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PubMed1997

New curcuminoids isolated from Zingiber cassumunar protect cells suffering from oxidative stress: a flow-cytometric study using rat thymocytes and H2O2.

Effects of new complex curcuminoids (cassumunin A and cassumunin B) isolated from tropical ginger, Zingiber cassumunar, were examined in dissociated rat thymocytes suffering from oxidative stress induced by 3 mM hydrogen peroxide by using a flow cytometer and ethidium bromide. The effects were compared with those of curcumin, a natural antioxidant, whose chemical structure is included in those of cassumunins A and B. Pretreatment of rat thymocytes with the respective cassumunins at concentrations ranging from 100 nM to 3 microM dose-dependently prevented the hydrogen peroxide (H2O2)-induced decrease in cell viability. It had the same action, although less effective, against the treatment with cassumunin A or B (3 microM) immediately after or 60 min after start of the oxidative stress. Respective potencies of cassumunins A and B in protecting the cells suffering from H2O2-induced oxidative stress were greater than that of curcumin. It is suggested that cassumunins A and B may possess a potent protective action on living cells suffering from oxidative stress.

Animals↗
PubMed1998

Specific and reversible inactivation of protein tyrosine phosphatases by hydrogen peroxide: evidence for a sulfenic acid intermediate and implications for redox regulation.

Protein tyrosine phosphatases (PTPs) catalyze the hydrolysis of phosphotyrosine from specific signal-transducing proteins. Although regulatory mechanisms for protein kinases have been described, no general mechanism for controlling PTPs has been demonstrated. Numerous reports have shown that cellular redox status plays an important role in tyrosine phosphorylation-dependent signal transduction pathways. This study explores the proposal that PTPs may be regulated by reversible reduction/oxidation involving cellular oxidants such as hydrogen peroxide (H2O2). Recent reports indicated that H2O2 is transiently generated during growth factor stimulation and that H2O2 production is concomitant with relevant tyrosine phosphorylation. By use of recombinant enzymes, the effects of H2O2 on three PTPs [PTP1, LAR (leukocyte antigen-related), and VHR (vaccinia H1-related)] and three distinct serine/threonine protein phosphatases (PPs: PP2Calpha, calcineurin, and lambda phosphatase) were determined. Hydrogen peroxide had no apparent effect on PP activity. In contrast, PTPs were rapidly inactivated (kinact = 10-20 M-1 s-1) with low micromolar concentrations of H2O2 but not with large alkyl hydroperoxides. PTP inactivation was fully reversible with glutathione and other thiols. Because of the slower rate of reduction, modification occurred even in the presence of physiological thiol concentrations. By utilization of a variety of biochemical techniques including chemical modification, pH kinetic studies, and mutagenesis, the catalytic cysteine thiolate of PTPs was determined to be the selective target of oxidation by H2O2. By use of the electrophilic reagent 7-chloro-4-nitrobenzo-2-oxa-1, 3-diazole (NBD-Cl), it was shown that a cysteine sulfenic acid intermediate (Cys-SOH) is formed after attack of the catalytic thiolate on H2O2. A chemical mechanism for reversible inactivation involving a cysteine sulfenic acid intermediate is proposed.

Animals↗
PubMed1995

Melatonin reduces H2O2-induced lipid peroxidation in homogenates of different rat brain regions.

The ability of melatonin to modify H2O2-induced lipid peroxidation in brain homogenates was determined. The concentrations of brain malonaldehyde (MDA) and 4-hydroxyalkenals (4-HDA) were assayed as an index of induced membrane oxidative damage. Homogenates from five different regions of the brain (cerebral cortex, cerebellum, hippocampus, hypothalamus, and corpus striatum) derived from two different strains of rats, Sprague-Dawley and Wistar, were incubated with either H2O2 (5 mM) alone or H2O2 together with melatonin at increasing concentrations ranging from 0.1 to 4 mM. The basal level of lipid peroxidation was strain-dependent and about 100% higher in homogenates from the brain of Wistar rats than those measured in Sprague-Dawley rats. MDA + 4-HDA levels increased after H2O2 treatment in homogenates obtained from each region of the brain in both rat strains but the sensitivity of the homogenates from Sprague-Dawley rats was greater than that for the homogenates from Wistar rats (increases after H2O2 from 45 to 165% compared 20 to 40% for Sprague-Dawley and Wistar rats, respectively). Melatonin co-treatment reduced H2O2-induced lipid peroxidation in brain homogenates in a concentration-dependent manner; the degree of protection against lipid peroxidation was similar in all brain regions.

Animals↗
PubMed1990

Decreased in vivo survival of hydrogen peroxide-damaged baboon red blood cells.

In this study we attempt to establish the consequence of in vitro hydrogen peroxide (H2O2)-induced membrane damage as manifested by spectrin-hemoglobin (Sp-Hb) complex formation and decreased red blood cell (RBC) deformability to in vivo RBC survival in baboons. After exposure to 135 to 581 mumols/L H2O2 and reduction with dithiothreitol (DTE), baboon RBCs were infused into the animal, and the fraction of cells remaining in circulation after 24 hours and the lifespan of surviving cells were quantitated. In a dose-dependent fashion, a positive correlation was observed between in vitro membrane alterations and the 24-hour in vivo survival. While 12% of the control cells were removed from circulation in 24 hours, 23% were removed after treatment with 339 mumols/L H2O2, and 36% following exposure to 581 mumols/L H2O2. Pretreatment with carbon monoxide before exposure with H2O2 increased the survival of oxidized RBCs. RBCs not removed from circulation in the first 24 hours had a normal lifespan. Moreover, by selectively isolating biotin-labeled, peroxide-treated cells that survived the first 24-hour posttransfusion period, a significant decrease in Sp-Hb crosslinking was observed in these cells. These results suggest that a subpopulation of cells sensitive to oxidation were removed during the first 24 hours. To identify this population, the survival of density-fractionated RBCs exposed to oxidant stress was quantitated. No differences in either the 24-hour survival or RBC life span were observed between untreated low-density (MCHC less than or equal to 32g/dL) and high-density cells (MCHC greater than or equal to 37g/dL). However, striking differences were noted after treatment with 339 mumols/L H2O2, with the 24-hour survival of high-density cells showing a marked decrease compared with low-density cells. These data support our hypothesis that during peroxidative membrane damage, Hb oxidation initiates a sequence of events resulting in skeletal changes that lead to membrane alterations and, eventually, in vivo destruction, and that the dense, dehydrated cells are more susceptible to oxidant damage.

Animals↗
PubMed1992

Different modifications by vanillin in cytotoxicity and genetic changes induced by EMS and H2O2 in cultured Chinese hamster cells.

The modifying effects of vanillin on the cytotoxicity and 6-thioguanine (6TG)-resistant mutations induced by two different types of chemical mutagens, ethyl methanesulfonate (EMS) and hydrogen peroxide (H2O2), were examined using cultured Chinese hamster V79 cells. The effects of vanillin on H2O2-induced chromosome aberrations were also examined. Vanillin had a dose-dependent enhancing effect on EMS-induced cytotoxicity and 6TG-resistant mutations, when cells were simultaneously treated with vanillin. The post-treatment with vanillin during the mutation expression time of cells after treatment with EMS also showed an enhancement of the frequency of mutations induced by EMS. However, vanillin suppressed the cytotoxicity induced by H2O2 when cells were post-treated with vanillin after H2O2 treatment. Vanillin showed no change in the absence of activity of H2O2 to induce mutations. Post-treatment with vanillin also suppressed the chromosome aberrations induced by H2O2. The differential effects of vanillin were probably due to the quality of mutagen-induced DNA lesions and vanillin might influence at least two different kinds of cellular repair functions. The mechanisms by which vanillin enhances or suppresses chemical-induced cytotoxicity, mutations and chromosome aberrations are discussed.

Animals↗
PubMed1985

Metal ions and oxygen radical reactions in human inflammatory joint disease.

Activated phagocytic cells produce superoxide (O2-) and hydrogen peroxide (H2O2); their production is important in bacterial killing by neutrophils and has been implicated in tissue damage by activated phagocytes. H2O2 and O2- are poorly reactive in aqueous solution and their damaging actions may be related to formation of more reactive species from them. One such species is hydroxyl radical (OH.), formed from H2O2 in the presence of iron- or copper-ion catalysts. A major determinant of the cytotoxicity of O2- and H2O2 is thus the availability and location of metal-ion catalysts of OH. formation. Hydroxyl radical is an initiator of lipid peroxidation. Iron promoters of OH. production present in vivo include ferritin, and loosely bound iron complexes detectable by the 'bleomycin assay'. The chelating agent Desferal (desferrioxamine B methanesulphonate) prevents iron-dependent formation of OH. and protects against phagocyte-dependent tissue injury in several animal models of human disease. The use of Desferal for human treatment should be approached with caution, because preliminary results upon human rheumatoid patients have revealed side effects. It is proposed that OH. radical is a major damaging agent in the inflamed rheumatoid joint and that its formation is facilitated by the release of iron from transferrin, which can be achieved at the low pH present in the micro-environment created by adherent activated phagocytic cells. It is further proposed that one function of lactoferrin is to protect against iron-dependent radical reactions rather than to act as a catalyst of OH. production.

Arthritis, Rheumatoid↗
PubMed1989

Intestinal post-ischemic reperfusion injury: studies with neonatal necrotizing enterocolitis.

In the feline intestine studies have implicated superoxide (O.-) and other oxygen derived free radicals as initiators of injury as measured by increased capillary permeability during the reperfusion period. Biochemical mechanisms of this free radical generation include: xanthine oxidase dependent O.- production, hydrogen peroxide (H2O2) formation by superoxide dismutase (SOD), hydroxyl radical (OH-) production via the Haber-Weiss reaction, and lipid radical formation from membrane peroxidation. Pathological consequences of these events include inflammatory neutrophil infiltration, damage to the collagen and mucosal basement membrane, increased capillary permeability, edema, cell degeneration and necrosis. Animal models of neonatal necrotizing enterocolitis (NNEC) indicate that intestinal injury occurs after the etiologic factors (hypothermia, hypoxia) are removed. In order to determine the role of active oxygen species in the pathogenesis of NNEC, weanling hamsters and neonatal piglets were cold stressed and activities of pro/antioxidant enzymes were determined, and histopathologic and ultrastructural studies were performed. Cold stressed weanling hamsters showed a 55.7% (P less than 0.05) decrease in xanthine dehydrogenase/xanthine oxidase activity ratio. Light microscopy revealed scattered colonic mucosal erosions and submucosal edema in 50% of cold stressed animals. Transmission electron microscopy demonstrated degeneration of colonic mucosal epithelial cells, enlarged intracellular spaces, cytoplasmic vacuolization, and nuclear membrane swelling. The colonic serosa was also edematous and infiltrated with bacteria. Large intestinal tissue from cold stressed neonatal piglets showed a significant increase (P less than 0.05) in Mn and Cu, Zn, SOD, CAT, GSH-Red, total GSH, and Glc6-PD at 0 and 12 hrs. post stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

Evidence for participation of hydroxyl radical in increased microvascular permeability.

Polymorphonuclear leukocytes undergo the respiratory burst when exposed to a variety of stimuli. This is associated with the production of superoxide anion radical (O-2). Dismutation of O-2 can occur spontaneously to produce hydrogen peroxide (H2O2) and in the presence of metal catalysts O-2 and H2O2 can react to form hydroxyl radical (OH.). Some of these reactive species are released into the interstitium and may cause lipid peroxidation and depolymerization of macromolecules. We have studied the effect of free radicals on vascular permeability. Hypoxanthine and xanthine oxidase were applied topically on the hamster cheek pouch microcirculation model, injected intravenously with FITC-dextran 150 (Mw 150,000) to visualize permeability changes. This caused a flux of O-2 and a significant increase in macromolecular leakage. An attempt was made to elucidate the roles of different radicals by addition of superoxide dismutase (SOD), catalase (CAT), dimethyl sulfoxide (DMSO) and L-methionine to the reaction mixture. A significant decrease in leakage was found with all these substances, indicating OH. or possibly singlet oxygen damage. These results indicate that a free radical flux can cause permeability changes, and we suggest that part of the permeability change seen during inflammation may be related to free radical flux produced by activated leukocytes.

Animals↗
PubMedDate not supplied

Determination of absolute chemiluminescence quantum yields for reactions of bis-(pentachlorophenyl) oxalate, hydrogen peroxide and fluorescent compounds.

Absolute chemiluminescence quantum yields (phi CL) for reactions of bis-(pentachlorophenyl) oxalate (PCPO), hydrogen peroxide (H2O2) and 9:10 diphenyl anthracene (DPA) have been determined. A fully corrected chemiluminescence monitoring spectrometer was calibrated for spectral sensitivity using the chemiluminescence of the bis-(pentachlorophenyl) oxalate system as a liquid light source, the total photon output of which had previously been determined by chemical actinometry. At high (PCPO)/(H2O2) ratios phi CL was found to be independent of PCPO and H2O2 concentrations.

Anthracenes↗
PubMed1987

The biological activity of hydrogen peroxide. III. Induction of Epstein-Barr virus via indirect action, as compared with TPA and teleocidin.

Hydrogen peroxide (H2O2) was found to be a potent inducer of the production of the early antigen complex (EA) and/or virus capsid antigen (VCA), determined by Epstein-Barr virus (EBV). Maximum synthesis of EBV antigens was induced by 0.2 mM H2O2, 5 days after a single 10-min treatment, in both B95-8 cells (30.2%) and P3HR-I cells (17.4%). These induction frequencies by H2O2 of proteins encoded by the EBV genome were almost the same as those obtained by 10 min treatment with the potent inducers, 12-O-tetradecanoylphorbol-13-acetate (TPA) and teleocidin. In combination with n-butyrate (4mM), H2O2 showed an additive induction of EBV antigens (1.9- and 1.7-fold in B95-8 and P3HR-I cells, respectively) and was as efficient as TPA and teleocidin. H2O2 induced EBV antigens at a very low level (less than 1%) in Raji cells by itself, but it induced EBV antigens synergistically in combination with n-butyrate (about 25-fold). In combined treatments using H2O2, TPA and teleocidin, the combination of H2O2 and TPA or H2O2 and teleocidin showed additive effects on the induction of synthesis of EBV antigens, but the combination of TPA and teleocidin showed almost the same induction level as that produced by H2O2, TPA or teleocidin alone. The inducing activities of H2O2, TPA and teleocidin were suppressed completely, in the case of H2O2, and slightly, in the cases of TPA and teleocidin, by treatment with catalase. Moreover, the effects of H2O2 were largely suppressed by scavengers of hydroxyl radical (X OH) and singlet oxygen (1O2), but not by superoxide dismutase (SOD), whereas the induction of EBV proteins by TPA and teleocidin was largely suppressed by SOD, but only slightly by scavengers of X OH and 1O2. Thus, the biological actions of H2O2 on the activation of the EBV genome seem to be essentially different from those of TPA and teleocidin, though the biological actions of TPA and teleocidin may be partially ascribed to those of H2O2.

Animals↗
PubMed1998

In vivo fluorometric measurement of cerebral oxidative stress using 2'-7'-dichlorofluorescein (DCF).

The time course of oxidative stress following cerebral ischemia and reperfusion has been obscure, although oxygen-derived free radicals have been postulated to play an important role in the progression of reperfusion injury. We have examined the time profile of hydrogen peroxide (H2O2) generation in the rat cortex following incomplete forebrain ischemia and reperfusion. We used 20 male Sprague-Dawley rats anesthetized with alpha-chloralose and urethane. A closed cranial window was created in the temporoparietal skull, and 2'-7'-dichlorofluorescein (DCF), a sensitive fluorescent probe for H2O2, was loaded intracellularly by the superfusion technique. We simultaneously monitored DCF fluorescence and reflectance from the cortex with an in vivo fluoromicroscope having two photomultiplier tubes, and subtracted the hemodynamic artifact from DCF fluorescence. Incomplete forebrain ischemia was induced by temporal ligation of both common carotid arteries combined with hypotension. The results showed that corrected DCF fluorescence remained unchanged during ischemia, but increased following reperfusion, indicating enhanced H2O2 generation. Pretreatment by intraperitoneal injection of catalase attenuated H2O2 generation significantly. that H2O2 generation is mainly enhanced following reperfusion.

Animals↗
PubMed1998

H2O2 causes endothelial barrier dysfunction without disrupting the arginine-nitric oxide pathway.

We have previously demonstrated that nitric oxide (.NO) donors attenuate and that inhibition of endogenous nitric oxide synthase (NOS) enhances hydrogen peroxide (H2O2)-mediated porcine pulmonary artery endothelial cell (PAEC) injury. The current study investigates the hypothesis that oxidant-mediated inhibition of NOS contributes to PAEC injury. PAEC barrier function, measured as the transmonolayer clearance of albumin, was significantly impaired by H2O2 (10-100 microM) in the absence of cytotoxicity. Treatment with H2O2 did not alter NOS activity, measured as the conversion of [3H]arginine to [3H]citrulline in PAEC lysates, either immediately after treatment with 0-250 microM H2O2 for 30 min or for up to 120 min after treatment with 100 microM H2O2. H2O2 had little effect on NOS activity in intact PAECs, measured as 1) the formation of [3H]citrulline in [3H]arginine-loaded PAECs, 2) PAEC guanosine 3',5'-cyclic monophosphate content, and 3) PAEC.NO release to the culture media. These results indicate that the arginine-.NO pathway remains intact after exposure to oxidant conditions sufficient to promote functional derangements of vascular endothelial cells.

Animals↗
PubMed1992

Multicellular oxidant defense in unicellular organisms.

Although catalase is thought to be a major defense against hydrogen peroxide (H2O2), the catalase activity within individual Escherichia coli fails to protect against exogenous H2O2. Contrary to earlier reports, we find that dilute suspensions of wild-type and catalase-deficient E. coli are identical in their sensitivity to H2O2, perhaps because even wild-type, catalase-positive E. coli cannot maintain an internal/external concentration gradient of this highly diffusible oxidant. However, concentrated suspensions or colonies of catalase-positive E. coli do preferentially survive H2O2 challenge and can even cross-protect adjacent catalase-deficient organisms. Furthermore, high-density catalase-positive--but not catalase-negative--E. coli can survive and multiply in the presence of competitive, peroxide-generating streptococci. These observations support the concept that bacterial catalase may defend colonial, but not individual, E. coli against environmental H2O2. Group protection by the activity of enzymes that mitigate oxidative stress may have been a driving force in the evolution of multicellular organisms.

Biological Evolution↗
PubMed1995

Effect of in vitro incorporation of prostanoid precursors, superoxide radical and hydrogen peroxide on platelet function.

The level of cyclic adenosine monophosphate (cAMP) in human platelets is known to be an important regulator of platelet function. The polyunsaturated fatty acids (PUFA) dihomo-gamma-linolenic acid (DHLA), and eicosapentaenoic acid (EPA), precursors of the prostaglandin (PG) 1 and 3 series respectively, were studied for their ability to stimulate platelet cAMP and/or PGE1 levels, and to inhibit platelet aggregation (PAg). Incubation of washed platelets (1 x 10(8)/ml) with 125 microM DHLA increased intraplatelet levels of PGE1 from 197 +/- 7 to 1622 +/- 9.7 picograms/10(8), cAMP from 3 +/- 0.8 to 31 +/- 1.9 picomoles/10(8), and inhibited collagen-induced PAg. Addition of 1 mumole of xanthine per unit of xanthine oxidase (a superoxide radical generating system) to the incubating medium potentiated the effects of both fatty acids, whereas 240 microM Hydrogen Peroxide (H2O2) inhibited these effects. These results suggest that: (1) DHLA may be more effective in inhibiting PAg than EPA, which has been reported to reduce the incidence of coronary diseases in some human populations; (2) That superoxide radical may activate the platelet cyclooxygenase system to increase lipid peroxidation of these PUFA prostanoid precursors and may result in the inhibition of PAg, whereas H2O2 may have an opposite effect.

8,11,14-Eicosatrienoic Acid↗
PubMed1996

K-7259, a novel dilazep derivative, and d-propranolol attenuate H2O2-induced cell damage.

We studied the effects of dilazep, K-7259 (a novel derivative of dilazep) and d-propranolol on the change in cell shape and accumulation of nonesterified fatty acids (NEFA) induced by hydrogen peroxide (H2O2) in isolated rat cardiac myocytes. Myocytes were incubated in a Krebs-Ringer bicarbonate buffer containing 2 mM diethyltriamine pentaacetic acid (DETAPAC) and 2mM FeSO4 for 10 min, and then treated with 2mM H2O2 for 50 min. Before the treatment with H2O2, the percentage of the number of rod-shaped cells to that of total cells was 66 +/- 2%, and decreased to 35 +/- 3%, 25 +/- 4% and 14 +/- 2%, after 30, 40 and 50 min of the H2O2 treatment, respectively. The levels of NEFA (lauric, myristic, palmitoleic, arachidonic, linoleic, palmitic, oleic and stearic acids) increased after the treatment with H2O2. In the absence of FeSO4 and DETAPAC, however, H2O2 did not have these effects, and therefore all the experiments with drugs were performed in the presence of Fe2SO4 and DETAPAC. K-7259 (30 microM) and d-propranolol (50 microM) attenuated both the changes in cell shape and accumulation of NEFA induced by H2O2, whereas dilazep (30 or 50 microM) did not. N-(2-mercaptopropionyl)glycine (2 mM), an .OH scavenger, inhibited the H2O2-induced changes completely. These results suggest that K-7259 and d-propranolol attenuate the H2O2-induced changes in cell shape and accumulation of NEFA, probably because of their .OH-scavenging effect.

Animals↗
PubMed1994

Reduction by NG-nitro-L-arginine of H2O2-induced endothelial cell injury.

1. The effects of three analogues of NG-nitro-L-arginine (L-NOARG) and NG-monomethyl-L-arginine (L-NMMA), inhibitors of nitric oxide (NO) synthase, on hydrogen peroxide (H2O2)-induced endothelial cell injury were studied. 2. Endothelial cell injury was assessed by measuring the release of intracellular lactate dehydrogenase (LDH) and 51Cr. 3. Addition of H2O2 (250-1,000 microM) to endothelial cells induced the release of LDH dose-dependently. The release of LDH was reduced by pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 10(-4)-4 x 10(-3) M), L-NOARG (10(-4)-4 x 10(-3) M) and NG-nitro-L-arginine benzyl ester (L-NABE, 10(-4)-4 x 10(-3) M), inhibitors of NO synthase. 4. L-NOARG analogues also reduced H2O2-induced 51Cr release from endothelial cells, while L-NMMA had no effect. 5. The protective effect of L-NAME was not reversed by addition of L-arginine (L-Arg, 1-10 mM). 6. Both L-NAME and L-NMMA completely inhibited L-Arg metabolism to L-citrulline coupled with NO synthesis. 7. These findings suggest that L-NOARG analogues but not L-NMMA reduced H2O2-induced endothelial cell injury, and that these effects may not be related to inhibition of NO production.

Amino Acid Oxidoreductases↗
PubMed1998

Constitutive and inducible hsp70s are involved in oxidative resistance evoked by heat shock or ethanol.

Improved cardiac post-ischemic recovery after whole-body hyperthermia is correlated with an increased expression of the heat shock proteins (hsps). The inducible hsp70 (hsp70i) has a known cardioprotective effect against ischemia/reperfusion injury. Here, we studied whether other hsps are also involved in cardioprotection. Using rat heart-derived H9c2 myocytes, we observed that preheating at 43 degreesC for 20 min conferred resistance to hydrogen peroxide (H2O2). The resistance to mild H2O2 toxicity (3-5 micro mol/10(7) cells) appeared early and persisted, whereas the resistance to moderate H2O2 toxicity (6-9 micro mol/10(7) cells) was detectable only at 20-44 h post heat shock. No resistance was observed at higher doses of hydrogen peroxide (10-12 micro mol/10(7) cells), indicating that severe toxicity exceeds the capacity of the induced protective mechanism. Coincidentally, this thermal regimen elicited a rapid and prolonged increase in the cellular level of hsp70i, and a delayed and transient induction of the constitutive hsp70 (hsp70c). Nuclear translocations of hsp70i and hsp70c also occurred upon heat stimulation. A homogeneous distribution of the accumulated hsp70i and hsp70c throughout the nuclei and cytoplasm paralleled the development of heat-induced resistance to moderate H2O2 challenge. Application of another hsp inducer, ethyl alcohol, evoked a similar pattern of H2O2 resistance, and hsp induction and distribution. Our results suggest that induction and subcellular distribution of hsp70s contribute importantly to cellular antioxidant defenses, and that a co-operation between hsp70i and hsp70c may improve cardiac preservation during oxidative insult.

Animals↗
PubMed1984

Role of oxygen radicals in cardiac injury due to reoxygenation.

The ability of oxygen derived free radicals to induce irreversible cellular injuries during reoxygenation was studied on isolated potassium-arrested heart preparation. Enzymatic scavengers of hydrogen peroxide (H2O2) and superoxide anion (O-2), catalase and superoxide dismutase, were not effective in reversing the cardiac alterations induced by hypoxia. Cellular injuries induced by reoxygenation, 'Oxygen paradox', were partially prevented by scavengers of H2O2 (glutathione reduced form, catalase) and O-2 (superoxide dismutase). The 'oxygen paradox' was associated with a release of malonaldehyde. The inhibition of lipid peroxidation by alpha-tocopherol prevented the toxic effect of molecular oxygen on hypoxic hearts. The specific quenchers of singlet oxygen (histidine) and hydroxyl radical (mannitol) reduced the peroxidation of unsaturated lipids and the intensity of the 'oxygen paradox' phenomenon. The results indicate that in cardiac muscle (i) oxygen derived free radicals are important byproducts of abnormal oxidative metabolism present during the post hypoxic period; (ii) the 'oxygen paradox' phenomenon is related to the formation of lipid hydroperoxides leading to the cellular membrane disruption and to the irreversible alteration of cardiac integrity.

Adenosine Triphosphate↗