title: Melatonin ameliorates oxidative stress, modulates death receptor pathway proteins, and protects the rat cerebrum against bisphenol-A-induced apoptosis.
abstract: Epidemiological reports have indicated a correlation between the increasing of bisphenol-A (BPA) levels in the environment and the incidence of neurodegenerative diseases. In the present study, the protective effect of melatonin on oxidative stress and the death receptor apoptotic proteins in the cerebrum of the bisphenol-A-treated rats were examined. Adult male rats were orally administered melatonin (10mg/kg bw) concurrently with BPA (50mg/kg bw) 3 days a week for 6 weeks. BPA exposure resulted in significant elevations of oxidative stress, as evidenced by the increased malondialdehyde level and the decreased glutathione level and superoxide dismutase activity in the cerebrum. BPA caused an upregulation of p53 and CD95-Fas and activation of capsases-3 and 8, resulting in cerebral cell apoptosis. Melatonin significantly attenuated the BPA-evoked brain oxidative stress, modulated apoptotic-regulating proteins and protected against apoptosis. These data suggest that melatonin modulated important steps in the death receptor apoptotic pathway which likely related to its redox control properties. Melatonin is a promising pharmacological agent for preventing the potential neurotoxicity of BPA following occupational or environmental exposures.
authors.affiliation: Zoology Department, Faculty of Science, Mansoura University, Mansoura, Egypt. Electronic address: maelmissiry@yahoo.com.
authors.forename: Mohamed A
authors.initials: MA
authors.lastname: El-Missiry
authors.affiliation: Zoology Department, Faculty of Science, Mansoura University, Mansoura, Egypt.
authors.forename: Azza I
authors.initials: AI
authors.lastname: Othman
authors.affiliation: Biology Department, Princess Nora University, Riyadh, Saudi Arabia.
authors.forename: Monera A
authors.initials: MA
authors.lastname: Al-Abdan
authors.affiliation: Zoology Department, Faculty of Science, Mansoura University, Mansoura, Egypt.
authors.forename: Aml A
authors.initials: AA
authors.lastname: El-Sayed
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D001559:Benzhydryl Compounds / Q000633:toxicity*; D054022:Cerebrum / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D005978:Glutathione / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008550:Melatonin / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects*; D010636:Phenols / Q000633:toxicity*; D051381:Rats; D017207:Rats, Sprague-Dawley; D053218:Receptors, Death Domain / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D000098826:Bisphenol A Compounds
chemical_list: D000975:Antioxidants; D001559:Benzhydryl Compounds; D005978:Glutathione; D008315:Malondialdehyde; D008550:Melatonin; D010636:Phenols; D053218:Receptors, Death Domain; D013482:Superoxide Dismutase; C006780:bisphenol A; D000098826:Bisphenol A Compounds
keywords: Antioxidants; Apoptosis; Brain; CD95-Fas; Caspases-3 and 8; Death receptor pathway