Abstract
Abstract Piper nigrum a spice, has widely used in various systems of traditional medicine. Therefore, the present study was designed to investigate the chemopreventive potential of P. nigrum on cell proliferation, apoptosis in DMBA-induced skin papillomagenesis and its influence on the levels/activity of enzymes associated with xenobiotic metabolism and antioxidant status in mice. Two different doses (2 and 4%) of P. nigrum were given orally to the mice in the test diet at peri-initiational stage. DMBA and croton oil was used to induce and promote skin papillomagenesis respectively. For biochemical studies, mice were given with the same doses of P. nigrum in the test diet for two weeks. There was a significant reduction in (i) tumor burden to 3.0 and 2.4 (positive control: 6.4); (ii) tumor volume to 1.7 and 2.4 (positive control: 4.7); and (iii) tumor incidence 60 % and 50 %, respectively in case of 2 and 4% test diet treated animals relative control (100%). P. nigrum treatment resulted in upregulation of Bax with concomitant decrease in antiapoptotic protein Bcl-2 and PCNA in mouse skin tumors. P. nigrum showed a significant increase in the content/activities of phase I and phase II enzymes with the test diets. A significant enhancement in the activities of antioxidant enzymes were observed at 2 and 4% test diets of P. nigrum. Glyoxalase I activity and the content of reduced glutathione were significantly elevated. Expectedly, the activity of lactate dehydrogenase, exhibited a significant reduction at both the doses of test diets. The Chemopreventive effect of P. nigrum could be credited to its ability to inhibit cell proliferation and enhance apoptosis as well as to modulate phase I, phase II enzyme systems and also antioxidant status. The present findings may have some significance from the point of view of lowering the risk of cancer in human population. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1594. doi:1538-7445.AM2012-1594
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