Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glutathion (GSH) plays an important role in maintenance of the redox state of the myocardium and acts as the membrane stabilizer. Seventeen patients who underwent cardiac surgery were subjected to cardiopulmonary bypass (CPB) and ischemic cardioplegia. The effect of GSH on ischemic myocardium was evaluated by serum lysosomal enzymes (acid phosphatase, beta-glucuronidase), isoenzymes of creatine phosphokinase (MB-CPK) and aspartate aminotransferase (m-GOT). standard CPB was instituted and systemic hypothermia was employed. GSH was administered to 8 patients in a dose of 200 mg/kg i.v. prior to institution of CPB. Mixed venous blood was sampled before administration of GSH, 10 min after institution of CPB and 0, 1, 6, 24 and 48 hr of reperfusion period following cardioplegia. Activity of acid phosphatase and beta-glucuronidase were significantly suppressed in the GSH-treated group compared to the non-treated group at 24 hours of reperfusion and immediately after aortic unclamping, respectively. Serum MB-CPK levels remained stable during reperfusion, but in the non-treated group, the level increased significantly at 6 hours of reperfusion. Increment of serum m-GOT levels was significantly suppressed at 1, 6 and 24 hours of reperfusion, compared to the non-treated group. These data suggest that pretreatment of GSH can protect the myocardium subjected to CPB from ischemic insult.
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PMID:Effect of glutathion pretreatment on hypothermic ischemic cardioplegia. 710 61

The extent and time course of recovery on return to normothermia were studied in isolated rat hearts, perfused with oxygen-saturated Tyrode's solution at 5-7 degrees C. After a 1-h hypothermia period, complete recovery was obtained on rewarming; after 3 h hypothermia irreversible deterioration of electrical and mechanical activities resulted. The level of lipid peroxidation, evaluated by the thiobarbituric acid (TBA) reaction, showed a dramatic transient increase on return to normothermia, accompanied by a decrease in the levels of reduced glutathione (GSH). Perfusion with iron chelator-containing saline completely prevented both the deterioration and the peak of lipid peroxidation. These results show that lipid peroxidation is responsible for the cold injury. It is proposed that lipid peroxidation is produced as the result of a cold-induced oxidative stress.
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PMID:Hypothermia triggers iron-dependent lipoperoxidative damage in the isolated rat heart. 800 32

The role of the glutathione (GSH) system in vivo or in drug resistance has received much attention, since GSH is a major component of the cellular detoxification system. We Studied the effect of GSH depletion by buthionine sulfoximine (BSO), a potent inhibitor of gamma-glutamylcysteine synthetase, on doxorubicin (DOX) toxicity in mice. The administration of BSO (30 mM in drinking water for 5 days) significantly decreased the tissue GSH. The GSH depletion in various tissues by BSO was associated with a decrease in the detoxification of DOX in mice. A single dose of 20 mg/kg of DOX significantly reduced body weight and rectal temperature in mice 3 days after injection. The combination with BSO and cepharanthine (biscoclaurine alkaloid), a P-glycoprotein (P-gp) inhibitor, significantly potentiated decrease in body and hypothermia induced by DOX. The study demonstrates that BSO markedly increases the toxicological effect of DOX with the alterations in GSH of tissues and Suggests that the intracellular accumulation of DOX is not a factor.
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PMID:Effect of glutathione depletion by buthionine sulfoximine on doxorubicin toxicity in mice. 868 Aug 8

Russian knapweed is a perennial weed found in many parts of the world, including southern California. Chronic ingestion of this plant by horses has been reported to cause equine nigropallidal encephalomalacia (ENE), which is associated with a movement disorder simulating Parkinson's disease (PD). Repin, a principal ingredient purified from Russian knapweed, is a sesquiterpene lactone containing an alpha-methylenebutyrolactone moiety and epoxides and is a highly reactive electrophile that can readily undergo conjugation with various biological nucleophiles, such as proteins, DNA, and glutathione (GSH). We show in this study that repin is highly toxic to C57BL/6J mice and Sprague-Dawley rats and acutely induces uncoordinated locomotion associated with postural tremors, hypothermia, and inability to respond to sonic and tactile stimuli. We also show that repin intoxication reduces striatal and hippocampal GSH and increases total striatal dopamine (DA) levels in mice. Striatal microdialysis in rats, however, has demonstrated a significant reduction of extracellular DA levels. These findings, coupled with the absence of any demonstrable change in striatal DOPAC levels, suggest that repin acts by inhibiting DA release, a hypothesis that is further supported by our demonstration that, in cultured PC12 cells, repin inhibits the release of DA without affecting its uptake. We believe, therefore, that inhibition of DA release represents one of the earliest pathogenetic events in ENE, leading eventually to striatal extracellular DA denervation, oxidative stress, and degeneration of nigrostriatal pathways. Since the neurotoxic effects of repin appear to be mediated via oxidative stress, and since repin is a natural product isolated from a plant in our environment that can cause a movement disorder associated with degeneration of nigrostriatal pathways, clarification of the mechanism of repin neurotoxicity may provide new insights into our understanding of the pathogenesis of PD.
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PMID:Repin-induced neurotoxicity in rodents. 968 20

An important factor in the production of myocardial damage following cardiopulmonary bypass in the creation of oxygen derived free radicals. Few sources for these radicals have been identified but experimentally activated neutrophils are known to release free radical which contribute to myocyte necrosis. The aim of this pilot study was to identify whether, by depleting patients of leukocytes and particularly neutrophils on bypass, a better degree of myocardial protection could be observed using specific identifiers of myocardial damage. Ten patients undergoing urgent coronary artery bypass for unstable angina with impaired left ventricular function were leuko-depleted using a PALL medical leukocyte filter in the extra corporeal circulation together with leukocyte depletion of all transfused blood. A similar group of matched controls had only an arterial line filter without leukodepletion. All patients were operated by one surgeon using identical techniques of intermittent cross clamping and fibrillation at moderate hypothermia. Full blood count, Glutathione, Troponin T and CPK/MB were measured before, during and at identified intervals up to 72 hour after bypass. Preliminary results show little change in the total leukocyte count but the Troponin T and CPK/MB values were lower in the filtered group than in the control group and an increased level of total Glutathione in the filter group showed that there was less oxidated stress on the myocardium. Currently this filter is an expensive addition to bypass surgery but these preliminary results suggest that activated neutrophil depletion on bypass may be of benefit to patients with unstable angina, impending myocardial necrosis and low ejection fraction.
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PMID:Does activated neutrophil depletion on bypass by leukocyte filtration reduce myocardial damage? A preliminary report. 1006 58

The effect of mild hypothermia on Na(+)-K+ ATPase and lipid peroxidation in canine brain tissue following a 18-minute cardiac arrest and resuscitation for 8 hours were studied. Mild hypothermia improved the restoration of the activity of Na(+)-K+ ATPase, LDH, protect the activity of SOD, decrease the loss of GSH, but not completely blocked the ischemia reperfusion induced lipid peroxidation.
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PMID:[Effects of mild hypothermia on Na(+)-K+ ATPase and lipid peroxidation in canine brain tissue following cardiac arrest and resuscitation]. 1068 82

Oxidative stress is one of the major causes of cellular injury. Various reactive oxygen (ROS) and nitrogen (RNS) species such as superoxide, hydroxyl radical, peroxynitrite, and nitric oxide are involved in the manifestations of different types of organ toxicity and the resultant syndromes, symptoms, or diseases. Hypothermic conditions have been reported to reduce the oxidative stress in various in vitro and in vivo studies. In the present study, we sought to determine the effect of lowered temperatures on oxidative stress-induced cell death in Chinese hamster ovary (CHO) cells. We also investigated the oxidative stress-induced alterations in the expression of anti-apoptotic protein, bcl-2, in CHO cells at lowered temperatures. CHO cells were incubated at four different temperatures of 30, 32, 35, and 37 degrees C (control temperature) from 1 to 4 d. In another set, the cells were incubated with 100 microM hydrogen peroxide (H(2)O(2)) for 30 min before harvesting at different time points. The cells were harvested at 1, 2, 3, and 4 d. Cell survival was significantly higher at 30 degrees C as compared to 37 degrees C over 4 d of incubation. In cells incubated with H(2)O(2), significantly higher cell viability was observed at lower temperatures as compared to the cells incubated at 37 degrees C. The activity of glutathione peroxidase (GSH-Px) also increased significantly at lower temperatures. Lowered temperature also provided a significant increase in the expression of anti-apoptotic protein, bcl-2 after 4 d of incubation. These data suggest that hypothermic conditions lowers the risk of oxidative stress-induced cellular damage and programmed cell death by increasing the activity of GSH-Px and by the induction in the expression of the anti-apoptotic protein, bcl-2.
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PMID:Hypothermia enhances bcl-2 expression and protects against oxidative stress-induced cell death in Chinese hamster ovary cells. 1146 79

This experiment was carried out to determine the effect of short-term hypothermia on blood malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glucose-6-phosphate dehydrogenase (G-6-PD) concentrations in rats. Twenty Sprague-Dawley rats were used weighing 180-200 g and on average 3.5 months old. They were randomly divided into two experimental groups: control (without cooling) and hypothermic (with cooling). The rats of the hypothermic group were cooled by immersion into cold water (10-12 degrees C), and the control rats were immersed into water of body temperature (37 degrees C) up to the neck without using any anaesthetic or tranquilizer for 3 min Rectal body temperatures of both groups were measured and blood samples to analyse MDA, GSH, SOD, GSH, GSH-Px and G-6-PD were collected immediately after the treatment. It was found that the MDA level was higher and the GSH and G-6-PD levels were lower in the hypothermic group than those in the controls. There was no difference between the control or hypothermic group regarding SOD or GSH-Px levels. It is concluded that acute hypothermia increased the lipid peroxidation and decreased the GSH and G-6-PD levels in rats.
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PMID:Effect of short-term hypothermia on lipid peroxidation and antioxidant enzyme activity in rats. 1222 69

The effects of normothermia and delayed hypothermia on the levels of N-acetylaspartate (NAA), reduced glutathione (GSH) and the activities of mitochondrial complex I, II-III, IV and citrate synthase were measured in brain homogenates obtained from anaesthetized neonatal pigs following transient in vivo hypoxia-ischaemia. In the normothermic animals there was a significant decrease in complex I activity and in the levels of GSH and NAA when compared to the controls. Delayed hypothermia preserved NAA and GSH at control levels and enhanced the rate of complex II-III activity. There was correlation (R = 0.79) between GSH and NAA levels when data from all three experimental groups were analyzed. Citrate synthase activity was not significantly different in the three groups, indicating maintenance of mitochondrial integrity. These data suggest that delayed hypothermia affords protection of integrated mitochondrial function in the neonatal brain following transient hypoxia-ischaemia.
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PMID:Delayed hypothermia prevents decreases in N-acetylaspartate and reduced glutathione in the cerebral cortex of the neonatal pig following transient hypoxia-ischaemia. 1251 11

With the aim of evaluating the effect of interaction between physical training or exercise only during pregnancy and thermal stress on oxidative stress, and antioxidant mechanism sedentary pregnant rats (PS), exercised pregnant rats only during pregnancy (PE) and trained rats submitted to also exercise during pregnancy (PT) were compared (N=63). Exercise sessions consisted of swimming at 80% of maximal work load supported into water at 28 degrees C (hypothermia, PS 28, PE28, PT28) or 35 degrees C (thermal neutrality, PS35, PE35, PT35) or 39 degrees C (hyperthermia, PS39, PE39, PT39), for 30 min. The initial body weight in all groups of rats was from 177 to 207 g. On the 20th day of pregnancy, 24 h after the last immersion or swimming session venous blood was collected to determine oxidative stress. Plasma concentrations of means malondialdehyde (MDA) values measured as thiobarbituric acid reactive substances (TBARS); total glutathione (GSH) and vitamin E were determined. The oxidative stress index was calculated from the ratio TBARS/GSH and TBARS/Vitamin E. TBARS did not change on the group PE at different temperatures of water; TBARS were higher for PS28 than PS35 and PS39; PT35 had higher values than PT28 and PT39. For GSH, PS39 was lower than PS35; PE28 was higher than PE35 and PE39 and PT35 were lower than PT28 and PT39. Plasma concentration of vitamin E did not present any difference for sedentary rats at different water temperatures, but for PE28, the values were lower than for PE35 and PE39, whereas PT39 was lower than PT35 and PT28. In relation to TBARS/GSH, it was verified an increase in oxidative stress for PS28 (in relation to PS35 and PS39), PE35, and PT35 (in relation to PE28 and PE39 or PT28 and PT39); regarding the ratio TBARS/vitamin E, the highest values were obtained at 35 degrees C for PS and PT groups and at 39 for PE group. These results have shown the great complexity of the interaction between physical training, thermal stress and pregnancy. Apparently, hypothermia produces large index of oxidative stress only in sedentary rats, but this index was greater at 35 degrees C in relation to extreme temperatures for trained rats. These results have suggested that physical training allows a more efficient activation of antioxidant mechanisms under thermal stress.
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PMID:Reactive oxygen species in pregnant rats: effects of exercise and thermal stress. 1278 44


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