The ADW protection against see more BPA induced cytotoxicity was evaluated by MTT assay (Fig. 4). The cells were incubated with ADW (100 μg/mL) and BPA (100 nM) for 0-72 h and the cell viability was measured. BPA induced 6%, 35% and 56% cytotoxicity in HepG2 cells at 24, 48 and 72 h. The mitochondrial

respiration inhibitor Antimycin A was used as negative control was very effective and caused 57%, 65% and 84% cytotoxicity to cells at 24, 48 and 72 h respectively. When ADW (100 μg/mL) was co-incubated with BPA, cell viability was significantly increased from 45% to 78% compared to BPA treated group and showed rescue effect of ADW against BPA induced toxicity. The oxygen consumption rate in the mitochondria of HepG2 cells treated with BPA was evaluated and the results are given in Fig. 5(a). The results show that BPA and antimycin A treated cells showed to decreased oxygen consumption compared to control which was measured as fluorescent life time signal (μs) over a period of 0-200 mins. When the cells were treated with ADW along with BPA the oxygen consumption was increased significantly over 0-200 mins and the oxygen consumption pattern was comparable to control cells. The ATP concentration was measured in the HepG2 cells treated with BPA and the results are presented in Fig. 5(b). The results

show that ATP level in the cells treated with BPA www.selleckchem.com/products/Sunitinib-Malate-(Sutent).html and antimycin A was significantly reduced by 7.5 folds and 5.45 folds compared to control at 24 h incubation time. While cells treated with ADW along with BPA could withstand the ATP depletion in a significant manner. The mitochondrial membrane potential (ΔΨM) using JC-1 stain was measured in HepG2 cells treated with BPA and the results are given in Fig. 5(c). At 24 h the ΔΨM was increased significantly by 3.9 and 5.25 folds in cells treated with BPA and antimycin A. Whereas, the cells treated with ADW along with BPA significantly inhibited the increase in ΔΨM and inhibited mitochondrial membrane damage. Ureohydrolase The lipid peroxidation was significantly increased by 2.4 folds upon addition of BPA in HepG2 cells as shown in Fig.

6. The cells treated with antioxidants such as Vitamin E and BHA could significantly inhibit the lipid peroxidation induced by BPA. In similar lines, ADW addition was very effective and significantly reduced the lipid peroxidation by 63.16% compared to BPA treated cells. The effect of BPA treatment on GSH and GSSG levels in the HepG2 cells was evaluated and the results are given in Table 2. The results showed that non-enzymic antioxidant glutathione content was significantly reduced by 2.94 folds upon BPA treatment compared to control cells. The antimycin A treated group showed 4.29 folds reduction in GSH content. While, addition of ADW and Vitamin E to cells treated with BPA showed to inhibit GSH depletion significantly.