Abstract: Oral administration of arsenic trioxide (3 and 6 mg/kg body
weight/d) for 30 d caused, as compared with vehicle control, dose-dependent
significant reductions in body weight, absolute weight, protein, glycogen, as
well as, total, dehydro and reduced ascorbic acid contents both in the liver
and kidney of arsenic-treated mice. Succinic dehydrogenase (SDH) and
phosphorylase only in the liver activities were significantly reduced in a
dose-dependent manner. Acid phosphatase activity was significantly decreased in
the liver of low dose arsenic-treated animals; however, significant rise in its
activity was observed in high dose group. As compared with vehicle control,
treatment also caused significant dose-dependent reductions in SDH, alkaline
phosphatase and acid phosphatase activities in the kidney of mice. Vitamin E
cotreatment as well as, 30 d withdrawal of arsenic trioxide treatment with or
without vitamin E caused significant amelioration in arsenic-induced toxicity
in mice. Administration of vitamin E during withdrawal of treatment also caused
significant amelioration as compared from only withdrawal of the treatment. It
is concluded that vitamin E ameliorates arsenic-induced toxicities in the liver
and kidney of mice.
