Ameliorative effects of quercetin against bisphenol A-caused oxidative stress in human erythrocytes: an in vitro and in silico study.

Bisphenol A (BPA) is an endocrine disruptor of xenobiotic type, mainly used for the production of polycarbonate plastic, epoxy resins and non-polymer additives. Because of its wide usages in the environment, the toxic effects of BPA have proved to be harmful to human health. However, its effects on human haemoglobin remain unclear. The affinity between BPA and haemoglobin, as well as erythrocytes, is an important factor in understanding the mechanism of the toxicity of BPA. Flavonoids are strong antioxidants that prevent oxidative stress and Quercetin is a flavonoid found in numerous vegetables and fruits. Therefore, the present investigation was undertaken to investigate whether Quercetin can be used to alleviate the toxic effects of BPA in vitro in human red blood cells (RBC). Venous blood samples were collected from healthy, well-nourished adult volunteers (25-30 years old) by phlebotomy. In a RBC suspension with a cell density of 2 × 104 cell per mL, the concentration of BPA (25-150 µg mL-1) was found to cause an increase in the lipid peroxidation (LPO) and a decrease in the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in human RBC. However, the concurrent addition of BPA (150 µg mL-1) and quercetin (10-50 µg mL-1) lead to significant amelioration. In silico studies gave structural insight into BPA and quercetin to decipher the plausible binding mechanism and molecular level recognition.

Testing the efficacy of quercetin in mitigating bisphenol A toxicity in liver and kidney of mice.

Quercetin (3,5,7,3',4'-pentahydroxy flavone) is a potent antioxidant found in various fruits and vegetables. The present investigation was an attempt to evaluate the mitigatory effect of quercetin on the damage caused by bisphenol A (BPA; 2,2-bis (4-hydroxyphenyl) propane), a well-known xenoestrogen, on liver and kidney of mice. Swiss strain adult male albino mice were orally administered with 120 and 240 mg/kg body weight (bw)/day BPA with or without quercetin (60 mg/kg bw/day) for 30 days. On the completion of the treatment period, animals were killed; organs were isolated and used for the study. Results revealed that oral administration of BPA for 30 days caused significant and dose-dependent decrease in body weight. Absolute and relative organ weights, total lipid and cholesterol contents were significantly increased in liver and kidney of mice when compared with vehicle control. BPA treatment also caused, when compared with vehicle control, a statistically significant reductions in the activities of catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase as well as in glutathione and total ascorbic acid contents; however, significant increase was found in malondialdehyde (MDA) levels. Histopathological studies revealed hepatocellular necrosis, cytoplasmic vacuolization and decrease in hepatocellular compactness in liver as well as distortion of the tubules, increased vacuolization, necrosis and disorganization of glomerulus in the kidney of BPA-treated mice. All these effects were dose-dependent. Co-treatment with quercetin (60 mg/kg bw) and BPA (low dose and high dose) alleviates the changes in body weight, as well as absolute and relative organ weights of mice. It also ameliorates the oxidative stress created by BPA by lowering MDA levels and by increasing enzymatic and nonenzymatic antioxidants as well as it brings back the normal histoarchitecture of liver and kidney of mice. The present results revealed that graded doses of BPA caused oxidative damage in liver and kidney of mice, which is mitigated by quercetin.

Quercetin alleviates bisphenol A-induced changes in nucleic acid and protein contents in mice.

The present study was an attempt to examine toxic effects of bisphenol A in liver and kidney of mice and its alleviation by quercetin. Oral administration of bisphenol A (60 and 120 mg/kg b. w./day) for 30 days caused, as compared to vehicle control significant, dose-dependent decrease in DNA, RNA and protein contents in liver and kidney of mice. Supplementation of quercetin (60 mg/kg b. w./day) along with bisphenol A for 30 days caused, as compared to bisphenol A alone treated groups, significant alleviation in DNA, RNA and protein contents. The amelioration was comparatively higher for high dose bisphenol A plus quercetin treated group than that of low dose plus quercetin treated group.

The ameliorative effect of black tea extract and quercetin on bisphenol A-induced cytotoxicity.

The purpose of our study was, to explore the possible ameliorating effects of black tea extract and quercetin, against bisphenol A-induced cytotoxicity. For this, human red blood corpuscles (RBC) were taken as the model. Blood samples collected in EDTA vials from healthy adults were used for preparation of RBC suspension. This suspension was treated with bisphenol A (0-150 microg/mL) with and without black tea extract or quercetin (0-200 microg/mL). The results showed that addition of bisphenol A causes concentration-dependent increase in rate of hemolysis. Addition of black tea extract or quercetin alone to RBC suspension did not cause any significant reduction. However, concurrent addition of bisphenol A (0-150 microg/mL) and black tea extract or quercetin caused concentration-dependent amelioration in bisphenol A-induced cytotoxicity.