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PubMed1998

Response of lens epithelial cells to hydrogen peroxide stress and the protective effect of caloric restriction.

Hydrogen peroxide (H2O2) has been reported to be present at significant levels in the lens and aqueous humor in some cataract patients and suggested as a possible source of chronically inflicted damage to lens epithelial (LE) cells. We measured H2O2 effects on bovine and mouse LE cells and determined whether LE cells from old calorically restricted mice were more resistant to H2O2-induced cellular damage than those of same age ad libitum fed (AL) mice. Bovine lens epithelial cells were exposed to H2O2 at 40 or 400 microM for 2 h and then allowed to recover from the stress. The cells were assayed for DNA damage, DNA synthesis, cell viability, cell morphology, response to growth stimuli, and proliferation potential. Hydrogen peroxide-treated cells showed an increased DNA unwinding 50% greater than that for untreated controls. These DNA strand breaks appeared to be almost completely rejoined by 30 min following removal of the cells from a 2-h exposure. The 40 microM exposure did not produce a significantly lower DNA synthesis rate than the control, it responded to growth factor stimuli, and it replicated as did the control cells after removal of H2O2. The 400 microM H2O2 severely affected DNA synthesis and replication, as shown by increased cell size and by markedly reduced clonal cell growth. The cells did not respond to growth stimulation by serum or growth factors and lost irreversibly the capacity to proliferate. The responses of LE cells from old adlib diet (AL) and calorically restricted (CR) mice to H2O2 were significantly different. Exposure of LE cells to 20, 40, or 100 microM H2O2 for 1 h induces a significant loss of cellular proliferation in cells from old AL mice. LE cells from long-term CR mice of the same strain and age were more resistant to oxidative damage at all three concentrations of H2O2 than those of both old and young AL mice and showed a significantly higher proliferation potential following treatment. It is concluded that CR results in superior resistance to reactive oxygen radicals in the lens epithelium.

Age Factors↗
PubMed1991

Hydrogen peroxide alters the physical state and function of the plasma membrane of pulmonary artery endothelial cells.

Hydrogen peroxide (H2O2) is an important mediator of acute oxidative injury to vascular endothelium. Because the plasma membrane is the initial site of interaction between endothelial cells and extracellular H2O2 produced by stimulated neutrophils or macrophages, we evaluated the effect of H2O2 on the physical state, i.e., fluidity, and function of porcine pulmonary artery endothelial cell plasma membranes. Lactate dehydrogenase (LDH) release, 5-hydroxytryptamine (5-HT) uptake, limiting fluorescence anisotropy (r infinity) for trimethylamino-diphenylhexatriene (TMA-DPH), and conjugated dienes were measured 0.5, 6, and 24 hr after cells were exposed for 30 min to 50-microM H2O2 or Hank's Balanced Salt Solution (control). Compared with control cells, H2O2 caused significant increases in LDH release and in 5-HT uptake 6 hr after exposure. The increase in 5-HT uptake was not blocked by imipramine. H2O2 also caused a significant increase in r infinity for TMA-DPH 0.5 hr after exposure and a significant reduction in r infinity for TMA-DPH 6 hr after exposure. Cellular contents of conjugated dienes were increased 0.5 and 6 hr after exposure to H2O2. Twenty-four hours after exposure LDH release, r infinity, 5-HT uptake, and conjugated dienes had returned to control levels. Preincubation with 50-microM alpha-tocopherol (vitamin E) or 1-mM or 10-mM dimethylthiourea (DMTU) for 1 hr or 24 hr prevented endothelial cell injury, whereas addition of vitamin E or DMTU to the medium 1 hr or 3 hr after H2O2 exposure did not protect against injury. These results indicate that H2O2 causes significant damage to the plasma membrane of pulmonary artery endothelial cells in vitro, leading to alterations in fluidity and leakiness of the membrane. This injury is associated with membrane lipid peroxidation, is reversible, and can be prevented by pretreatment, but not by post-treatment, with vitamin E or DMTU.

Animals↗
PubMed1994

[Superoxide formation and lipid peroxidation by the mitochondrial electron-transfer chain].

Isolated mitochondria supplemented with succinate or NAD(+)-linked substrates generate hydrogen peroxide (H2O2) in State 4 and the generation is enhanced by antimycin A, an inhibitor of the respiratory chain. Superoxide is a stoichiometric precursor of mitochondrial H2O2 because the ratio of O2-/H2O2 generation rates is close to 2.0 and is generated by an autoxidizable component in the NADH dehydrogenase and the ubiquinone-cytochrome b site. Lipid peroxidation is a free radical-mediated degradation of polyunsaturated fatty acids. Lipid-peroxidation reactions by bovine submitochondrial particles are supported by NADH or NADPH in the presence of ADP-Fe3+ chelate. Electrons from NADH are supplied to the reactions from a component between the substrate site and the rotenone-sensitive site of the NADH dehydrogenase. The peroxidation is dependent on the rate of electron input into the respiratory chain and on the concentration of reduced ubiquinone. Alteration of inner-membrane components and damage to electron-transfer activities of submitochondrial particles are induced by lipid peroxidation. 1-Melhyl-4-phenylpyridinium (MPP+), a metabolite of a parkinsonism-inducing drug, induces NADH-dependent superoxide formation and enhances NADH-dependent lipid peroxidation in submitochondrial particles, indicating that the oxidative stress induced by MPP+ may potentiate its toxicity in dopamine neurons.

Electron Transport↗
PubMed2000

UVA-induced oxidative damage in retinal pigment epithelial cells after H2O2 or sparfloxacin exposure.

Retinal impairment is one of the leading causes of visual loss in an aging human population. To explore a possible cause for retinal damage in the human population, we have monitored DNA oxidation in human retinal pigment epithelial (RPE) cells after exposure to hydrogen peroxide (H2O2) or the quinolone antibacterial sparfloxacin. When H2O2- or sparfloxacin-exposed cells were further exposed to ultraviolet A (UVA) irradiation, oxidative damage to the DNA of these cells was greatly increased over baseline values. This RPE+pharmaceutical-UVA cell system was developed to mimic in vivo retinal degeneration, seen in mouse studies using quinolone and UVA exposure. DNA damage produced by sparfloxacin and UVA in RPE cells could be remedied by the use of antioxidants, indicating a possible in vivo method for prevention or minimization of retinal damage in humans

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1986

The effects of Con A-induced lymphokines from the T-lymphocyte subpopulations on human monocyte leishmanicidal capacity and H2O2 production.

The effects of concanavilin A (Con A)-induced lymphokines from human peripheral blood mononuclear cells, enriched helper and suppressor lymphocyte populations and recombinant interferon-gamma (IFN-gamma) on the ability of monocytes to promote killing of intracellular Leishmania major (L. major) amastigotes and to induce the production of hydrogen peroxide (H2O2) was examined. All these mitogen-induced supernatants contained active IFN-gamma. There were no differences in the ability of these supernatants or IFN-gamma to promote the monocyte killing of the L. major amastigotes or H2O2 production. An increase in H2O2 production by monocyte monolayers was observed following the addition of either of these supernatants or IFN-gamma alone. In addition, a marked increase in the production of H2O2 was observed following priming with either of these mitogen-induced supernatants or IFN-gamma and the addition of a second stimulus, phorbol myristate acetate (PMA). Monoclonal antibody to IFN-gamma abrogated the increase in production of H2O2 by all these mitogen-induced supernatants; however, this antibody only resulted in partial inhibition of the leishmaniacidal effect of these lymphokines on human monocytes. These results would suggest that IFN-gamma is the component of the lymphokine that is largely or exclusively responsible for H2O2 production, while other factors in addition to IFN-gamma are important in promoting oxygen-independent mechanisms for the killing of intracellular L. major amastigotes.

Cells, Cultured↗
PubMed2000

Epithelial and stromal uterine cells cultured in vitro protect bovine sperm from hydrogen peroxide.

It is known that large amounts of leukocytes colonize the uterus, and that these leukocytes can produce considerable quantities of hydrogen peroxide (H2O2) and other reactive oxygen species that are toxic to sperm. It has been shown recently that oviductal fluid has a catalase that helps to maintain sperm motility. Therefore, the current experiment was performed to determine if a similar mechanism of protection exists against peroxides within uterine cells. Sperm motility and velocity were recorded after a 6h incubation in 1) conditioned media in the presence of endometrial cells, 2) conditioned media without endometrial cells, 3) control media (48h without cells) over endometrial cells, or 4) control media alone. All these treatments were performed in the presence or absence of added catalase. Conditioned media, endometrial cells and catalase had a significant positive effect on the maintenance of sperm motility and velocity. Addition of anti-catalase antibodies did not neutralize the beneficial effect of the conditioned media. However, the concentrations of aromatic amino acids, known substrates for sperm amino acid oxidase, were significantly lower in uterine conditioned media as compared to control medium. This reduction of aromatic amino acids was in correlation with reduced H2O2 production by sperm as estimated by chemiluminescence. These results suggest that epithelial and stromal uterine cells do not maintain sperm motility by secreting catalase in the conditioned media, but rather by reducing the levels of aromatic amino acids and thus of peroxides generated in the presence of spermatozoa.

Animals↗
PubMed1998

Hydrogen peroxide-induced cytoskeletal rearrangement in cultured pulmonary endothelial cells.

Although the signaling pathways leading to hydrogen peroxide (H2O2)-induced endothelial monolayer permeability remain ambiguous, cytoskeletal proteins are known to be essential for maintaining endothelial integrity and regulating solute flux through the monolayer. We have recently demonstrated that thrombin-induced actin reorganization in bovine pulmonary artery endothelial cells (BPAEC) requires activation of both myosin light chain kinase (MLCK) and protein kinase C (PKC). Therefore, the present study was designed to investigate the effects of H2O2 on actin reorganization in BPAEC. H2O2 initiated sustained recruitment of actin to the cytoskeleton and transient myosin recruitment in a time- and concentration-dependent manner. The H2O2-induced actin recruitment was significantly inhibited by the calmodulin antagonists, W7 and TFP, but not by the MLCK inhibitor, KT5926, nor the PKC inhibitors, H7 and calphostin C. H2O2 also caused actin filament rearrangement in BPAEC with disruption of the dense peripheral bands and formation of stress fibers. These alterations occurred prior to actin translocation to the cytoskeleton and are prevented by inhibition of either MLCK or PKC. High concentrations of H2O2 transiently attenuated PKC activity but slightly increased the phosphorylation of the prominent PKC substrate and actin-binding protein, myristoylated alanine-rich C kinase substrate (MARCKS), by 5 min. However, MARCKS phosphorylation was reduced to below basal levels by 30 min. On the other hand, H2O2 induced a time- and dose-dependent phosphorylation of myosin light chains which was eliminated by both MLCK and PKC inhibitors. These data suggest that MLCK contributes to H2O2-induced myosin light chain phosphorylation and actin rearrangement and that PKC may play a permissive role. Neither of these enzymes appears to be involved in the H2O2-induced recruitment of actin to the cytoskeleton.

Actins↗
PubMed1987

1 alpha,25 Dihydroxyvitamin D3 and mononuclear phagocytes: enhancement of mouse macrophage and human monocyte hydrogen peroxide production without alteration of tumor cytolysis.

1 alpha,25 dihydroxyvitamin D3 (1,25 D3) is known to interact with hematopoietic cells. The purpose of this study was to determine the effect of 1,25 D3 on hydrogen peroxide (H2O2) production and tumor cell killing by mouse peritoneal macrophages and human blood monocytes. Enhanced monocyte and macrophages phorbol myristate acetate (PMA)-stimulated H2O2 production was observed at concentrations of 0.13 to 130 nM 1,25 D3 and and was maximal at 1.3 nM. At concentrations of 100 U/ml, gamma interferon (IFN-gamma) alone had a similar effect but, in combination with 1,25 D3, there was no cooperative effect. At concentrations ranging from 0.13 to 130 nM, 1,25 D3 failed to augment tumor cell lysis by macrophages from peptone-injected normal or bacillus Calmette-Guerin (BCG)-infected mice, or by blood monocytes from normal humans. Our results indicate that 1,25 D3 can activate the monocyte and macrophage for H2O2 secretion without concomitant activation for tumor cell killing.

Animals↗
PubMed1993

Stimulation of the bactericidal activity of polymorphonuclear leukocytes by manganese.

An antioxidant effect of manganese (Mn) complexes due to the scavenging of the superoxide anion (O2-.) or to the decomposition of hydrogen peroxide (H2O2) has been described. We report here that Mn also can exert a prooxidant effect under certain experimental conditions. Thus Mn2+ in phosphate buffer increased the bactericidal effect of phorbol myristate acetate-stimulated polymorphonuclear leukocytes (PMNs) on extracellular Escherichia coli. This effect was inhibited by azide, catalase, and a decrease in chloride concentration and was not observed when normal PMNs were replaced by those of patients with chronic granulomatous disease or myeloperoxidase (MPO) deficiency. Mn2+ could be replaced by Mn3+ or by superoxide dismutase (SOD). These findings suggest that Mn (or SOD), by increasing the conversion of O2-. to H2O2, can increase the activity of the MPO-H2O2-chloride antimicrobial system released by stimulated PMNs.

Blood Bactericidal Activity↗
PubMed2001

Activation of rho is involved in the mechanism of hydrogen-peroxide-induced lung edema in isolated perfused rabbit lung.

Acute lung injury is attributed primarily to increased vascular permeability caused by reactive oxygen species derived from neutrophils, such as hydrogen peroxide (H2O2). Increased permeability is accompanied by the contraction and cytoskeleton reorganization of endothelial cells, resulting in intercellular gap formation. The Rho family of Ras-like GTPases is implicated in the regulation of the cytoskeleton and cell contraction. We examined the role of Rho in H2O2-induced pulmonary edema with the use of isolated perfused rabbit lungs. To our knowledge, this is the first study to examine the role of Rho in increased vascular permeability induced by H2O2 in perfused lungs. Vascular permeability was evaluated on the basis of the capillary filtration coefficient (Kfc, ml/min/cm H2O/100 g). We found that H2O2 (300 microM) increased lung weight, Kfc, and pulmonary capillary pressure. These effects of H2O2 were abolished by treatment with Y-27632 (50 microM), an inhibitor of the Rho effector p160 ROCK. In contrast, the muscular relaxant papaverine inhibited the H2O2-induced rise in pulmonary capillary pressure, but did not suppress the increases in lung weight and Kfc. These findings indicate that H2O2 causes pulmonary edema by elevating hydrostatic pressure and increasing vascular permeability. Y-27632 inhibited the formation of pulmonary edema by blocking both of these H2O2-induced effects. Our results suggest that Rho-related pathways have a part in the mechanism of H2O2-induced pulmonary edema.

Amides↗
PubMed1989

Measurement of hydrogen peroxide in plasma and blood.

Measurement of the oxygen metabolite hydrogen peroxide (H2O2) in biological fluids such as plasma could be of interest because it might indicate participation of toxic oxygen species in tissue injury. Recently several reports claimed to measure H2O2 using spectrophotometric and high pressure liquid chromatographic (HPLC) techniques that utilize oxidation of a substrate to a product by a peroxidase. In such a system it is crucial to perform two control experiments to verify whether the measured substance is H2O2. The specificity of the assay for H2O2 should be checked with catalase, and the degradation of H2O2 or inhibition of the assay system by the sample should be checked by determining the recovery of exogenously added H2O2. We performed both types of controls for HPLC and spectrophotometric determinations of H2O2 in plasma and blood. Our results indicate that contrary to previous reports in the literature the measured substance(s) in plasma or blood is not H2O2. Moreover, quantitative measurements of H2O2 in plasma or blood by HPLC was unreliable due to the irreversible binding of H2O2 to the column surface.

Animals↗
PubMed1998

Impairment of the mitochondrial electron chain transport prevents NF-kappa B activation by hydrogen peroxide.

A large body of work has been devoted to mechanisms leading to the activation of the transcription factor NF-kappa B in various cell types. Several studies have indicated that NF-kappa B activation by numerous stimuli depends on the intracellular generation of reactive oxygen species (ROS). In this report, we first demonstrated that inhibition of the electron transport chain by either rotenone or antimycine A gave rise to dose-dependent inhibition of NF-kappa B translocation induced by 150 microM of hydrogen peroxide (H2O2). Conversely, the impairment of the mitochondrial respiratory chain did not affect T lymphocyte treatment by TNF-alpha (tumor necrosis factor alpha) or pre-B lymphocyte treatment with LPS (lipopolysaccharide). We also showed that oligomycine which inhibits ATP synthase and FCCP, which uncouples respiration also led to dose-dependent inhibition of NF-kappa B activation by H2O2. All these inhibitors were also shown to inhibit mitochondrial respiration in lymphocytes assessed by oxygen consumption. Although only a transient drop in ATP concentration was observed when lymphocytes were treated by H2O2, this effect was remarkably reinforced in the presence of oligomycine demonstrating the crucial role of ATP in the signal transduction pathway induced by H2O2.

Adenosine Triphosphate↗
PubMed1997

Differential induction of adaptive responses by paraquat and hydrogen peroxide against the genotoxicity of methyl mercuric chloride, maleic hydrazide and ethyl methane sulfonate in plant cells in vivo.

Induction of adaptive response by conditioning doses of paraquat (PQ) and hydrogen peroxide (H2O2) in embryonic shoot cells of Hordeum vulgare and root meristem cells of Allium cepa was tested against the genotoxicity of challenge doses of methyl mercuric chloride (MMCl), maleic hydrazide (MH) or ethylmethane sulfonate (EMS). Plant tissue fixed at different recovery hours following the challenge treatments was analysed for cells with genotoxicity markers that include spindle or chromosome aberrations and micronuclei. The results provided clear-cut evidence that whereas H2O2 induced adaptive response for the chromosome damage caused by MMCl and MH, PQ induced the same for MMCl and EMS, but not for damage caused by MH. The findings pointed to the differences in the underlying mechanisms of oxidative responses induced by H2O2 and O2-.

Adaptation, Physiological↗
PubMed1985

A study of the sensitivity of Leishmania donovani promastigotes and amastigotes to hydrogen peroxide. I. Differences in sensitivity correlate with parasite-mediated removal of hydrogen peroxide.

The sensitivities of promastigotes and amastigotes of Leishmania donovani to reagent or glucose oxidase-generated hydrogen peroxide (H2O2) were examined in a phagocyte-free system and compared with direct measurements of loss of H2O2 due to reaction with the parasite. Using a combined fluorescence dye uptake/dye exclusion viability assay in conjunction with motility and transformation data it was shown that log-phase promastigotes harvested from recently transformed cultures were intermediate in their H2O2 sensitivity between amastigotes and log-phase promastigotes harvested from long-term subcultures. It was also observed that, while promastigotes are equally sensitive to either form of H2O2 stress, amastigotes are more resistant to single larger amounts of reagent H2O2 than to equivalent amounts of H2O2 generated over a 1 h period. In each case the respective LD50 values obtained for each form of the parasite under each type of H2O2 stress correlated with saturation of their ability to remove H2O2 from the phagocyte-free system. For both promastigotes and amastigotes there was always a time delay after removal of either form of H2O2 stress before H2O2-mediated damage to membranes became apparent. The results suggest that the differential responses of promastigotes and amastigotes to different forms of H2O2 stress may depend upon different H2O2 scavenging mechanisms examined in more detail in the accompanying paper.

Animals↗
PubMed1999

The identification of primary sites of superoxide and hydrogen peroxide formation in the aerobic respiratory chain and sulfite reductase complex of Escherichia coli.

The fitness of organisms depends upon the rate at which they generate superoxide (O-2) and hydrogen peroxide (H2O2) as toxic by-products of aerobic metabolism. In Escherichia coli these oxidants arise primarily from the autoxidation of components of its respiratory chain. Inverted vesicles that were incubated with NADH generated O-2 and H2O2 at accelerated rates either when treated with cyanide or when devoid of quinones, implicating an NADH dehydrogenase as their source. Null mutations in the gene encoding NADH dehydrogenase II averted autoxidation of vesicles, and its overproduction accelerated it. Thus NADH dehydrogenase II but not NADH dehydrogenase I, respiratory quinones, or cytochrome oxidases formed substantial O-2 and H2O2. NADH dehydrogenase II that was purified from both wild-type and quinone-deficient cells generated approximately 130 H2O2 and 15 O-2 min-1 by autoxidation of its reduced FAD cofactor. Sulfite reductase is a second autoxidizable electron transport chain of E. coli, containing FAD, FMN, [4Fe-4S], and siroheme moieties. Purified flavoprotein that contained only the FAD and FMN cofactors had about the same oxidation turnover number as did the holoenzyme, 7 min-1 FAD-1. Oxidase activity was largely lost upon FMN removal. Thus the autoxidation of sulfite reductase, like that of the respiratory chain, occurs primarily by autoxidation of an exposed flavin cofactor. Great variability in the oxidation turnover numbers of these and other flavoproteins suggests that endogenous oxidants will be predominantly formed by only a few oxidizable enzymes. Thus the degree of oxidative stress in a cell may depend upon the titer of such enzymes and accordingly may vary with growth conditions and among different cell types. Furthermore, the chemical nature of these reactions was manifested by their acceleration at high temperatures and oxygen concentrations. Thus these environmental parameters may also directly affect the O-2 and H2O2 loads that organisms must bear.

Aerobiosis↗
PubMed2001

Pyrite-induced hydrogen peroxide formation as a driving force in the evolution of photosynthetic organisms on an early earth.

The remarkable discovery of pyrite-induced hydrogen peroxide (H2O2) provides a key step in the evolution of oxygenic photosynthesis. Here we show that H2O2 can be generated rapidly via a reaction between pyrite and H2O in the absence of dissolved oxygen. The reaction proceeds in the dark, and H2O2 levels increase upon illumination with visible light. Since pyrite was stable in most photic environments prior to the rise of O2 levels, this finding represents an important mechanism for the formation of H2O2 on early Earth.

Biological Evolution↗
PubMed2000

Peroxide processing in photosynthesis: antioxidant coupling and redox signalling.

Photosynthesis has a high capacity for production of hydrogen peroxide (H2O2), but the intracellular levels of this relatively weak oxidant are controlled by the antioxidant system, comprising a network of enzymatic and non-enzymatic components that notably includes reactions linked to the intracellular ascorbate and glutathione pools. Mutants and transformed plants with specific decreases in key components offer the opp ortunity to dissect the complex system that maintains redox homeostasis. Since H2O2 is a signal-transducing molecule relaying information on intracellular redox state, the pool size must be rigorously controlled within each compartment of the cell. This review focuses on compartment-specific differences in the stringency of redox coupling between ascorbate and glutathione, and the significance this may have for the flexibility of the control of gene expression that is linked to photosynthetic H2O2 production.

Antioxidants↗
PubMed1986

The glutathione redox cycle as a defense system against hydrogen-peroxide-induced prostanoid formation and vasoconstriction in rabbit lungs.

Leukocyte-derived oxidants have been described as causing vasoconstriction and edema formation in isolated lungs. In the present study, dose-dependent and reversible pressor responses were achieved reproducibly by injection of hydrogen peroxide (H2O2) into the pulmonary artery of blood-free, perfused, isolated rabbit lungs in a dose-dependent manner. The pressor responses were accompanied by an instantaneous release of thromboxane A2 and a more delayed but quantitatively larger release of prostaglandin I2 into the recirculating perfusion fluid. There was no release of potassium or LDH, indicating the absence of overt cell damage. The H2O2-induced pressor responses were blocked by indomethacin (cyclooxygenase inhibitor), imidazole (inhibitor of thromboxane synthetase), mepacrine (phospholipase inhibitor), and W7 and trifluoperazine (agents that interfere with calcium-calmodulin function). Treatment with 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) dose-dependently inhibited the lung glutathione reductase activity and augmented the metabolic (prostanoid release) and functional (vasoconstriction) responsiveness of the pulmonary vascular bed to H2O2. Application of 1-(2-chloroethyl)-1-nitrosourea (CCNU), a control to BCNU, and inhibition of catalase activity by aminotriazole did not increase the sensitivity to externally applied H2O2. We conclude that calcium-calmodium function and thromboxane generation may be involved in the pulmonary vasoconstrictive response to H2O2 and that the lung glutathione redox cycle is active in limiting the responsiveness of the pulmonary vascular bed to externally generated H2O2.

Animals↗