Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The levels of some organochlorine pesticides (OCP)s (hexachlorobenzene, HCB, alpha-hexachlorocyclohexane, alpha-HCH, beta-HCH, gamma-HCH, heptachlorepoxide, HE, bis (4-chlorophenyl)-1,1-dichloroethene, p.p'DDE, bis (4-chlorophenyl)-1,1,1-trichloroethane, p.p' DDT and total DDT (E-DDT) and antioxidant enzyme activities namely Cu, Zn superoxide dismutase (SOD), catalase (CAT), selenium-dependent glutathione peroxidase (Se-GSH-Px), total glutathione peroxidase (T-GSH-Px), selenium independent glutathione peroxidase (GSH-Px II), glutathione reductase (GRd), level of reduced glutathione (GSH) and lipid peroxidation (LP), glutathione S-transferase (GST) activity toward several substrates including 1-chloro-2,4-dinitrobenzene (CDNB), 1,2-dichloro-4-nitrobenzene (DCNB), ethacrynic acid (EAA), 1,2-epoxy-3-(p-nitrophenoxy)-propane (ENPP) were measured in tumor and surrounding tumor free tissues of 24 female breast cancer patients and was evaluated whether there exist any association between the levels of OCPs and antioxidants. The mean levels of GSH, alpha-BHC, gamma-BHC and HE, and activities of SOD, Se-GSH-Px, T-GSH-Px, GSH-Px II,GRd, GST CDNB, and GST DCNB were significantly higher in tumors than in controls. In tumors, significant correlations were noted between: SOD and y-BHC; Se-GSH-Px and gamma-BHC; T-GSH-Px and gamma-BHC; GSH-Px II and alpha-BHC, gamma-BHC; GSH and alpha-BHC, gamma-BHC, HE; GRd and alpha-BHC; CDNB GST and alpha-BHC, gamma-BHC. These results show that free-radical mediated oxidative stress is, at least partly, associated with some of these OCP residues in human breast tumors.
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PMID:The organochlorine pesticide residues and antioxidant enzyme activities in human breast tumors: is there any association? 1203 8

Exposure of marine animals to certain pollutants can enhance reactive oxygen species (ROS) production with subsequent damage to macromolecules and alterations in oxidant defences levels. Aimed at correlating the tissue concentration of certain contaminants (PCBs, DDT) with antioxidant defence levels and oxidative damages, two fish species with different life strategies (mullet, Mugil cephalus, and flounder, Platichthys flesus) were collected in the Douro Estuary (NW Portugal). After capture, the fish were left to depurate for 1 month in clean seawater. The levels of the two antioxidant enzyme activities revealed that they are species-dependent with mullet's livers showing higher superoxide dismutase (SOD) (13.2+/-0.5 U/mg protein) and catalase (CAT) (15.5+/-1.0 mmol/min/mg protein) activities than flounder (SOD: 7.9+/-0.9 U/mg protein; CAT: 11.1+/-0.8 mmol/min/mg protein). After 1 month in captivity the antioxidant enzymes activities in liver decreased in mullets, while for flounders the responses were not consistent because during the experimental period flounders did not ate and responses of antioxidant enzymes and oxidative damages were dependent on the fasting condition. The liver oxidative damages were evaluated by estimating oxidised lipids and proteins. Both species showed similar levels for these two parameters. The hepatic lipid peroxidation in flounder increased after 1 month in captivity, while in mullet an increase was observed only in summer and autumn. The oxidised protein content increased for both species after the depuration period. This study reveals differences between species under oxidative stress when exposed to pollutants. In a clean environment, the mullet's primary antioxidant defences decreased indicating that the animals living in Douro estuary were facing an oxidative stress. The data indicate that, namely in mullet, the presence of pollutants induce oxidative stress responses.
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PMID:Oxidative stress biomarkers in two resident species, mullet (Mugil cephalus) and flounder (Platichthys flesus), from a polluted site in River Douro Estuary, Portugal. 1564 30

Acrylonitrile (ACN), an environmental toxic pollutant, has been detected in drinking water, food products and occupational environment. The objective of the present work was to investigate the cytotoxic effects as well as the oxidative stress induced by ACN in cultured rat colonocytes. Colonocytes were exposed in vitro to different concentrations of ACN (0.1-2.0mM) for 60min. Also, colonocytes were incubated with ACN (1.0mM) for different time intervals extending to 180min. Cytotoxicity was determined by assessing cell viability and lactate dehydrogenase (LDH) release. Oxidative stress was assessed by determining reduced glutathione (GSH) level and lipid peroxidation as indicated by thiobarbituric acid reactive substances (TBARS) production. Exposure of colonocytes to ACN (1.0mM) for 60min caused nearly a 50% decrease in cell viability and induced a 2.5-fold increase of LDH leakage. In the same experiment, ACN caused a significant decrease in cellular GSH content as well as a significant enhancement of TBARS accumulation. These toxic responses to ACN were dependent on both concentration and duration of exposure to ACN. There was a good correlation between LDH release and TBARS formation (r(2)=0.97, p<0.05). Treatment of colonocytes with GSH, N-acetyl-l-cysteine (NAC) or dithiothreitol (DDT) prior to exposure to ACN afforded different degrees of protection as indicated by significant decrease in the LDH leakage and TBARS formation as compared to ACN alone-treated cells. Also, pretreatment of colonocytes with the antioxidant enzyme superoxide dismutase (SOD) or catalase (CAT) significantly inhibited LDH leakage and TBARS production. Preincubation with dimethyl sulfoxide (DMSO), a hydroxyl radical scavenger or desferroxiamine (DFO), an iron chelator, diminished ACN-induced LDH leakage and TBARS generation. Our results suggest that ACN has a potential cytotoxic effect in rat colonocytes; and thiol group-donors, antioxidant enzymes, hydroxyl radical scavengers and iron chelators can play an important role against ACN-induced colonotoxicity.
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PMID:Acrylonitrile-induced toxicity and oxidative stress in isolated rat colonocytes. 2178 98