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)

Increased oxidative stress and antioxidant deficit have been suggested to play a major role in adriamycin-induced cardiomyopathy and congestive heart failure due to multiple treatments with adriamycin (doxorubicin). In this study, we investigated the acute effects of a single dose of adriamycin on myocardial antioxidant enzymes in rats. Adriamycin (2.5 mg/kg) was injected (i.p.) and myocardial antioxidant enzyme activities, mRNA abundance and protein levels at 1, 2, 4 and 24 h were examined. While manganese superoxide dismutase (MnSOD), glutathione peroxidase (GSHPx) and catalase (CAT) activities were not significantly changed, copper-zinc superoxide dismutase (CuZnSOD) activity was reduced at all time points and this change correlated with a decrease in its protein content. CuZnSOD mRNA was increased at 1 and 24 h. GSHPx mRNA and protein levels were transiently decreased by 20 and 25% respectively at 2 h. MnSOD mRNA was not significantly changed, but its protein levels were significantly decreased at 1 h. Lipid peroxidation was increased transiently at 1, 2 and 4 h. A transient depression in antioxidant enzyme as well as transient increase in oxidative stress with a single dose of adriamycin may precede more sustained changes seen with the repeated administration of the drug and contribute to the development of cardiomyopathy and heart failure.
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PMID:Early changes in myocardial antioxidant enzymes in rats treated with adriamycin. 1203 Mar 76

Zinc is a structural constituent of many proteins, including Cu/Zn superoxide dismutase (SOD), an endogenous antioxidant enzyme. Hypozincemia has been found in patients hospitalized with congestive heart failure, where neurohormonal activation, including the renin-angiotensin-aldosterone system (RAAS), is expected and oxidative stress is present. This study was undertaken to elucidate potential pathophysiological mechanisms involved in Zn dyshomeostasis in aldosteronism. In rats receiving aldosterone/salt treatment (ALDOST) alone for 1 and 4 wk or in combination with spironolactone (Spiro), an ALDO receptor antagonist, we monitored 24-h urinary and fecal Zn excretion and tissue Zn levels in heart, liver, and skeletal muscle, together with tissue metallothionein (MT)-I, a Zn(2+)-binding protein, and Cu/Zn-SOD activities in plasma and tissues. When compared with unoperated, untreated, age-/sex-matched controls, urinary and, in particular, fecal Zn losses were markedly increased (P < 0.05) at days 7 and 28 of ALDOST, leading to hypozincemia and a fall (P < 0.05) in plasma Cu/Zn-SOD activity. Microscopic scars and perivascular fibrosis of intramural coronary arteries first appeared in the right and left ventricles at week 4 of ALDOST and were accompanied by increased (P < 0.05) tissue Zn, MT-I, and Cu/Zn-SOD activity, which were not found in uninjured liver or skeletal muscle. Spiro cotreatment prevented cardiac injury and Zn redistribution to the heart. Thus increased urinary and fecal Zn losses, together with their preferential translocation to sites of cardiac injury, where MT-I overexpression and increased Cu/Zn-SOD activity appeared, contribute to Zn dyshomeostasis in rats with aldosteronism, which were each prevented by Spiro. These findings may shed light on Zn dyshomeostasis found in patients with decompensated heart failure.
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PMID:Zinc dyshomeostasis in rats with aldosteronism. Response to spironolactone. 1761 52

We recently reported two novel breeding lines of rats known as Carioca high-and low-conditioned freezing (CHF and CLF), based on defensive freezing responses to contextual cues previously associated with electric footshock. The anxiety-like profile of these animals from the 7th generation was tested in the elevated plus maze. The results indicated that CHF animals presented a significantly more "anxious" phenotype compared with CLF animals. Animals from the 12th generation were used to evaluate the oxidative stress status of the cortex, hippocampus, and cerebellum. Reactive oxidative species (ROS) were evaluated using 2,7-dichlorofluorescin diacetate (DCFH-DA; a sensor of reactive oxygen species [ROS]), and the levels of malondialdehyde (MDA), an early marker of lipid peroxidation, were assessed. The results indicated that free radical concentrations and MDA levels were significantly higher in all three brain structures in CHF rats compared with CLF rats. Our data also showed that the hippocampus had the highest reactive species and MDA concentrations compared with the cortex and cerebellum in CHF rats. Animals from the 16th generation were used to evaluate the antioxidant enzyme activity of catalase (CAT) and glutathione peroxidase (GPx) within these three brain structures. The results indicated that CAT activity was lower in the cortex and hippocampus in CHF rats compared with CLF rats. No significant difference was observed in the cerebellum. The enzymatic activity of GPx was significantly decreased in all three structures in CHF rats compared with CLF rats. The hippocampus exhibited the highest GPx activity compared with the other two brain structures. These findings suggest the involvement of a redox system in these two bidirectional lines, and the hippocampus might be one of the prime brain structures involved in this state of oxidative stress imbalance.
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PMID:Association between oxidative stress and contextual fear conditioning in Carioca high- and low-conditioned freezing rats. 2356 16