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Query: UNIPROT:P06889 (Mol)
630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It was previously shown that polyunsaturated and saturated fatty acid rich diets affected metabolic and functional changes in macrophages and a variety of immune tissues (thymus, mesenteric lymph nodes and spleen). This study reports metabolic and functional changes in peritoneal macrophages and lymphocytes of Walker-256 ascites cell tumour-bearing rats which were fed (a) normal balanced diet (3% fat), (b) diet enriched (15% fat) with polyunsaturated fatty acids or (c) diet fortified (15% fat) with saturated fatty acids. Neither of the fatty acid enriched diets affected macrophage migration following tumour cell implantation and ascitic cell growth. However both of these fortified fatty acid regimes enhanced the production of H2O2 by macrophages and lymphocytes. The maximum catalytic capacities of hexokinase, glutaminase, glucose-6-phosphate dehydrogenase and glutathione peroxidase were measured in resident and tumour activated macrophages and lymphocytes obtained from rats fed the three fatty acid dietary regimes during seven days of tumour ascites cell growth. Tumour growth caused an increase in the activities of all of the above enzymes in macrophages irrespective of the fatty acid composition of the diet and notably decreased, independent of dietary fatty acid composition, the activities of the enzymes in lymphocytes. Only glutaminase activity in the lymphocytes of tumour bearing animals fed an unsaturated fatty acid-rich diet was not reduced, but was increased by 78%. Moreover macrophages from control rats fed an enriched polyunsaturated fatty acid diet had increased hexokinase activity (21%), decreased glutaminase (48%) and citrate synthase (decreased 41%) relative to the activities of these enzymes in macrophages of animals maintained on a balanced fatty acid diet. The feeding of both fatty acid rich diets did not modify the pattern of lymphocyte responses during the growth of tumour cells in these animals. None of the fatty acid diets modified the growth rate nor the yield of tumour cells in the peritoneal cavity.
Biochem Mol Biol Int 1993 Jan
PMID:Effects of various dietary fatty acids on enzyme activities of carbohydrate and glutamine metabolism and the metabolic response of lymphocytes and macrophages during Walker-256 ascites cell tumour growth in rats. 849 May 66

Adriamycin elicited a stimulation of rat central nervous system lipid peroxidation, both in vivo and in vitro, as evidenced by the increase in the content of thiobarbituric acid reactants, which was found to be NADPH-dependent. The antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase were seen to decrease on exposure to adriamycin (1 mg/kg for a period of 7 days), together with a significant decrement in the GSH/GSSG ratio, thus contributing to the oxidative insult to the tissue. The in vitro addition of GSH or vitamin E to brain homogenates offered protection against adriamycin-induced lipid peroxidation, suggesting that supplementation with these antioxidants could improve the therapeutic value of the drug.
Biochem Mol Biol Int 1993 Apr
PMID:Adriamycin-induced oxidative stress in rat central nervous system. 850 33

We hypothesized that oxygen free radicals (OFRs) may be involved in pathogenesis of diabetic complications. We therefore investigated the levels of lipid peroxidation by measuring thiobarbituric acid reactive substances (TBARS) and activity of antioxidant enzymes [superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT)] in tissues and blood of streptozotocin (STZ)-induced diabetic rats. The animals were divided into two groups: control and diabetic. After 10 weeks (wks) of diabetes the animals were sacrificed and liver, heart, pancreas, kidney and blood were collected for measurement of various biochemical parameters. Diabetes was associated with a significant increase in TBARS in pancreas, heart and blood. The activity of CAT increased in liver, heart and blood but decreased in kidney. GSH-Px activity increased in pancreas and kidney while SOD activity increased in liver, heart and pancreas. Our findings suggest that oxidative stress occurs in diabetic state and that oxidative damage to tissues may be a contributory factor in complications associated with diabetes.
Mol Cell Biochem 1995 Oct 18
PMID:Lipid peroxidation and activity of antioxidant enzymes in diabetic rats. 856 56

Intracerebroventricular t-butyl hydroperoxide has been reported to induce damage to many types of brain cells. t-Butyl hydroperoxide administration increases glutathione disulfide levels and decreases levels of glutathione. Young adult mice may be more protected from t-butyl hydroperoxide than mature mice due to their higher glutathione levels, even after the administration of t-butyl hydroperoxide. This leads to our current study, investigating glutathione peroxidase and glutathione disulfide reductase in 2-mo-old and 8-mo-old mice. Furthermore, malondialdehyde levels were measured with the thiobarbituric acid assay and compared between the two age groups. Mature mice detoxify glutathione disulfide less readily than young adult mice. Glutathione disulfide reductase activity increases in young adult mice after t-butyl hydroperoxide administration, but not in mature mice. Glutathione peroxidase activity is significantly lower in 8-mo-old than 2-mo-old mouse striatum after t-butyl hydroperoxide administration. Furthermore, malondialdehyde levels in the 8-mo-old striatum increase significantly 20 min after t-butyl hydroperoxide administration. This suggests that age plays a factor in protective mechanisms that are involved in oxidative stress in the brain.
Mol Chem Neuropathol 1995 Oct
PMID:Age-dependent effects of t-BuOOH on glutathione disulfide reductase, glutathione peroxidase, and malondialdehyde in the brain. 857 45

We are currently using caprine arthritis encephalitis virus (CAEV) infection in goats as a model to understand changes in some clinical parameters and host response to infection with human immunodeficiency virus (HIV). The objective of this study was to measure changes in serum antioxidant activities in various age groups of goats infected with CAEV. Serum from CAEV-infected goats had significantly higher catalase activity (105.47 +/- 5.96 kU/l) than serum from healthy control goats (79.92 +/- 17.06 kU/l). Moreover, serum catalase activity increased with increase in the time after infection with CAEV. No change was observed in total superoxide dismutase (SOD) or glutathione peroxidase activity although CuZn SOD levels were elevated in infected goats. There was a positive correlation between serum catalase activity and hydrogen peroxide (H2O2) scavenging activity (r = 0.70, p < 0.05). In order to investigate cell membrane integrity, we determined lactate dehydrogenase (LDH) activity in infected goats. Although there was a transient increase in LDH no correlation was observed between increased serum catalase activity and LDH activity (r = 0.16, p > 0.05). We have earlier observed decreased oxyradical production in CAEV infected goats. This observed increase in serum catalase, a scavenger of endogenous free radicals such as H2O2 may be partly responsible for the observed decrease in oxygen radicals found in vivo.
Cell Mol Biol (Noisy-le-grand) 1995
PMID:Changes in serum antioxidant concentrations during infection with caprine lentivirus. 857 49

Over a 10-week period, female Wistar rats received a diet containing various levels of four trace elements (Zn, Cu, Mn, Se), co-factors of antioxidant enzymes (superoxide dismutase SOD, glutathione peroxidase GPx), in order to examine the influence of supplementation or deficiency of these elements (i) on tissue antioxidant enzyme defence systems, and (ii) on the susceptibility of the myocardium to ischemia-reperfusion injury. At the end of the dietary treatment, hearts were perfused at constant flow (11 ml/min) before being subjected to 15 min of total global normothermic ischemia, followed by reperfusion. The effects of the various diets (deficient, standard or supplemented) were estimated by studying functional recovery of various cardiac parameters (left ventricular developed pressure LVDP, dP/dtmax, heart rate x LVDP) as well as ultrastructural tissue characteristics. Furthermore, SOD and GPx activities were measured before ischemia and at the end of the reperfusion period. Results suggest that: (a) the activity of antioxidant enzymes increased or decreased significantly when diet was respectively supplemented with, or deficient in, trace elements, but was not further modified by an ischemia-reperfusion episode: (b) the recovery of cardiac function during reperfusion, and ventricular myocardial ultrastructure were significantly improved under the influence of trace element supplementation when compared to both standard and deficient groups. These results illustrate the protective effect of trace elements which are co-factors of antioxidant enzymes in limiting ischemia-reperfusion induced injury, and suggest a possible use in the field of anti-ischemic therapy.
J Mol Cell Cardiol 1995 Oct
PMID:Effect of dietary antioxidant trace element supply on cardiac tolerance to ischemia-reperfusion in the rat. 857 45

Intact human sperm incorporated radiolabelled fatty acids into membrane phospholipids when incubated in medium containing bovine serum albumin as a fatty acid carrier. The polyunsaturated fatty acids were preferentially incorporated into the plasmalogen fraction of phospholipid. Uptake was linear with time over 2 hr; at this time sufficient label was available to determine the loss of fatty acids under conditions of spontaneous lipid peroxidation. Loss of the various phospholipid types, the loss of the various fatty acids from these phospholipids, and the overall loss of fatty acids were all first order. The loss of saturated fatty acids was slow with first order rate constant k1 = 0.003 hr-1; for the polyunsaturated fatty acids, arachidonic and docosahexaenoic acids, k1 = 0.145 and 0.162 hr-1, respectively. The rate of loss of fatty acids from the various phospholipid types was dependent on the type, with loss from phosphatidylethanolamine being the most rapid. Among the phospholipid types, phosphatidylethanolamine was lost at the greatest rate. Analysis of fatty acid loss through oxidation products was determined for radiolabelled arachidonic acid. Under conditions of spontaneous lipid peroxidation at 37 degrees C under air in the absence of albumin, free arachidonic acid was found in the medium, along with minor amounts of hydroxylated derivative. All the hydroperoxy fatty acid remained in the cells. In the presence of albumin, all the hydroperoxy fatty acid was found in the supernatant bound to albumin; none could be detected in the cells. Albumin is known as a very potent inhibitor of lipid peroxidation in sperm; its action may be explained, based on these results, as binding the damaging hydroperoxy fatty acids. These results also indicate that a phospholipase A2 may act in peroxidative defense by excising a hydroperoxy acyl group from phospholipid and providing the hydroperoxy fatty acid product as substrate to glutathione peroxidase. This formulation targets hydroperoxy fatty acid as a key intermediate in peroxidative degradation.
Mol Reprod Dev 1995 Nov
PMID:Differential incorporation of fatty acids into and peroxidative loss of fatty acids from phospholipids of human spermatozoa. 857 48

Enzymatic and non-enzymatic antioxidant profiles of the gastric and duodenal mucosa of rat, rabbit, cat and pig were investigated and found to exhibit significant variations. Rat gastric and duodenal mucosa exhibited the highest levels of basal glutathione of the various tissues examined. The highest activity of glutathione reductase was found in the gastric and duodenal mucosa of rat as compared with that in these tissues from the other species. The gastric mucosa of cat and pig showed similar activities of glutathione peroxidase, which was significantly lower than those in rat or rabbit gastric mucosa. The activity of this antioxidant enzyme was similar in rat, rabbit and pig duodenal mucosa and lower than that in cat duodenal mucosa. Strong correlations were found between activities of the functionally coupled antioxidant enzymes glutathione peroxidase and glutathione reductase in gastric but not in duodenal mucosa. The activity of superoxide dismutase showed negligible regional or species-related variations in activity.
Comp Biochem Physiol B Biochem Mol Biol 1995 Dec
PMID:Species-related variations in antioxidant components of gastric and duodenal mucosa. 859 Mar 84

The influence of altered levels of endogenous catecholamines following adrenalectomy or 6-hydroxydopamine (6-OH) treatment (alone or in combination) on enzymatic (glutathione reductase, catalase, glutathione peroxidase and Cu, Zn superoxide dismutase) and non-enzymatic (glutathione) antioxidant components of heart, liver, kidney, lung and erythrocytes in male Wistar rats was investigated. Functional antioxidant status was assessed in terms of susceptibility to t-butylhydroperoxide-induced sulfhydryl group oxidation (an indirect measure of glutathione depletion) and lipid peroxidation, as measured by thiobarbituric acid-reactive substance (TBARS) formation. Reduced levels of adrenaline and noradrenaline resulted from adrenalectomy and 6-OH treatment, respectively, while a combination of these treatments led to a reduction in the levels of both catecholamines. Adrenalectomy was associated with alterations in glutathione reductase activity in the heart and liver (increased). 6-OH treatment alone produced an elevation in glutathione reductase activity only in the heart. In adrenalectomized animals, 6-OH treatment produced no further increases in glutathione reductase activities of heart or liver. In lung, however, the combination of adrenalectomy and 6-OH treatment caused an elevation in both glutathione peroxidase and glutathione reductase activities. Glutathione levels of liver alone were elevated following adrenalectomy, while those of erythrocytes and liver (but not other tissues investigated) were increased by the combination of adrenalectomy and 6-OH treatment. The kidney was relatively resistant to the effects of sympathectomy and showed no changes in any of the antioxidant components measured. Adrenalectomy alone or in combination with 6-OH produced an increased in susceptibility to peroxide-induced sulfhydryl group oxidation only in the heart. 6-OH treatment caused a reduction in peroxide-induced TBARS formation only in the kidney. Both adrenalectomy and the combination of adrenalectomy and 6-OH treatment were associated with reduced TBARS formation in the liver, lung and kidney, but not heart. Results from this study demonstrate that the effects of sympathectomy on antioxidant status vary among tissues. Differences between adrenalectomy and 6-OH treatment on antioxidant components are suggestive of differential actions of adrenaline and noradrenaline on tissue antioxidant status which may have important implications under conditions associated with elevations in levels of these catecholamines including chronic stress and myocardial infarction.
Mol Cell Biochem 1995 Nov 08
PMID:Alteration of antioxidant status following sympathectomy: differential effects of modified plasma levels of adrenaline and noradrenaline. 860 10

The stress response to reactive oxygen species is an important defence system which can reduce their potential to induce biomolecule damage. In this investigation the effect of exposing Molt-3 lymphoblastoid cells or peripheral blood lymphocytes to a non-toxic dose of hydrogen peroxide (10 microM) was studied. Cellular response to a subsequent high dose of hydrogen peroxide (100-200 microM) was assessed by measurement of growth, viability, proliferation and DNA damage (lymphocytes only) and intracellular activities of the enzymes, superoxide dismutase, glutathione peroxidase and catalase (Molt-3 only). The results indicate that pretreatment of lymphocytes with 10 microM hydrogen peroxide can elicit a response which is protective against DNA damage normally inducible in these cells by subsequent exposure to toxic doses of hydrogen peroxide. It appears from the results with Molt-3 cells that altered activities of glutathione peroxidase may contribute to this enhanced resistance to hydrogen peroxide.
Biochem Mol Biol Int 1995 Oct
PMID:Oxidant-induced stress response in lymphoid cells. 867 10


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