title: [Effects of bisphenol A exposure during lactation on testicular mitochondria in male mouse offspring].
abstract: OBJECTIVE
  To study whether maternal bisphenol A (BPA) exposure during lactation stage will induce oxidative stress and apoptosis in male offspring's testis by mitochondrial pathway.
  
  
  METHODS
  After delivery, maternal mice were randomly divided into four groups, including high dose group (50 mg/kg), medium dose group (5 mg/kg), low dose group (0.01 mg/kg) and solvent control group. BPA were given daily by gavage to maternal mice during lactation stage. The pups were raised and sacrificed at PND 75. The effect of BPA exposure on the activity of testicular mitochondrial succinate dehydrogenase (SDH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in male offspring were detected. The expressions of cytochrome C (Cyt C), caspase 3 and apoptosis-inducing factor (AIF) in testes of male offspring were detected by Western blot. Changes of mitochondrial substructure in testicular cells were observed by transmission electron microscopy.
  
  
  RESULTS
  The exposed mice had a significant decrease in the activities of testicular mitochondrial SDH (P < 0.05) in all groups and with notable decrease in the activities of GSH-Px and SOD in the high and medium-dose groups (P < 0.05). BPA also caused testicular mitochondrial MDA increased markedly (P < 0.05). Western blot showed that the expression levels of Cyt C, caspase 3 and AIF increased significantly in the testes of BPA-treated groups (P < 0.05). Under transmission electron microscopy, mitochondria swell, crests obscure and disappear were founded in the high and medium-dose groups.
  
  
  CONCLUSIONS
  During lactation stage, maternal exposed to BPA induce oxidative stress and apoptosis of testicular cells by possible mechanisms of mitochondrial pathway,which would cause adverse effects on the early development of testis.
authors.affiliation: Medicine Experiment Center, Weifang Medical University, Weifang 261053, China. xiemeina@wfmc.edu.cn
authors.forename: Meina
authors.initials: M
authors.lastname: Xie
authors.forename: Fengjie
authors.initials: F
authors.lastname: Li
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D051033:Apoptosis Inducing Factor; D001559:Benzhydryl Compounds / Q000009:adverse effects*; D015153:Blotting, Western; D001942:Breast Feeding; D053148:Caspase 3 / Q000378:metabolism; D045304:Cytochromes c / Q000032:analysis; D005260:Female; D005979:Glutathione Peroxidase; D006801:Humans; D007774:Lactation; D008297:Male; D008315:Malondialdehyde; D018811:Maternal Exposure / Q000009:adverse effects*; D051379:Mice; D046529:Microscopy, Electron, Transmission; D008928:Mitochondria / Q000187:drug effects* / Q000502:physiology; D018384:Oxidative Stress; D010636:Phenols / Q000009:adverse effects*; D013482:Superoxide Dismutase; D013737:Testis / Q000187:drug effects* / Q000473:pathology; D000098826:Bisphenol A Compounds
chemical_list: D051033:Apoptosis Inducing Factor; D001559:Benzhydryl Compounds; D053148:Caspase 3; D045304:Cytochromes c; D005979:Glutathione Peroxidase; D008315:Malondialdehyde; D010636:Phenols; D013482:Superoxide Dismutase; C006780:bisphenol A; D000098826:Bisphenol A Compounds