Quercetin protects hamster spermatogenic cells from oxidative damage induced by diethylstilboestrol

Abstract

Quercetin has been reported to be an efficient antioxidant which protects chicken spermatogonial cells from oxidative damage through increasing intracellular antioxidants and decreasing lipid peroxidation. Exposure to diethylstilboestrol (DES) could cause reproductive damage in males, which is associated with oxidative stress. This study was conducted to investigate the protective effects of quercetin on DES-induced oxidative damage in cultured hamster spermatogenic cells. The cells were treated with different concentrations of DES, and their growth status was observed under inverted microscope. The viability of spermatogenic cells was detected by 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT). The contents of superoxide dismutase (SOD) in supernatants and glutathione peroxidase (GSH-Px) in cells were detected with spectrophotography. The results showed that quercetin significantly inhibited the DES-induced damage on spermatogenic cells, with the exception of the low-dose group in which no significant difference was observed. The cell survival rate increased significantly in the middle- and high-dose groups. The contents of SOD and GSH-Px were significantly elevated after medication with quercetin (P < 0.01). It can be concluded that quercetin protects spermatogenic cells against DES-induced oxidative damage through increasing intracellular antioxidants and decreasing lipid peroxidation. Quercetin plays a very important role in ameliorating reproductive toxicity induced by environmental oestrogens.

Effects of the hydroalcoholic extract of Phyllanthus niruri and its isolated compounds on cyclophosphamide-induced hemorrhagic cystitis in mouse

“…Although quercetin displayed carcinogenic activity in the kidney of male rats when administered in the feed for 2-years (Dunnick and Hailey 1992), it is well known that this compound has protective effects in several in vivo models of oxidative stress (Hapner et al 2010;Li et al 2010;Mi et al 2010). Furthermore, a recent paper has shown that quercetin reduced cisplatin-induced nephrotoxicity in rats, without compromising its anti-tumor activity (Sanchez-Gonzalez et al 2011).…”

A New Perspective on the Quercetin Paradox in Male Reproductive Dysfunction

“…Chronic alcohol consumption (Ezzatabadipour et al ., in press; Muthusami and Chinnaswamy, ), cigarette smoking (Hassa et al ., ), occupational exposure to high temperatures (Dada et al ., ) and certain chemicals such as phthalate esters are among other causes of male infertility (Foster et al ., ). Thus, male infertility and abnormal progeny outcome are some of the consequences resulting from exposure of germ cells to various stressors (Ezzatabadipour et al ., in press; Li et al ., ). Of these, oxidative stress emerges as one of the most important mediator of testicular dysfunctions (Saleh and Agarwal, ; Sikka, ).…”

“…(Pflieger‐Bruss et al ., ). Diethylstilboestrol (DES) is a synthetic estrogen and is an ideal drug for studying the deleterious effects of estrogenic endocrine disruptors on male animals (Li et al ., ). Experiments have demonstrated that exposure to DES, in embryonic period, peri‐natally or in adult animals, could cause reproductive damage in males (Pflieger‐Bruss et al ., ; Yang et al ., ) by decreasing the specific activities of SOD (Superoxide dismutase), GSH‐Px (Glutathione peroxidase), GR (Glutathione reductase) with concomittant increase in lipid peroxidation through generation of ROS (Ma et al ., ; Nair and Shaha, ).…”

“…This controversy is because of the fact that not much is known about the bioavailability and bioefficacy of quercetin till date. However, work reported so far on quercetin has been done on laboratory animals showing its protective effects on male reproductive function (Li et al ., ; Mi et al ., ). Human trials have not been taken up yet and the data generated so far accounts only for the in vitro work published using human semen samples (Khanduja et al ., ).…”

“…Experiments have demonstrated that exposure to DES, in embryonic period, peri‐natally or in adult animals, could cause reproductive damage in males (Pflieger‐Bruss et al ., ; Yang et al ., ) by decreasing the specific activities of SOD (Superoxide dismutase), GSH‐Px (Glutathione peroxidase), GR (Glutathione reductase) with concomittant increase in lipid peroxidation through generation of ROS (Ma et al ., ; Nair and Shaha, ). Quercetin has been reported to attenuate the oxidative damage caused by DES by restoring the activity of SOD and GSH‐Px (Guzy et al ., ; Li et al ., ; Li et al ., ).…”