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

During reperfusion of ischemic brain tissue, the production of reactive oxygen species initiates several modifications of the astroglial functional and ultrastructural integrity. During 24 h after ischemic treatment, modification of cellular superoxide free radical scavenging systems have been observed in primary culture of rat astroglial cell. Mitochondrial Mn superoxide dismutase activity (Mn-SOD) gradually decreases, whereas that of the cytosolic Cu,Zn form of the enzyme remains unaffected. We observed in parallel a significant decrease of glutamine synthetase (GS), an astrocyte specifically located enzyme. Addition of almitrine (dialylamine-4',6'-triazinyl 2')-1-(bis-parafluoro-benzydryl)-4-piperazine or dibucaine (a phospholipase A2 inhibitor) antagonizes the decrease of Mn-SOD activity, but does not affect modification of GS activity. Combined effects are observed by simultaneous addition of both drugs. Our data demonstrate that almitrine may increase the synthesis of some mitochondrial proteins, like Mn-SOD, and provide support for further study on the therapeutic potential of almitrine in ischemic astroglial cell injury.
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PMID:Almitrine prevents some hypoxia-induced metabolic injury in rat astrocytes. 790 67

Male Sprague-Dawley rats (150-200 g) were randomly assigned to sham operation (n=6) or 5/6 nephrectomy (n=12) procedures. Two weeks after the completion of the 5/6 nephrectomy, these animals were again randomly assigned to two groups: non-treatment or treatment with vitamin E supplementation at 200 IU/kg chow. Two weeks later, all animals were sacrificed and the kidneys harvested. The secretory phospholipase A(2) (PLA(2)) activity was elevated (150%) in the untreated remnant kidney but returned to sham values in the vitamin E-treated kidneys. The cytoprotective heat shock protein (HSP70) and the intracellular antioxidant superoxide dismutase (MnSOD, Cu/ZnSOD) were similar in sham, remnant, and vitamin E-treated remnant kidneys. We conclude that the sudden reduction of renal mass secondary to the 5/6 nephrectomy procedure stimulates PLA(2) activity but not HSP70, MnSOD, or Cu/ZnSOD. This increased activity of PLA(2) in the remnant kidney returned to sham values after vitamin E treatment. The intrinsic cellular antioxidant enzymes, MnSOD, Cu/ZnSOD, as well as the cytoprotective heat shock protein HSP70, showed no significant changes in either vitamin E-treated or untreated kidneys compared with sham. These data are suggestive that the elevation of PLA(2) is a specific and localized response to the sudden reduction of renal mass.
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PMID:Phospholipase A(2) activity, heat shock protein, and superoxide dismutase in rat remnant kidney. 1068 62

Increased awareness of obesity has led to a dietary shift toward "heart-friendly" vegetable oils containing omega-6 polyunsaturated fatty acid (omega-6 PUFA). In addition to its beneficial effects, omega-6 PUFA also exhibits proinflammatory and prooxidative properties. We hypothesized that chronic dietary omega-6 PUFA can induce free radical generation, predisposing the cardiac mitochondria to oxidative damage. Male Wistar rats were fed a diet supplemented with 20% w/w sunflower oil, rich in omega-6 PUFA (HP) or normal laboratory chow (LP) for 4 weeks. HP feeding augmented phospholipase A(2) activity and breakdown of cardiolipin, a mitochondrial phospholipid. HP hearts also demonstrated elevated inducible nitric oxide synthase expression, loss of Mn superoxide dismutase, and increased mitochondrial nitrotyrosine levels. In these hearts, oxidative damage to mitochondrial DNA (mDNA) was demonstrated by 8-hydroxyguanosine immunopositivity, overexpression of DNA repair enzymes, and a decrease in the mRNA expression of specific respiratory subunits encoded by the mDNA. Functionally, at higher workloads, HP hearts also demonstrated a greater decline in cardiac work than LP, suggesting a compromised mitochondrial reserve. Our study, for the first time, demonstrates that consumption of a high fat diet rich in omega-6 PUFA for only 4 weeks instigates mitochondrial nitrosative damage and causes cardiac dysfunction at high afterloads.
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PMID:Induction of mitochondrial nitrative damage and cardiac dysfunction by chronic provision of dietary omega-6 polyunsaturated fatty acids. 1702 68