effects of resveratrol and tannic acid on apoptosis in colon adenocarcinoma cell line

To investigate the effects of resveratrol and tannic acid on apoptosis, and Bcl-2 homologous antagonist/killer [Bak] and fas associated death domain [FADD] proteins in the CaCo-2 cell line. In the present study, resveratrol and tannic acid were administrated in the CaCo-2 cell line at doses of 25, 50, and 100 uM. The CaCo-2 cells were grown and cultured in the Medical Biology Department, Eskisehir Osmangazi University, Eskisehir, Turkey in 2007. The effects of these agents on apoptotic index were determined by Apop Taq peroxidase kit and their effects on the ratios of Bak and FADD proteins by the immunohistochemical staining method at 24, 48, and 72 hours. Stained and non-stained cells in 30 separate areas of the 3 separate chamber slides, prepared for each group, were counted. The percentage of apoptosis, and Bak and FADD proteins was calculated with the control. Mean +/- standard error values were calculated for the 3 experiments. Apoptotic index, Bak protein percentage ratio, and FADD protein percentage ratio values in all groups that received tannic acid and resveratrol increased when compared within the groups. This increase was found to be time and dose independent in all parameters. Cells undergo apoptosis in 2 pathways [mitochondrial and death receptor] in resveratrol and tannic acid induced CaCo-2 cells

effect of paclitaxel on rats following benzo [a] pyrene treatment

To observe the effects of paclitaxel on rats that received benzoapyrene. In this study, 45 male Sprague-Dawley rats aged 2-month-old were used, which were housed at the Medical Biology Department of Eskisehir Osmangazi University, Eskisehir, Turkey in 2006. Urine, blood, liver, and kidney tissue samples of Sprague Dawley rats treated with benzoapyrene and paclitaxel were examined in our study. Biochemical data were evaluated on urine and blood samples, and liver and kidney tissue samples were investigated by light microscopy. Superoxide dismutase, catalase activities, and malondialdehyde values in the group which received benzoapyrene were significantly different than the control, and most of these parameters came close to control values in the group that received paclitaxel following benzoapyrene application. Histological appearances of the samples of all rats also supported the biochemical results. The present study indicated that liver and kidney structures damaged by benzoapyrene may be restored by paclitaxel