestion of the central veins, mild dilatation of blood sinusoids but with no portal vein congestion and hepatocytes appeared normal throughout the study period. Conclusion: It could be concluded that chronic exposure to aluminium induced reversible hepatotoxicity manifested clinically as significant elevation of liver function tests and coadministration of vitamin C could ameliorate both biochemical and histological effect of chronic aluminium exposure on liver.