Arsenic (As) is a well-known human
carcinogen and a potent hepatotoxin. Environmental exposure to
arsenic imposes a serious health hazard to humans and other animals worldwide.
Tetrahydrocurcumin (
THC), one of the major metabolites of
curcumin, exhibits many of the same physiological and pharmacological activities as
curcumin and in some systems may exert greater
antioxidant activity than the
curcumin. It has been reported that
THC has
antioxidant efficacy attributable to the presence of identical β-diketone of 3rd and 5th substitution in
heptane moiety. In the present study, rats were orally treated with
arsenic alone (5 mg kg(-1) bw/day) with
THC (80 mg kg(-1) bw/day) for 28 days. Hepatotoxicity was measured by the increased activities of serum hepatospecific
enzymes, namely
aspartate transaminase,
alanine transaminase,
alkaline phosphatase and
bilirubin along with increased elevation of
lipid peroxidative markers,
thiobarbituric acid reactive substances. And also elevated levels of serum
cholesterol,
triglycerides,
free fatty acids and
phospholipids were observed in
arsenic intoxicated rats. These effects of
arsenic were coupled with enhanced mitochondrial swelling, inhibition of
cytochrome c oxidase, Ca(2+)
ATPase and a decrease in mitochondrial
calcium content. The toxic effect of
arsenic was also indicated by significantly decreased activities of enzymatic
antioxidants such as
superoxide dismutase,
catalase, and
glutathione peroxidase along with non-enzymatic
antioxidant such as
reduced glutathione. Administration of
THC exhibited significant reversal of
arsenic induced toxicity in hepatic tissue. All these changes were supported by the reduction of
arsenic concentration and histopathological observations of the liver. These results suggest that
THC has a protective effect over
arsenic induced toxicity in rat.