Abstract
Abstract Lovastatin, an inhibitor of the rate-limiting enzyme in the cholesterol biosynthetic pathway, hydroxymethylglutaryl coenzyme A reductase, has shown interesting antiproliferative activities in cell culture and in animal models of cancer. The present study was carried out to evaluate the anticancer potentials of lovastatin against Dalton's lymphoma ascites (DLA). The lovastatin given orally to mice at the dose of 5, 25, 50 mg/kg body weight for 10 days caused significant reduction in percent increase in body weight when compared to the mice of the DLA control group. Restoration of hematological and biochemical parameters towards normal was also observed. Tumor control animals inoculated with DLA showed a major decrease in the level of catalase (CAT), superoxide dismutase (SOD) and increase in thio-barbituric acid reactive substances (TBARS) levels in liver. Treatment with lovastatin (5, 25, and 50 mg/kg body weight) doses given orally caused a reversal of these changes towards the normal. This confirms the potent hepatoprotective and antioxidant nature of lovastatin. Lovastatin (50 mg/kg body wt, i.p) was effective to accelerate the apoptosis in the ascites tumor bearing mice that was evident from the fragmentation of DNA in gel electrophoresis. Further the morphological analysis of DLA cells aspirated from the lovastatin treated animals showed a significant (P<0.01) increase of apoptotic cells than the control animals. The proapoptotic and antioxidant activities of the lipid lowering drug lovastatin may further suggest its possible therapeutic use as a cancer chemopreventive agent. Citation Information: Mol Cancer Ther 2013;12(11 Suppl):A255. Citation Format: Kavitha Velusamy, Janani Balraj, Palaniswamy Muthusamy, Angayarkanni Jayaraman. Antitumor activity and antioxidant status of fungal lovastatin against Dalton's lymphoma ascites in Swiss albino mice. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2013 Oct 19-23; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2013;12(11 Suppl):Abstract nr A255.
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