KOSEN 한인과학기술자네트워크

>식품산업에서 천연 항산화제로 알려진 SOD에 대한 최근 국내외 연구동향을 알고자 합니다. SOD에 관해 발표된 최근 보고서들입니다.

>식품산업에서 천연 항산화제로 알려진 SOD에 대한 최근 국내외 연구동향을 알고자 합니다. 다음의 웹사이트에는 "Superoxide dismutases: Recent advances and clinical applications Book, 1999" 라는 책에 대한 소개가 나와 있습니다. http://membres.tripod.fr/DISMUTASE/SOD.html 또한 다음의 문헌들을 참조하시기 바랍니다. 1. Curr Top Cell Regul 2000;36:117-32 Superoxide dismutase, oxidative stress, and cell metabolism. Culotta VC Department of Environmental Health Sciences, Johns Hopkins University School of Public Health, Baltimore, Maryland 21205, USA. 2. Cell Mol Neurobiol 1998 Dec;18(6):609-20 Role of superoxide dismutase in ischemic brain injury: a study using SOD-1 transgenic mice. Kinouchi H, Kamii H, Mikawa S, Epstein CJ, Yoshimoto T, Chan PH Department of Neurosurgery, Tohoku University School of Medicine, Sendai, Japan. Nitric oxide radicals (NO) play an important role in the pathophysiology of focal cerebral ischemia. 2. Vascular NO can reduce ischemic brain injury by increasing CBF, whereas neuronal NO may mediate neurotoxicity following brain ischemia, mainly by its reaction with superoxide to generate peroxynitrite. 3. These findings could contribute to a strategy for the treatment of cerebral ischemia. 3. J Inherit Metab Dis 1998 Aug;21(5):598-603 The role of manganese superoxide dismutase in health and disease. Robinson BH Department of Biochemistry, University of Toronto, Ontario, Canada. Manganese superoxide dismutase (MnSOD) is the mitochondrial enzyme that disposes of superoxide generated by respiratory chain activity. Of all electrons passing down the mitochondrial respiratory chain, 1-2% are diverted to form superoxide; thus production of hydrogen peroxide occurs at a constant rate due to MnSOD activity. Mice lacking MnSOD develop cardiomyopathy and basal ganglia lesions, have no lipid peroxidation products, but show destruction of enzymes with 4Fe-4S centres. Patients with complex I (NADH-CoQ oxidoreductase) deficiency show variable hyperinduction of MnSOD that is at least partially dependent on the extent of disturbance of redox state. This in turn appears to result in production of excess hydroxyl radicals, which are damaging to proteins, lipids and DNA. An alternative method of protection from oxygen radicals is employed by complex I-deficient cell types that do not induce MnSOD in that they show induction of the bcl-2 protein. 4. Curr Opin Neurol 1996 Dec;9(6):486-91 Superoxide dismutase and oxygen radical neurotoxicity. Hosler BA, Brown RH Cecil B. Day Laboratory for Neuromuscular Research, Massachusetts General Hospital-East, Charlestown, USA. Although reactive oxygen species are natural metabolic products, they can be toxic to cells and are implicated in some neurodegenerative disease. Cytosolic Cu, Zn superoxide dismutase normally defends against damage by reactive oxygen species; however, mutant forms of the enzyme might instead contribute to damage of motor neurons n some amyotrophic lateral sclerosis patients. Possible mechanisms of oxidative injury to neurons are discussed with reference to cytosolic Cu, Zn superoxide dismutase mutations and other factors which might enhance oxygen radical toxicity.