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

Using a mouse model with intraluminal blockade of the middle cerebral artery (MCA) which produced both cortical and striatal infarction, the effect that superoxide radicals have on cerebral infarction, local cerebral blood flow, and neurological deficits after 24 h of permanent focal cerebral ischemia in transgenic mice (Tg) overexpressing human CuZn-superoxide dismutase (SOD-1) was examined. There were no difference between SOD-1 Tg mice and non-Tg littermates observed in the infarct areas of brain slices, the infarct volume, the local cerebral blood flow, or the neurological deficits. These data suggest that pre-existing high levels of antioxidant enzyme failed to provide neuronal protection against permanent focal cerebral ischemia.
 ...
PMID:Brain infarction is not reduced in SOD-1 transgenic mice after a permanent focal cerebral ischemia. 829 91

Three forms of non-injurious ischemic preconditioning were tested for their effects on endogenous antioxidant activity and subsequent ischemic injury. Test ischemia alone, consisting of 1 h occlusion of both carotid arteries (BCAs) and one middle cerebral artery (MCA), elicited an average volume of cerebral infarction of 143.4 +/- 15.0 mm3 (mean +/- s.e.m.). Twenty minutes occlusion of the MCA only or MCA and BCAs (but not BCAs only) 24 h before test ischemia significantly increased the activity of the antioxidant enzyme superoxide dismutase and significantly reduced the cerebral infarction volume. These findings demonstrate that brief focal ischemia can attenuate the injurious impact of subsequent ischemia and that an upregulation of endogenous antioxidant activity may play a key role in this neuroprotective effect.
 ...
PMID:Induction of ischemic tolerance and antioxidant activity by brief focal ischemia. 914 Oct 50

Cerebrovascular disease is one of the major causes of morbidity and mortality in recent. Oxygen free radicals produced during cerebral infarction increases the damage to neurons. Superoxide dismutase (SOD) is the endogenous antioxidant enzyme that can effectively scavenge superoxide radicals. Trilinolein is a lipophilic antioxidant purified from the herb of Panax pseudoginseng. In the cultured rat brain astrocytes (RBA), the activity of SOD (both Cu,Zn-SOD and Mn-SOD subtypes) was markedly increased by incubation with trilinolein at low concentration (0.1 microM) for 2 days. This stimulatory effect of trilinolein was not related to the incubating concentration. However, long-term (7 days) incubation with trilinolein at same concentration decreased the activity. Similar changes were also observed in the gene expression of SOD in RBA; short-term (2 days) incubation of RBA by 0.1 microM trilinolein increased the mRNA level that was lowered in RBA received a long-term incubation with 0.1 microM trilinolein. This result shows that trilinolein is an effective antioxidant to increase the activity of SOD in RBA which would be beneficial to neurons subjected to oxygen free radical damage. However, long-term medication of antioxidant shall be concerned.
 ...
PMID:Effect of trilinolein on the activity and gene expression of superoxide dismutase in cultured rat brain astrocytes. 1082 34

Stroke is one of the major causes of morbidity and mortality in recent. Oxygen free radicals produced during cerebral infarction increases the damage to neurons. Superoxide dismutase (SOD) is the endogenous antioxidant enzyme that can effectively scavenge superoxide radicals. Catechin is a hydrophilic antioxidant usually existed in tea, fruits and vegetables. In the cultured rat brain astrocytes (RBA), the activity of SOD (both Cu, Zn-SOD and Mn-SOD subtypes) was markedly increased by incubation with catechin at low concentration (0.1 microM) for 2 days (short-term) and 7 days (long-term). This stimulatory effect of catechin was not related to the incubating concentration. Similar changes were also observed in the gene expression of SOD in RBA. The increase in quantity of SOD-messenger RNA was remarkable and seemed to be more obvious than the other antioxidants such as vitamin E. This result shows that catechin is an effective antioxidant to increase the activity of SOD in RBA which would be beneficial to neurons subjected to oxygen free radical damage.
 ...
PMID:Effect of catechin on the activity and gene expression of superoxide dismutase in cultured rat brain astrocytes. 1214 26

Reactive oxygen species can be scavenged by superoxide dismutase (SOD) and glutathione peroxidase (GPx). During ischemia-reperfusion, the normal functioning of these antioxidant enzymes may be insufficient for the prevention of oxidant-induced peroxidation of membrane lipids and hence cerebral infarction. We therefore investigated whether electroacupuncture (EA) treatment at Fengchi points in post-ischemic rats could increase the antioxidant enzyme activities and thereby reduce the extent of lipid peroxidation. The results indicated that while EA did not alter the antioxidant enzyme activities in non-ischemic normal rat brains, ischemia-reperfusion caused significant increases in SOD and GPx activities. EA treatment further increased the antioxidant enzyme activities in ischemic-reperfused brain tissues, with a concomitant decrease in the extent of lipid peroxidation. Our finding suggests that EA treatment at Fengchi reduced the extent of lipid peroxidation in ischemic-reperfused rat brains, possibly by increasing the activities of SOD and GPx.
 ...
PMID:Electroacupuncture reduces the extent of lipid peroxidation by increasing superoxide dismutase and glutathione peroxidase activities in ischemic-reperfused rat brains. 1469 62

This study investigated the neuroprotective effects of dietary supplementation of fish oil on both brain infarction and the activities of antioxidant enzymes. Male Sprague-Dawley rats (4-weeks old) were divided into two groups and received either a regular diet (RD) or a fish-oil-supplemented diet (FOD) for 6 weeks prior to middle cerebral artery (MCA) occlusion. The infarction volume of the brain was calculated using image analysis after staining. Antioxidant enzymes were measured before ischemia (BI), after 2 h of ischemia (AI) and after 24 h (24hR), 48 h (48hR) and after 7 days (7dR) of reperfusion. The infarction volume of the brain was significantly smaller in the FOD group than in the RD group after 24 h of reperfusion (p<0.05). Before ischemia, the levels of lipid peroxide and the glutathione peroxidase (GPx) activity were higher in the FOD group than in the RD group. During reperfusion, the catalase (CAT) activity in the FOD group remained at the preischemia level until after 48 h of reperfusion, while those in the RD group did not. The Mn-superoxide dismutase (SOD) activity and GPx activity were higher in the FOD group than in the RD group only after 2 h of ischemia. In the fatty acid analysis, the ratio of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) were higher in the FOD group than in the RD group (p<0.05). Our results demonstrate that supplementing the diet with fish oil could decrease the cerebral infarction volume following ischemia and reperfusion (I/R) partly by working directly as an antioxidant and partly by modulating antioxidant enzyme activities.
 ...
PMID:Temporal changes in cerebral antioxidant enzyme activities after ischemia and reperfusion in a rat focal brain ischemia model: effect of dietary fish oil. 1528 90

The present work examined the hypothesis that brain ischemic tolerance induced by ischemic preconditioning (IPC) is triggered by an initial oxidative stress and is associated with an increase in antioxidant enzyme activities as one end-effector of the neuroprotection. Wistar rats were preconditioned by a single 3-min occlusion of the middle cerebral artery. After a various duration of reperfusion (30 min, 24, 72 or 168 h), rats were subjected to a 60-min focal ischemia and sacrificed 24 h later. Cerebral infarcts were significantly reduced when performed during the 24- to 72-h time window after IPC. The pretreatment with the protein synthesis inhibitor, cycloheximide (1 mg/kg, i.p., 30 min prior to IPC), completely suppressed the neuroprotection. The free radical scavenger, dimethylthiourea (DMTU; 300 mg/kg, i.p., 30 min prior to IPC) and the antioxidant ebselen (10 mg/kg, oral cramming, 2 h before and 12 h after IPC) also abolished the IPC-induced protection of the brain. Nevertheless, IPC did not induce any delayed changes in antioxidant enzyme (superoxide dismutase, glutathion peroxidase) activities nor in the neuronal expression of Mn and Cu/Zn superoxide dismutase. These results indicate that an initial oxidative stress could be involved as a trigger of IPC, while antioxidant enzymes do not play a key role as end-effectors in such a neuroprotection.
 ...
PMID:Brain ischemic preconditioning is abolished by antioxidant drugs but does not up-regulate superoxide dismutase and glutathion peroxidase. 1549 54