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)

Although much evidence favors the concept that dilated cardiomyopathy could be a postviral disease, the actual prevalence and pathogenesis of viral heart disease in dilated cardiomyopathy has not been well explored, since the diagnosis of viral infection is still difficult. The recently developed polymerase chain reaction (PCR) has made it possible to amplify a few copies of viral genome and has shown that viral genomes persist long after viral infection. The PCR is a promising method for testing possible viral etiology. We have found that antiheart antibodies associated with a murine model of myocarditis increased the intracellular free Ca2+ concentration through the activation of Ca(2+)-permeable cation channels in isolated ventricular cells. Marked induction of Mn-SOD and Cu/Zn-SOD mRNA was found in the heart with viral myocarditis and oxygen radicals may play an important role in the pathogenesis of viral myocarditis. Our recent studies revealed an increase in the circulating cytokines in patients with acute myocarditis and cardiomyopathy and suggested that cytokines play some role in the pathogenesis of myocardial injury in these diseases. In our animal model of EMC virus myocarditis, plasma tumor necrosis factor (TNF)-alpha was elevated in the acute stage and exogenously administered anti TNF-alpha antibody improved the survival and myocardial lesion, suggesting the importance of TNF-alpha in the pathogenesis.
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PMID:[Detection of viral genomes in myocarditis]. 773 17

The pathogenesis of influenza virus infections of the lungs is in part mediated by oxidative stress. Such infections might therefore be expected to induce expression of stress-response genes and genes encoding antioxidant enzymes and to activate transcriptional regulatory proteins. Mice (C57B1/6 and C3H/HeJ) were infected intranasally with influenza virus A/PR/8/34 (H1N1). Expression of the genes encoding the antioxidant enzymes manganese superoxide dismutase (Mn- SOD), indoleamine-2, 3-dioxygenase (IDO), heme oxygenase-1, and glutathione peroxidase were increased in the lungs of virus-infected animals. Cu/ZnSOD and catalase mRNA were not induced by viral infection. Activation of the transcriptional regulatory proteins AP-1, C/EBP, and NF-kappa B (which are known to be affected by oxidant stress) was demonstrated by electrophoretic mobility shift assay after viral infection. In the case of MnSOD, despite increased gene expression enzyme activity was not increased. In contrast, for heme oxygenase-1 both mRNA and activity were increased. C3H/ HeJ and C57B1/6 mice, which are known to have different responses to other types of oxidant stress, also differed in their responses to viral infection. Induction of heme oxygenase-1 expression was greater in C57B1/6 mice than in C3H/ HeJ mice, although inhibiting this enzyme did not alter virus-induced mortality. In contrast, IDO was more strongly induced in C3H/HeJ mice. Activation of NF-kappa B was much more marked in C57B1/6 mice than in C3H/HeJ mice. Although virus replication and inflammatory responses were equivalent in the two strains, lung injury (as measured by wet-to-dry wt ratios) and mortality were greater in C3H/HeJ mice than in C57B1/6 mice, a difference that may be related to differing oxidant stress responses. Thus influenza pneumonia causes an oxidant stress response in the lungs, the nature of which is determined in part by the genetic background of the host.
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PMID:Oxidant stress responses in influenza virus pneumonia: gene expression and transcription factor activation. 884 86

Hydrophobic bile acids lead to generation of oxygen free radicals in mitochondria. Accordingly, this study investigated if gene delivery of superoxide dismutase (SOD) would reduce hepatic injury caused by experimental cholestasis. Rats were given adenovirus (Ad; 3 x 10(9) p.f.u., i.v.) carrying the bacterial control gene lacZ, mitochondrial Mn-SOD or cytosolic Cu/Zn-SOD genes 3 days before bile duct ligation. Both Mn- and Cu/Zn-SOD activity was increased in the liver about four-fold 3 days after viral infection. Serum alanine transaminase increased to about 710 U/l after bile duct ligation, which was blunted by about 70% in rats receiving Ad-Mn-SOD, but by only 30% in rats receiving Ad-Cu/Zn-SOD. Bile duct ligation caused focal necrosis, apoptosis and fibrosis in the liver and increased collagen alpha1 mRNA about 20-fold. These effects were reduced significantly by Ad-Mn-SOD, but not by Ad-Cu/Zn-SOD. In addition, bile duct ligation increased 4-hydroxynonenal, a product of lipid peroxidation, activated NF-kappaB and increased synthesis of TNF(alpha) and TGF-beta. These effects were also blunted significantly by Ad-Mn-SOD, but not by Ad-Cu/Zn-SOD. Taken together, it is concluded that cholestasis causes liver injury by mechanisms involving mitochondrial oxidative stress. Gene delivery of mitochondrial Mn-SOD blocks formation of oxygen radicals and production of toxic cytokines thereby minimizing liver injury caused by cholestasis.
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PMID:Viral gene delivery of superoxide dismutase attenuates experimental cholestasis-induced liver fibrosis in the rat. 1185 21

The present study investigated the in vivo hemocytic and hepatopancreatic response to Vibrio parahaemolyticus and white spot syndrome virus (WSSV) injection in shrimp Litopenaeus vannamei. The proliferation of bacteria and virus in shrimp, animal mortality, total hemocyte counts (THCs), phenoloxidase (PO) activity, respiratory burst, and gene expression of immune factors associated with immune recognition (lectin), prophenoloxidase (proPO) activation, and the anti-microorganism (lysozyme) and active oxygen defense response (including respiratory burst, cytosolic manganese superoxide dismutase [C-MnSOD], and catalase [CAT]) were quantified. Shrimp death rate increased significantly and was time-dependent after V. parahaemolyticus or WSSV injection. The production of superoxide anion, and the gene expression including lectin in hemocytes, proPO in the hepatopancreas, lysozyme, C-MnSOD and CAT could be induced by injection with V parahaemolyticus and WSSV. The highest value of lysozyme was in the hemocytes with 66.59 times (at 3 h) greater expression than in the control group after WSSV injection and 3.69 times (24 h) greater than in the control group after V parahaemolyticus injection. In the hepatopancreas, CAT expression showed a significant increase, with up to 16 times greater expression than in the control group at 6 h postinjection with WSSV and 7.02 times greater expression than in the control group at 48 h postinjection with V parahaemolyticus (p < 0.05). However, significant decreases in PO activity and proPO transcripts in hemocytes and lectin transcripts in the hepatopancreas were detected after V parahaemolyticus and WSSV injection (p < 0.05). The results suggest that lysozyme, the antioxidase system, and reactive oxygen species might play a crucial role in shrimp defense against bacterial and viral infection.
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PMID:Reactive oxygen system plays an important role in shrimp Litopenaeus vannamei defense against Vibrio parahaemolyticus and WSSV infection. 2199 61