Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04179 (MnSOD)
 2,777 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The studies using an immunohistological technique revealed that overexpression of oxidative stress-related substance such as HNE was observed in the liver of primary biliary cirrhosis patients. These data suggested that oxidative stress participated in the pathogenesis of primary biliary cirrhosis. Therefore we analyzed serum oxdative stress marker (8-OHdG) and anti oxidative substances (Mn-SOD and TRX) to evaluate their clinical significance. In addition we analyzed the genotype of anti oxidative substance GST that has been reported to relate susceptibility of autoimmune disease. Serum levels of 8-OHdG, Mn-SOD and TRX in PBC patients were significantly higher than those of healthy subjects (P<0.001). Though there was no relation between serum level of 8-OHdG and clinical data, positive correlation between serum level of Mn-SOD, TRX and serum level of ALP, IgM was observed. Positive correlation was also observed between serum level of Mn-SOD and TRX. Serum levels of Mn-SOD of patients who responded to UDCA therapy were significantly higher than those of patients who did not response to therapy (P<0.01). Although genotypic difference of GSTM1 and GSTT1 by peripheral blood mononuclear cells did not relate to susceptibility of PBC, serum titer of AMA of GSTM1 null and GSTT1 null patients were significantly higher than those of GSTM1 positive and/or GSTT1 positive patients (P< 0.05). These findings suggest that serum oxidative stress-related markers may reflect the extent of liver damage of PBC, and may relate to the efficacy of UDCA therapy on PBC. It also made clear that genotype of GST related to the titer of AMA.
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PMID:[Significance of serum oxidative stress related markers and genotype of GST gene in the pathogeneses of primary biliary cirrhosis]. 1555 21

Oxidative stress and mitochondrial dysfunction are common features in patients with sepsis and organ failure. Within mitochondria, superoxide is converted into hydrogen peroxide by MnSOD (manganese-containing superoxide dismutase), which is then detoxified by either the mGSH (mitochondrial glutathione) system, using the enzymes mGPx-1 (mitochondrial glutathione peroxidase-1), GRD (glutathione reductase) and mGSH, or the TRX-2 (thioredoxin-2) system, which uses the enzymes PRX-3 (peroxiredoxin-3) and TRX-2R (thioredoxin reductase-2) and TRX-2. In the present paper we investigated the relative contribution of these two systems, using selective inhibitors, in relation to mitochondrial dysfunction in endothelial cells cultured with LPS (lipopolysaccharide) and PepG (peptidoglycan). Specific inhibition of both the TRX-2 and mGSH systems increased the intracellular total radical production (P<0.05) and reduced mitochondrial membrane potentials (P<0.05). Inhibition of the TRX-2 system, but not mGSH, resulted in lower ATP production (P<0.001) with high metabolic activity (P<0.001), low oxygen consumption (P<0.001) and increased lactate production (P<0.001) and caspase 3/7 activation (P<0.05). Collectively these results show that the TRX-2 system appears to have a more important role in preventing mitochondrial dysfunction than the mGSH system in endothelial cells under conditions that mimic a septic insult.
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PMID:Mitochondrial protection by the thioredoxin-2 and glutathione systems in an in vitro endothelial model of sepsis. 2135 52