595-600<span style="font-size:12.0pt;line-height:
115%;font-family:" times="" new="" roman";mso-fareast-font-family:"times="" roman";="" mso-ansi-language:en-in;mso-fareast-language:en-in;mso-bidi-language:hi"="" lang="EN-IN">Effect
of prefeeding dehydrated amaranth (A. gangeticus) leaves at 10 and 20%
levels on a chemical toxicant, dimethylhydrazine (DMH)-induced free radical
stress in rat liver was evaluated. DMH-induced rise in hepatic malondialdehyde
(MDA), was diminished by AL. AL intake resulted in a significant increase in
hepatic glutathione (GSH). The feeding of AL at 10%level increased the hepatic
glucose-6- phosphate dehydrogenase (G-6-PDH) activity, while that at 20% level
increased the hepatic glutathione reductase (GSSGR) as well, in addition to
G-6-PDH. Amaranth leaves at 10 and 20% levels of feeding diminished the hepatic
superoxide dismutase and glutathione peroxidase (GSH-Px) activities. DMH influenced
adversely the hepatic antioxidant enzyme activities. Simultaneous
administration of DMH and feeding of AL enhanced the DMH-induced decrease in hepatic GSH-Px.
DMH enhanced formation of micronuclei was reverted significantly by AL intake. Hence, it was
concluded that the consumption of AL
at 20% level reduced DMH-induced impaired antioxidant status in rat liver.</span