were depleted, probably due to the augmentation of lipid
peroxidation. The activity of CAT also decreased in the
cisplatin treated group, which in turn increased lipid peroxidation.
Due to this, the free radicals and reactive oxygen
species were involved in cisplatin induced oxidative stress. T.
cordifolia treatment (200 and 400 mg/kg body weight, oral) was
found to prevent the lipid peroxidation by enhancing renal
antioxidant enzymes. These observations also support the
hypothesis that part of the mechanism of nephrotoxicity in
cisplatin treated animals is related to depletion of antioxidant
system. Histopathological studies also supported the above
results. The inhibition of antioxidant enzyme activity in
cisplatin induced nephrotoxicity and prevention of this
altered in rats treated with T. cordifolia support the rationale
for the use of antioxidants and antioxidant extracts to
improve cisplatin chemotherapy to treat cancers. The T. cordifolia
is one such a medicinal plant consists of antioxidant
properties which prevent the toxicity of cisplatin therapy. In
summary a single dose of cisplatin leads to the inhibition of
renal antioxidant enzyme activity, depletion of renal GSH
levels and increase in serum urea, creatinine and UTP levels.
A combined therapy with T. cordifolia and cisplatin would be
more beneficial than cisplatin alone. The findings suggest the
potential use of T. cordifolia in adjuvant therapy of cancer.