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. |
