Reactive oxygen species superoxide dismutase

Lipid peroxidation (see Fig. 17.2) is a chain reaction that can be attacked in many ways. The chain reaction can be inhibited by use of radical scavengers (chain termination). Initiation of the chain reaction can be blocked by either inhibiting synthesis. of reactive oxygen species (ROS) or by use of antioxidant enzymes like superoxide dismutase (SOD), complexes of SOD and catalase. Finally, agents that chelate iron can remove free iron and thus reduce Flaber-Weiss-mediated iron/oxygen injury. 

The mitochondrial dysfunctionality seen in manganese neurotoxicity might be related to the accumulation of reactive oxygen species (Verity, 1999). Mitochondrial Mn superoxide dismutase (MnSOD) is found to be low or absent in tumour cells and may act as a tumour suppressor. It is induced by inflammatory cytokines like TNF, presumably to protect host cells. In a rat model, iron-rich diets were found to decrease MnSOD activity, although a recent study reported that in rat epithelial cell cultures iron supplementation increased MnSOD protein levels and activity, but did not compromise the ability of inflammatory mediators like TNF to further increase the enzyme activity (Kuratko, 1999). 

The antioxidant system in humans is a complex network composed by several enzymatic and nonenzymatic antioxidants. In addition to being an antioxidant, lycopene also exerts indirect antioxidant properties by inducing the production of cellular enzymes such as superoxide dismutase, glutathione S-transferase, and quinone reductase that also protect cells from reactive oxygen species and other electrophilic molecules (Goo and others 2007). 

General descriptors may be related to the metabolism responses in the biofilm. Biofilm algae have several mechanisms to counterbalance the damage caused by the toxicants. Environmental stress produces oxidative damage in the cells, which can be tracked down by means of the analysis of many enzymes (superoxide dismutase, catalase, peroxidase, etc.) that function as effective quenchers of reactive oxygen species (ROS). 

Greenlund, L. J., Deckwerth, T. L. and Johnson, E. M. Jr. Superoxide dismutase delays neuronal apoptosis a role for reactive oxygen species in programmed neuronal death. Neuron 14 303-315,1995. 

Manganese is the cofactor for catalases, peroxidases and superoxide dismutases, which are all involved in the detoxification of reactive oxygen species (SOD). We consider here the widely distributed Mn SOD, and then briefly describe the dinuclear Mn catalases. 

All aerobic organisms contain substances that help prevent injury mediated by free radicals, and these include antioxidants such as a-tocopherol and the enzymes superoxide dismutase and glutathione peroxidase. When the protective effect of the antioxidants is overwhelmed by the production of reactive oxygen species, the intracellular milieu becomes oxidative, leading to a state known as oxidative stress (Halliwell and Gutteridge, 1999). Thus the balance between the generated free radicals and the efficiency of the protective antioxidant system determines the extent of cellular damage. 

Superoxide dismutase (SOD) Therapeutically active protein (detoxification of reactive oxygen species)... 

Reactive oxygen species produced in mitochondria are inactivated by a set of protective enzymes, including superoxide dismutase and glutathione peroxidase. 

The production of superoxide anions is one of the major factors involved in NO toxicity because superoxide anions can react with NO to form the highly toxic free-radical peroxynitrite. A pivotal role for superoxide anions in NO-related insults is emphasized by results showing that transgenic mice overexpressing superoxide dismutase (SOD) are resistant to brain ischemia. Superoxide can protect against SNP-induced toxicity. Thus, the superoxide-scavenging properties of EGb 761 are likely to explain, at least in part, its ability to block cell death and the increase in reactive oxygen species accumulation induced by the two NO donors used here, SNP and SIN-1. 

MPTP decreases glutathione levels and increases the levels of reactive oxygen species and the degree of lipid peroxidation in mouse brain slices in vitro and increases the levels of reactive oxygen species in mouse brain in vivo. MPTP neurotoxicity in vitro is reduced by glutathione. In vitro studies have shown that MPP neurotoxicity can be reduced by vitamin E, vitamin C, coenzyme Q, and mannitol (but not by superoxide dismutase, catalase, allopurinol, or dimethyl sulfoxide). P-Carotene, vitamin C, and /V-acctylcystcine partially protect against the neurotoxic effects of MPTP in mice, as do nicotinamide, coenzyme Q, and the free-radical spin trap A-tert-butyl-a-(sulfophenyl) nitrone. 

Zini, A., de Lamirande, E., and Gagnon, C. 1993. Reactive oxygen species in semen of infertile patients Levels of superoxide dismutase and catalase-like activities in seminal plasma and spermatozoa. Int. J. Androl. 16, 183-188. 

---