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route and time of exposure to the metal, the activity of SOD and CAT were significantly higher in the brain relative to the control, but the level of LPO was not significantly altered. Liver damage induced by oral cadmium after one and three months exposure was clearly shown by the increased activities of plasma hepatic marker enzymes namely, L-aspartate aminotransferase activity (L-AST), L-alanine aminotransferase activity (L-ALT), alkaline phosphatase activity (ALP) along with increased level of LPO indices and a corresponding decrease in the activities of SOD and CAT in the liver. Similarly, liver damage induced by ocular exposure to Cd for one month was manifested as increased plasma L-AST, L-ALT and ALP activities with an increased LPO and a corresponding decrease in the activities of SOD and CAT in the liver. However, the plasma parameters did not significantly change after three months of exposure to ocular Cd, except plasma ALP activity which remained significantly higher. The liver LPO was also not significantly different from the control after three months
exposure to ocular Cd, although the SOD and CAT activities significantly decreased. Thus the major finding of the present study was that in relation to ocular exposure, oral exposure to Cd was more toxic to the liver at the
end of three months of exposure.