Bukowska, B; Michalowicz, J; Pieniazek, D; Sicinska, P; Duda, W; ,
Superoxide dismutase (SODs, E.C.1.15.1.1) are metalloproteins, which are subdivided into four different catagories, as they contain different metals: copper/zinc (Cu/Zn) superoxide dismutase, manganese (Mn) superoxide dismutase, iron (Fe) superoxide dismutase, and nickel (Ni) superoxide dismutase. In mammalian tissues, due to location in cell, dismutases are divided into cytosolic dismutase - CuZnSOD (SOD1) that is present in cytoplasm and nucleus, mitochondrial dismutase - MnSOD (SOD-2) that is contained in mitochondrial matrix, and extracellular dismutase - EC-SOD (SOD-3) that exists in intracellular spaces of tissues and extracellular fluids (plasma, lymph, celebral-modulatory or synovial). SODs eliminate superoxide radicals from cell environment and prevents formation of reactive oxygen species and their derivatives. SODs are characterized by thier peroxidative activity: they degrades hydrogen peroxide at the participation of uric acid, HCO3- and other substrates such as formate, glutamate, tyrosine, etc. Superoxide dismutases may be only damaged by some xenobiotics, e.g., azide, cyanides, chloric acid or diethyl-dithio-carbamate and hydrogen peroxide. They play an essential role in stabilization of blood pressure and correct astrocytes blood supply. They are responsible for male fertility, lung function, NO metabolism, and also for development of numerous diseases. In this review, we describe the effect of age and some physical (ionization) and chemical factors (hydrogen peroxide, 2-methoxyestradiol, diethyl-dithio-carbamate, chlorophenols, 2,3,7,8-tetrachlorodibenzo-p-dioxin, microcystin-LR) on the activity of SODs. As their activity is decreased in many diseases and under influence of many physical and chemical factors, it is supposed that SOD supplementation may be very important in therapy. Administration of recombined EC-SOD may prevent cells from damages caused by radical activity. © 2006 Bentham Science Publishers Ltd.
Hydrogen peroxide; Oxidative stress; Peroxynitrite; SOD dysfunction; SOD inhibitors; Superoxide anion; Superoxide dismutases; 2 methoxyestradiol; 2,3,7,8 tetrachlorodibenzo para dioxin; 2,4 dichlorophenol; 2,4,5 trichlorophenol; copper zinc superoxide dismutase; cyanoginosin LR; diethyldithiocarbamic acid; dopamine; extracellular superoxide dismutase; fibroblast growth factor; hydrogen peroxide; iron superoxide dismutase; lecithinized superoxide dismutase; liposome; manganese; manganese superoxide dismutase; melatonin; n(g) nitroarginine methyl ester; neuroleptic agent; nickel superoxide dismutase; oxidoreductase; oxygen; oxygen radical; peroxynitrite; puerarin; reduced nicotinamide adenine dinucleotide phosphate; sivelestat; superoxide dismutase; unclassified drug; unindexed drug; vanadium derivative; aging; alcohol liver disease; alopecia areata; Alzheimer disease; amyotrophic lateral sclerosis; animal experiment; antioxidant activity; arthritis; blood pressure regulation; brain blood flow; brain ischemia; coronary artery disease; diabetic nephropathy; drug induced disease; drug potency; endothelial dysfunction; enzyme inhibition; enzyme localization; gene overexpression; gene therapy; human; hyperbaric oxygen; hyperoxia; hypoxia; lipid peroxidation; liver disease; lung function; lung injury; male fertility; mitochondrial respiration; nonhuman; oxidative stress; protein expression; protein function; radiation injury; radiation protection; review; schizophrenia; tardive dyskinesia; tonsillitis; traumatic brain injury; Mammalia