title: Protective effect of DHEA on hydrogen peroxide-induced oxidative damage and apoptosis in primary rat Leydig cells.
abstract: Dehydroepiandrosterone (DHEA) is widely used as a nutritional supplement due to its putative anti-aging properties. However, the effect of DHEA in Leydig cells, a major target cell of DHEA biotransformation in male, are not clear. The present study aimed to investigate the preventative effect of DHEA on oxidative damage and apoptosis after H2O2 treatment in Leydig cells. The results showed that DHEA treatment attenuated the reduction of cell viability induced by H2O2. No differences were observed on the superoxide anion (O2-) content, while DHEA treatment decreased reactive oxygen species (ROS) and hydroxyl radical (•OH) content in H2O2-treated Leydig cells. Pre-treatment with DHEA increased peroxidase (POD) activity and decreased glutathione peroxidase (GSH-Px) activity in H2O2-treated Leydig cell. DHEA treatment attenuated DNA damage as indicated by the decreasing of tail moment, comet length and olive tail moment. Total apoptosis ratio and early apoptosis ratio were significantly decreased in H2O2-treated Leydig cell that were pre-treatment with DHEA. DHEA treatment decreased Bax, capase-9 and capase-3 mRNA levels in H2O2-treated Leydig cells. Our results demonstrated that pre-treatment with DHEA prevented the Leydig cells oxidative damage caused by H2O2 through increasing POD activity, which resulted in inhibition of •OH generation. Meanwhile, pre-treatment with DHEA inhibited H2O2-induced Leydig cells early apoptosis which mainly by reducing the pro-apoptotic protein Bax and caspases-9, caspases-3 mRNA levels. This information is important to understand the molecular mechanism of anti-ageing effect and potential application in treatment of oxidative stress induced related diseases of DHEA.
authors.affiliation: Key Laboratory of Animal Physiology and Biochemistry, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
authors.forename: Xiao
authors.initials: X
authors.lastname: Ding
authors.affiliation: Key Laboratory of Animal Physiology and Biochemistry, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Yu
authors.affiliation: Key Laboratory of Animal Physiology and Biochemistry, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
authors.forename: Chongyang
authors.initials: C
authors.lastname: Ge
authors.affiliation: Key Laboratory of Animal Physiology and Biochemistry, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
authors.forename: Haitian
authors.initials: H
authors.lastname: Ma
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000235:genetics; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D020552:Comet Assay; D004249:DNA Damage; D003687:Dehydroepiandrosterone / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects; D005979:Glutathione Peroxidase / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000633:toxicity*; D007985:Leydig Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D016877:Oxidants / Q000633:toxicity; D018384:Oxidative Stress / Q000187:drug effects*; D009195:Peroxidase / Q000378:metabolism; D061251:Primary Cell Culture; D020011:Protective Agents / Q000494:pharmacology; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013739:Testosterone / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000235:genetics
chemical_list: C494828:Bax protein, rat; D016877:Oxidants; D020011:Protective Agents; D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein; D013739:Testosterone; D003687:Dehydroepiandrosterone; D008315:Malondialdehyde; D006861:Hydrogen Peroxide; D009195:Peroxidase; D005979:Glutathione Peroxidase; D053148:Caspase 3
keywords: Leydig cells; Pathology Section; apoptosis; dehydroepiandrosterone; oxidative damage