title: Heroin-administered mice involved in oxidative stress and exogenous antioxidant-alleviated withdrawal syndrome.
abstract: Heroin has been shown to elevate dopamine (DA) level. It is well known that an increase in DA oxidative metabolism leads to increased reactive oxygen species (ROS) formation, and thus, ROS have been frequently associated with neuronal cell death due to damage to carbohydrates, amino acids, phospholipids, and nucleic acids. This study investigated whether there are oxidative stress and effects of exogenous antioxidants in heroin-administered mice. The heroin-dependent mice model was made via intraperitoneal injection. Oxidative damage of DNA, protein, and lipid was measured by analysis of single cell electrophoresis, the 2,4-dinitrophenylhydrazine method, and thiobarbituric acid method respectively. The activities of antioxidative enzymes and total antioxidant capacity were assayed by spectrophotometry. After administration with heroin, the mice not only showed decrease of total antioxidant capacity in serum and antioxidant enzymes such as superoxide dismutase, catalase, and glutathione (GSH) peroxidase in brain, but also exhibited the oxidative damages of DNA, protein and lipid. On the other hand, exogenous antioxidants could restrain the oxidative stress, even alleviate withdrawal syndrome in heroin-administered mice. Our results also imply a possibility that ROS may participate in the whole process of dependence and withdrawal of heroin. Therefore, strategies of blocking oxidative stress may be useful in the development of therapy for opiate abuse.
authors.affiliation: School of Ocean Biology, Ocean University of China, Qingdao, People's Republic of China.
authors.forename: Bo
authors.initials: B
authors.lastname: Xu
authors.forename: Zhenhua
authors.initials: Z
authors.lastname: Wang
authors.forename: Gang
authors.initials: G
authors.lastname: Li
authors.forename: Bingjun
authors.initials: B
authors.lastname: Li
authors.forename: Hong
authors.initials: H
authors.lastname: Lin
authors.forename: Rongliang
authors.initials: R
authors.lastname: Zheng
authors.forename: Qiusheng
authors.initials: Q
authors.lastname: Zheng
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000627:therapeutic use*; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D001923:Brain Chemistry / Q000187:drug effects; D002374:Catalase / Q000378:metabolism; D004249:DNA Damage / Q000187:drug effects; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D003932:Heroin / Q000008:administration & dosage / Q000633:toxicity*; D006556:Heroin Dependence / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control; D007274:Injections, Intraperitoneal; D007279:Injections, Subcutaneous; D008214:Lymphocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D009270:Naloxone / Q000008:administration & dosage / Q000627:therapeutic use; D009292:Narcotic Antagonists / Q000008:administration & dosage / Q000627:therapeutic use; D009294:Narcotics / Q000008:administration & dosage / Q000633:toxicity; D018384:Oxidative Stress / Q000187:drug effects*; D013375:Substance Withdrawal Syndrome / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D009292:Narcotic Antagonists; D009294:Narcotics; D009270:Naloxone; D008315:Malondialdehyde; D003932:Heroin; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase