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At least 1,531 records · Page 85Linked to original sources
PubMed1991

Lipid peroxidation and antielastase activity in the lung under oxidant stress: role of antioxidant defenses.

The role of lipid peroxidation in the inactivation of alpha 1-protease inhibitor (alpha 1-PI) in the alveolar lining fluid of human subjects has been examined under oxidant stress. Exposure to nitrogen dioxide (NO2) at 4 ppm for 3 h resulted in a significant increase in the amount of lipid peroxidation products in the alveolar lining fluid, with conjugated dienes the predominant species. Four-week supplementation with vitamins C and E before NO2 exposure markedly decreased the levels of conjugated dienes (control 804 +/- 103 pmol/micrograms total phospholipids vs. vitamin-supplemented 369 +/- 58, P = 0.003). Malondialdehydes, although detectable in the lavage fluid, contributed little to the total amount of lipid peroxidation products, and the levels were comparable in both groups. NO2 exposure in the absence of vitamin supplementation caused a significant decrease in the elastase inhibitory capacity (EIC) of the alveolar lining fluid in the control group but not in the vitamin-supplemented group [control 3.67 +/- 0.32 micrograms alpha 1-PI/micrograms porcine pancreatic elastase (PPE) vs. vitamin-supplemented 2.75 +/- 0.17, P less than 0.03]. The vitamin-supplemented group had a lower level of conjugated dienes and a higher EIC. Conversely, the control group had higher levels of conjugated dienes and a lower EIC in their lavage fluid. These studies demonstrate that lipid peroxidation occurs as an early event during oxidant exposure in the lungs of normal subjects. The appearance of lipid peroxidation products in the lavage fluid is associated with a decrease in the EIC of the alveolar lining fluid. Vitamins C and E diminish lipid peroxidation and preserve the EIC of the lower respiratory tract fluid during oxidant stress.

Adult↗
PubMed1999

Oxidative damage in fetal rat brain induced by ischemia and subsequent reperfusion. Relation to arachidonic acid peroxidation.

To determine whether ischemia followed by subsequent reperfusion can induce fetal cerebral oxidative damage, we created a model of fetal ischemia/reperfusion using rats at day 19 of pregnancy. Fetal ischemia was induced by unilateral occlusion of the utero-ovarian artery for 20 min. Reperfusion was achieved by releasing the occlusion and restoring the circulation for 30 min. The opposite uterine horn was used as control. We measured brain mitochondrial respiratory control index (RCI) and the concentration of thiobarbituric acid-reactive substances (TBARS) in each group. Arachidonic acid (AA) peroxidation induced by the incubation of brain microvessel fraction and AA was measured. AA peroxidation was also evaluated with and without aspirin, an inhibitor of cyclooxygenase and phenidone, which inhibits both of cyclooxygenase and lipoxygenase. The RCI significantly decreased by the occlusion with (p < 0.01) or without reperfusion (p < 0.05). The TBARS level significantly increased with occlusion plus reperfusion (p < 0.01). AA peroxidation was significantly greater in the occlusion and occlusion plus reperfusion groups than in the control groups (p < 0. 01). Aspirin did not affect peroxidation, while phenidone significantly inhibited it in a concentration-dependent manner (p < 0.001). Accordingly, ischemia followed by reperfusion is likely to induce fetal cerebral lipid peroxidation, which may inhibit mitochondrial respiratory activity. The phenidone-inhibited enzyme lipoxygenase may participate importantly in this peroxidation.

Animals↗
PubMed2001

Effects of octreotide on liver metastasis and intrametastatic lipid peroxidation in experimental pancreatic cancer.

OBJECTIVES: In prospective clinical trials, octreotide improved the quality of life and survival time in patients with pancreatic cancer. In this study, we analyzed whether octreotide modulates the intrametastatic oxygen radical metabolism and might decrease liver metastasis in a model of pancreatic cancer. METHODS: Syrian hamsters received 0.9% NaCl or N-nitrosobis(2-oxopropyl)amine for 3 months. Therapy was performed for 12 weeks by 0.9% NaCl or octreotide. Hamsters received a standard diet or were fed a high-fat diet. In the 25th week, pancreas and liver were examined macroscopically and histologically. The level of lipid peroxidation and the activity of glutathione peroxidase and superoxide dismutase were determined intrahepatically and intrametastatically. RESULTS: The number and size of liver metastases per animal were increased by high-fat diet and decreased by octreotide. While high-fat diet increased intrahepatic extrametastatic lipid peroxidation, octreotide decreased intrahepatic extrametastatic lipid peroxidation and increased intrametastatic lipid peroxidation. CONCLUSIONS: Octreotide decreases the number and size of liver metastases in chemically induced pancreatic cancer in Syrian hamsters. Possible mechanisms are the prevention of high lipid peroxidation in non-metastatic liver as well as the increase in intrametastatic lipid peroxidation, leading to loss of integrity of spread tumor cells.

Animals↗
PubMed2005

Lipid peroxidation and Ca-ATPase activity of basal plasma membranes of syncytiotrophoblast from normotensive pregnant women.

BACKGROUND: The Ca-ATPase activity of the plasma membranes of several tissues of preeclamptic pregnant women is significantly reduced when compared with the values of normotensive pregnant women. This has been explained considering the raise in the level of lipid peroxidation of the plasma membranes with preeclampsia. In this work we studied the effect of lipid peroxidation of syncytiotrophoblast basal (fetal facing) plasma membranes from normotensive pregnant women, on their level of Ca-ATPase activity. METHODS: The syncytiotrophoblast basal (fetal facing) plasma membranes from normotensive pregnant women were isolated and irradiated with ultraviolet (UV) light (254 nm). The membranes were then assayed for Ca-ATPase activity and lipid peroxidation by TBARS. RESULTS: The UV irradiation raises the level of lipid peroxidation of the membranes, producing a concomitant inhibition of their Ca-ATPase activity. Presence of the antioxidant butylated hydroxytoluene during the UV irradiation of the membranes prevents increase in their level of lipid peroxidation and hence the inhibition of their Ca-ATPase activity. CONCLUSION: These results give a strong support to the hypothesis that the lowered Ca-ATPase activity already described for plasma membranes of several tissues of preeclamptic women is the consequence of the increased level of lipid peroxidation shown by these membranes.

Adult↗
PubMedDate not supplied

Lipid peroxidation and oxidative stress during acute allylamine-induced cardiovascular toxicity.

Allylamine is an aliphatic amine that causes vascular lesions in aorta and medium-sized arteries. This primary amine has been shown to be metabolized to acrolein both in vivo and in vitro. Acrolein may cause allylamine's toxic effects, since it acts as a strong peroxidizing agent itself; in addition, deamination of allylamine is accompanied by production of hydrogen peroxide. To investigate the relative roles of oxidative stress and lipid peroxidation in allylamine intoxication, we conducted an acute in vivo time-course study following administration of allylamine (150 mg/kg) to rats by gavage. Animals were sacrificed at 1, 3 and 5 h after allylamine treatment, and subcellular fractions of aorta, epicardium and endocardium were assayed for enzymes of the oxidant defense system and thiol (-SH) status, capacity for lipid peroxidation, and .OH radical generation. Results suggest that in vivo treatment with allylamine causes preferential damage to aortic mitochondria. A marked depletion of total and free -SH content was found in aorta, epicardium and endocardium, with a striking increase in the formation of thiobarbiturate-reactive substance by aortic mitochondria at all time points. A significant increase in the capacity to generate .OH was found in aorta (with lesser increases in epicardium and endocardium) after allylamine treatment. Levels of defense system enzymes were not consistently altered, however. In a totally in vitro experiment, liposomes incubated with acrolein (0.2-2 mM) showed a proportional increase in lipid peroxidation of liposomal membrane. A likely basis of allylamine's cardiovascular toxicity is acrolein-induced lipid peroxidation, especially in mitochondria.

Allylamine↗
PubMed1989

Lipid abnormalities and peroxidation of erythrocytes in nephrotic syndrome.

Serum lipid abnormalities are a common feature of the nephrotic syndrome. It is suggested that this may influence the membrane lipid composition of red cells, which on the other hand may result in an abnormal sensitivity of red cells to lipid peroxidation. Therefore, lipids of plasma and red cell membranes from 7 patients with nephrotic syndrome and from 31 healthy control subjects were examined. In addition, the consequences for the hydrogen-peroxide-induced lipid peroxidation of red cells as an index for their capacity to compensate for oxidant stress was measured. All patients were anemic. Their red cells exhibited a significantly increased susceptibility to lipid peroxidation. Fatty acid analysis revealed a decreased proportion of linoleic acid in plasma and red cell membrane. The content of cholesterol in patients' red cell membranes was clearly diminished. It is shown that this abnormality was related to the enhanced sensitivity of their red cells for peroxidative stress. The present study shows that in addition to an impairment of red cells' antioxidant enzymes, abnormalities of the membrane lipid composition should be considered investigating the cause for an increased susceptibility to lipid peroxidation.

Adolescent↗
PubMed1996

Decreased serum antioxidant activity of hemodialysis patients demonstrated by methylguanidine synthesis and microsomal lipid peroxidation.

This study aims to raise the possibility of methylguanidine, a peroxidative product of creatinine, as a measure of the peroxidative state. As a known standard, we measured the inhibitory effect of uremic serum on the NADPH-dependent microsomal lipid peroxidation. This is an established method for evaluating the peroxidative state and is compared to the effect of uremic serum on methylguanidine synthesis. The study shows decreased serum antioxidant activity in hemodialysis patients by both methods, though there is no correlation between them. These results support the use of methylguanidine as a peroxidative marker and suggest a difference in the reactive oxygen species involved in the reactions of methylguanidine synthesis and microsomal lipid peroxidation.

Adult↗
PubMed1999

Formation of nitric oxide-derived oxidants by myeloperoxidase in monocytes: pathways for monocyte-mediated protein nitration and lipid peroxidation In vivo.

Protein nitration and lipid peroxidation are implicated in the pathogenesis of atherosclerosis; however, neither the cellular mediators nor the reaction pathways for these events in vivo are established. In the present study, we examined the chemical pathways available to monocytes for generating reactive nitrogen species and explored their potential contribution to the protein nitration and lipid peroxidation of biological targets. Isolated human monocytes activated in media containing physiologically relevant levels of nitrite (NO(2)(-)), a major end product of nitric oxide ((*)NO) metabolism, nitrate apolipoprotein B-100 tyrosine residues and initiate LDL lipid peroxidation. LDL nitration (assessed by gas chromatography-mass spectrometry quantification of nitrotyrosine) and lipid peroxidation (assessed by high-performance liquid chromatography with online tandem mass spectrometric quantification of distinct products) required cell activation and NO(2)(-); occurred in the presence of metal chelators, superoxide dismutase (SOD), and scavengers of hypohalous acids; and was blocked by myeloperoxidase (MPO) inhibitors and catalase. Monocytes activated in the presence of the exogenous (*)NO generator PAPA NONOate (Z-[N-(3-aminopropyl)-N-(n-propyl)amino]diazen-1-ium-1,2- diolate) promoted LDL protein nitration and lipid peroxidation by a combination of pathways. At low rates of (*)NO flux, both protein nitration and lipid peroxidation were inhibited by catalase and peroxidase inhibitors but not SOD, suggesting a role for MPO. As rates of (*)NO flux increased, both nitrotyrosine formation and 9-hydroxy-10,12-octadecadienoate/9-hydroperoxy-10,12-octadecadieno ic acid production by monocytes became insensitive to the presence of catalase or peroxidase inhibitors, but they were increasingly inhibited by SOD and methionine, suggesting a role for peroxynitrite. Collectively, these results demonstrate that monocytes use distinct mechanisms for generating (*)NO-derived oxidants, and they identify MPO as a source of nitrating intermediates in monocytes.

Apolipoprotein B-100↗
PubMed1974

Lipid peroxidation by human blood phagocytes.

Cell suspensions enriched in human blood monocytes, obtained from normal peripheral blood by sedimentation on sodium diatrizoate-Ficoll gradients or from the blood of patients with neutropenia and monocytosis, accumulated malonyldialdehyde, a labile catabolite of lipid peroxidation, during incubations with polystyrene beads or heat-killed Staphylococcus epidermidis. Mixed blood leukocytes principally composed of granulocytes or granulocytes purified by density gradient sedimentation did not accumulate malonyldialdehyde during incubations with these particles, but did when ingesting particles containing linolenate. The phospholipid fatty acid composition of monocyte-enriched and purified granulocyte preparations from the same donors were compared. The molar fraction of arachidonate (20:4) in phospholipids from monocyte-rich preparations was 62% greater than that of purified granulocytes. The findings indicate that human monocytes, possibly because of a greater content of polyunsaturated fatty acids in their membranes, peroxidize a greater quantity of endogenous lipids than granulocytes during endocytosis. Normal human granulocytes have the capacity to peroxidize ingested lipids. However, mixed leukocytes from two patients with chronic granulomatous disease produced little malonyldialdehyde when engulfing linolenate-containing particles. Therefore the capacity to peroxidize lipid is related to cellular oxygen metabolism, a function in which chronic granulomatous disease granulocytes are dificient. Malonyldialdehyde chemically prepared by hydrolysis of tetramethoxypropane, by extraction from peroxidized linolenic acid, or purified from extracts of phagocytizing rabbit alveolar macrophages had bactericidal activity against Escherichia coli and S. epidermidis. Therefore, toxic catabolites of lipid hydroperoxides may potentiate the bactericidal activity of hydrogen peroxide in mononuclear phagocytes.

Aldehydes↗
PubMed1984

Role of hydrogen peroxide in the neutrophil-mediated release of prostacyclin from cultured endothelial cells.

We have examined the effect of activated neutrophils on the release of prostacyclin (PGI2) from cultured endothelial cells by radioimmunoassay and thin layer chromatography of its stable metabolite, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha). Phorbol myristate acetate-activated neutrophils induced a time- and dose-dependent release of 6-keto-PGF1 alpha from human and bovine endothelial cell monolayers, whereas phorbol myristate acetate alone and neutrophils alone did not. Pretreatment of the endothelial cells with aspirin prevented neutrophil-mediated 6-keto-PGF1 alpha release, indicating that it did not depend upon neutrophil-generated endoperoxides. Phorbol myristate acetate-activated neutrophils from a patient with chronic granulomatous disease failed to induce endothelial 6-keto-PGF1 alpha release. Addition of catalase but not of superoxide dismutase significantly reduced human and bovine endothelial 6-keto-PGF1 alpha release by phorbol myristate acetate-activated neutrophils. Catalase-inhibitable endothelial 6-keto-PGF1 alpha release was also observed after the addition of the hydrogen peroxide-generating system, glucose-glucose oxidase, to bovine and human endothelial cell monolayers. Bovine endothelial 6-keto-PGF1 alpha release induced by exogenously generated hydrogen peroxide was attenuated by the phospholipase inhibitor mepacrine, suggesting that hydrogen peroxide may act by triggering endothelial membrane phospholipase activation. The release of 6-keto-PGF1 alpha by enzymatically or neutrophil-generated hydrogen peroxide was not associated with endothelial cell lysis as assessed by 51Cr release. We conclude that exogenously generated hydrogen peroxide or a hydrogen peroxide-derived product mediates rapid nonlytic release of PGI2 from cultured endothelial cells.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Vitamin E suppresses increased lipid peroxidation in cigarette smokers.

Cigarette smoke contains many xenobiotics, including oxidants and free radicals, which can increase lipid peroxidation. Recently, breath pentane output (BPO) has been recognized as a good indicator of lipid peroxidation. Vitamin E is known to be a potent free radical scavenger which can protect biological membranes against oxidative damage. We investigated the effect of vitamin E (dl-alpha-tocopherol) on lipid peroxidation in 13 healthy smokers. The results showed (1) smokers had increased BPO as compared with 19 healthy non-smokers (16.3 +/- 1.9 vs 5.8 +/- 0.5, pmol/kg body weight/min, p less than 0.001) although both groups had comparable plasma vitamin E and selenium concentrations, (2) supplementation with vitamin E (800 mg/day for 2 weeks) decreased BPO in smokers, and (3) the concentration of plasma selenium-dependent glutathione peroxidase was restored to normal in those smokers (five out of 13) in whom this was low initially. We conclude that a normal plasma concentration of vitamin E does not prevent this increase of lipid peroxidation in smokers but that substantial doses of vitamin E will significantly reduce this increased lipid peroxidation. If a major function of vitamin E is to protect lipids from peroxidation, then smokers have a conditioned insufficiency of vitamin E on a normal diet.

Adult↗
PubMed2000

The ability of mineral dusts and fibres to initiate lipid peroxidation. Part II: relationship to different particle-induced pathological effects.

Exposure to pathogenic mineral dusts and fibres is associated with pulmonary changes including fibrosis and cancer. Investigations into aetiological mechanisms of these diseases have identified modifications in specific macromolecules as well as changes in certain early processes, which have preceded fibrosis and cancer. Peroxidation of lipids is one such modification, which is observed following exposure to mineral dusts and fibres. Their ability to initiate lipid peroxidation and the parameters that determine this ability have recently been reviewed. Part II of this review examines the relationship between the capacity of mineral dusts and fibres to initiate lipid peroxidation and a number of pathological changes they produce. The oxidative modification of polyunsaturated fatty acids is a major contributor to membrane damage in cells and has been implicated in a great variety of pathological processes. In most pathological conditions where an induction of lipid peroxidation is observed it is assumed to be the consequence of disease, without further establishing if the induction of lipid peroxidation may have preceded or accompanied the disease. In the great majority of instances, however, despite the difficulty in proving this association, a causal relationship between lipid peroxidation and disease cannot be ruled out.

Animals↗
PubMed2003

Biomarkers of lipid peroxidation, airway inflammation and asthma.

Oxidative stress, specifically lipid peroxidation, is believed to contribute to the pathophysiology of asthma. This review highlights the pathways through which reactive oxygen species (ROS) may lead to lipid peroxidation. The potential of both the innate and acquired immune systems to activate inflammatory cells and release ROS that may overwhelm the host antioxidant defences and cause lipid peroxidation, accompanied by detrimental pathophysiological effects, are discussed. Despite the evidence demonstrating the importance of lipid peroxidation, systematic characterisation of oxidative stress and antioxidant defences has not been undertaken, largely due to the lack of appropriate biomarkers. This review discusses the emergence of isoprostanes (specifically 8-iso-prostaglandin F2alpha) as reliable, in vivo markers of lipid peroxidation, which provides an appropriate tool for studying oxidative stress. Furthermore, the development of techniques to study induced sputum and breath condensate, derived directly from the airway surface, enables the site of oxidative damage to be closely assessed. Evidence suggests that dietary changes that have occurred over recent years have increased susceptibility to lipid peroxidation, due to reduced antioxidant defences. To date, the limited number of long-term (>1 week) supplementation trials have been promising. However, the development of techniques to study isoprostanes in airway-lining fluid pave the way for further studies investigating the potential for antioxidant supplements to be used as routine therapy in asthma.

Asthma↗
PubMed2004

Lipid peroxidation induced by DHA enrichment modifies paracellular permeability in Caco-2 cells: protective role of taurine.

Dietary enrichment with docosahexaenoic acid (DHA) has numerous beneficial effects on health. However, the intake of high doses of polyunsaturated fatty acids can promote lipid peroxidation and the subsequent propagation of oxygen radicals. The purpose of this study was to evaluate the effect of DHA on lipid peroxidation and tight junction structure and permeability in Caco-2 cell cultures. Moreover, the effects of taurine, a functional ingredient with antioxidant properties, were also tested. Differentiated Caco-2 cell monolayers were maintained in DHA-supplemented conditions with or without added taurine. Incubation with 100 microM DHA increased lipid peroxidation and paracellular permeability, in parallel with a redistribution of the tight junction proteins occludin and ZO-1. Taurine partially prevented all of these effects. The participation of reactive oxygen and nitrogen species in increased paracellular permeability was also examined using various agents that modify the formation of superoxide radical, hydrogen peroxide, nitric oxide, and peroxynitrite. We conclude that hydrogen peroxide and peroxynitrite may be involved in the DHA-induced increase in paracellular permeability and that the protective role of taurine may be in part related to its capacity to counteract the effects of hydrogen peroxide.

Caco-2 Cells↗
PubMed2003

Pro-oxidant activity of low doses of resveratrol inhibits hydrogen peroxide-induced apoptosis.

We have recently shown that efficient apoptotic signaling is a function of a permissive intracellular milieu created by a decrease in the ratio of superoxide to hydrogen peroxide and cytosolic acidification. Resveratrol, a phytoalexin found in grapes and wines, triggers apoptosis in some systems and inhibits the death signal in others. In this regard, the reported inhibitory effect on hydrogen peroxide-induced apoptosis has been attributed to its antioxidant property. Here, we provide evidence that exposure of human leukemia cells to low concentrations of resveratrol (4-8 micro M) inhibits caspase activation and DNA fragmentation induced by incubation with hydrogen peroxide or upon triggering apoptosis with a novel compound that kills via intracellular hydrogen peroxide production. At these concentrations, resveratrol elicits pro-oxidant properties as evidenced by an increase in intracellular superoxide concentration. This pro-oxidant effect is further supported by our observations that the drop in intracellular superoxide and cytosolic acidification induced by hydrogen peroxide is completely blocked in cells preincubated with resveratrol. Thus, the inhibitory effect of resveratrol on hydrogen peroxide-induced apoptosis is not due to its antioxidant activity, but contrarily via a pro-oxidant effect that creates an intracellular environment nonconducive for apoptotic execution.

Antineoplastic Agents, Phytogenic↗
PubMed1987

Lipid peroxidation and superoxide dismutase-1 and glutathione peroxidase activities in trisomy 16 fetal mice and human trisomy 21 fibroblasts.

An increase in lipid peroxidation has been reported in fetal human trisomy 21 brains. To determine whether this change can be regarded as a consequence of the increase in soluble Cu, Zn-superoxide dismutase (SOD-1) activity caused by the trisomy, we have made use of the trisomy 16 mouse, a model for human trisomy 21. Lipid peroxidation, as malonaldehyde, and the activities of SOD-1 and glutathione peroxidase were studied in diploid and trisomy 16 mouse fetuses and fetal brains and, for comparison, in diploid and trisomy 21 human fibroblasts. SOD-1 activity in diploid mouse brain increased during fetal and postnatal development, but glutathione peroxidase activity was unchanged. Mean SOD-1 activity was almost exactly 50% increased in trisomy 16 fetuses and fetal brains and in human trisomy 21 fibroblasts, confirming the gene dosage effect in both species. The SOD-1 activity in the trisomic fetuses was correlated with that in their matched diploid littermates, suggesting that factors other than the gene dosage also determine activity. Mean glutathione peroxidase activity was not increased in trisomy 16 fetuses or brains and only slightly increased in human trisomy 21 fibroblasts. Mean lipid peroxidation was decreased in fetal trisomy 16 brains but was increased in human trisomy 21 fibroblasts. These results do not lend support to the notion that increased SOD-1 activity is developmentally deleterious and necessarily increases lipid peroxidation and, secondarily, the activity of glutathione peroxidase. The difference between the human and mouse data concerning lipid peroxidation in trisomic brains may be related to structural differences in the lipids which provide the substrate for lipid peroxidation.

Animals↗
PubMed1986

Relative inactivation of steroidogenic enzyme activities of in vitro vitamin E-depleted human adrenal microsomes by lipid peroxidation.

The effects of lipid peroxidation and vitamin E on the steroidogenic activities of human adrenal microsomes were studied. The vitamin E content in the microsomes could be varied by treating the lyophilized microsomes with n-pentane, without affecting the steroidogenic enzyme activities. When the level of microsomal vitamin E in the adrenal was reduced to that in other tissues such as liver and kidney, NADPH-supported lipid peroxidation increased about 200-fold, and concomitantly, the steroidogenic enzyme activities decreased. After 5 min of the lipid peroxidation reaction, 17 alpha-hydroxylase and C17,20-lyase activities were inactivated to 13% and 18%, respectively, of the original activities. 3 beta-Hydroxysteroid dehydrogenase-isomerase and 21-hydroxylase, however, retained 89% and 84%, respectively, of the original activities. When vitamin E was reincorporated into the original activities. When vitamin E was reincorporated into the extracted microsomes, neither the lipid peroxidation reaction nor the inactivation of the enzyme activities was observed. These results indicate that the high concentration of vitamin E in adrenal protects the enzymes from oxidative damage, and that the microsomal C19 steroidogenic cytochrome P-450 activities are highly sensitive to lipid peroxidation. This suggests an association between adrenal lipid peroxidation and a decrease in C19 steroid synthesis with advancing age.

3-Hydroxysteroid Dehydrogenases↗
PubMed1991

In vivo generation of hydrogen peroxide in the rat corpus luteum during luteolysis.

The hypothesis that hydrogen peroxide generation occurs in the corpora lutea of superovulated rats during luteolysis was tested using a peroxide-dependent inhibitor of catalase, 3-amino-1,2,4-triazole (AT). Luteal regression was induced during midpseudopregnancy by injection of 500 micrograms prostaglandin F2 alpha (PGF2 alpha) 1 h before administration of AT (0.1 g/kg, ip) and was confirmed by progesterone analysis of peripheral blood serum. Within groups of both PGF2 alpha-treated and untreated control rats, other rats also received ethanol (0.2 g/kg, ip), which prevents hydrogen peroxide-mediated inhibition of catalase by AT. Diluted homogenates of ovaries removed 1 h after AT administration were assayed for catalase activity by measuring the decrease in absorbance at 240 nm for 30 sec after the addition of hydrogen peroxide (10 mM). Ethanol-sensitive catalase inhibition by AT was significantly higher (47.9 +/- 3.38%) in samples from PGF2 alpha-treated groups than in controls (23.1 +/- 4.82%; P less than 0.01; n = 9). Similar increases in catalase inhibition by AT were found in luteal tissue of rats treated with PGF2 alpha 24 h earlier and in rats in which luteolysis was allowed to occur spontaneously in late pseudopregnancy. Hemoglobin an AT assays revealed that the changes in catalase activity were not the result of altered blood contamination or AT concentration in the luteal homogenates. Since catalase inhibition by AT is only seen in the presence of hydrogen peroxide, these results support the conclusion that an early and sustained component of corpus luteum regression is the generation of hydrogen peroxide in luteal tissue.

Amitrole↗