In vivo formation of H2O2 in red cells during exposure to hyperoxia

Jefferson, D; Mengel, Charles E.

doi:10.1172/jci107029

Cited by 12 publications

(5 citation statements)

References 6 publications

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“…No significant change was found in glutathione reductase, but glutathione peroxidase and glucose 6-phosphate dehydrogenase showed a remarkable enhancement of activity in organs from tocopherol-deficient rats over the control values: in lung, 74 and 230% respectively, and in liver, 35 and 154% (see Table 1). Since stimulation of lipid peroxidation has been observed in tocopherol-deficient animals in vitro (Raskin et al, 1971;Riely et al, 1974) and in vivo (Johnson et al, 1972;Jerret et al, 1973), the observed increases in the activity of glucose 6-phosphate dehydrogenase and glutathione peroxidase indicate their adaptive response to an enhanced production of lipid peroxides and suggest keyroles for these enzymes in lipid-peroxide metabolism in lung and liver.…”

Section: Resultsmentioning

confidence: 98%

“…Boveris & Chance (1973) showed that hyperbaric 02 increased the formation of H202 in mitochondria isolated from normal rat livers. After exposure to hyperoxia, an increased H202 production in vivo was detected qualitatively in the erythrocytes (Johnson et al, 1972) and in the brain (Jerret et al, 1973) of tocopherol-deficient rats, but Oshino et al (1975a,b) were unable to detect this phenomenon in perfused liver and liver in situ in the normal anaesthetized rat. This discrepancy suggests differences in the biological systems, which make it difficult to determine the primary effect of hyperbaric 02.…”

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confidence: 99%

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Oxygen toxicity in the perfused rat liver and lung under hyperbaric conditions

Nishiki

Jamieson

Oshino

et al. 1976

Biochemical Journal

119

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1. In the lung and liver of tocopherol-deficient rats, the activities of glutathione peroxidase and glucose 6-phosphate dehydrogenase were increased substantially, suggesting an important role for both enzymes in protecting the organ against the deleterious effects of lipid peroxides. 2. Facilitation of the glutathione peroxidase reaction by infusing t-butyl hydroperoxide caused the oxidation of nicotinamide nucleotides and glutathione, resulting in a concomitant increase in the rate of release of oxidized glutathione into the perfusate. Thus the rate of production of lipid peroxide and H2O2 in the perfused organ could be compared by simultaneous measurement of the rate of glutathione release and the turnover number of the catalase reaction. 3. On hyperbaric oxygenation at 4 X 10(5)Pa, H2O2 production, estimated from the turnover of the catalase reaction, was increased slightly in the liver, and glutathione release was increased slightly, in both lung and liver. 4. Tocopherol deficiency caused a marked increase in lipid-peroxide formation as indicated by a corresponding increase in glutathione release under hyperbaric oxygenation, with a further enhancement when the tocopherol-deficient rats were also starved. 5. The study demonstrates that the primary response to hyperbaric oxygenation is an elevation of the rate of lipid peroxidation rather than of the rate of formation of H2O2 or superoxide.

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Section: Resultsmentioning

confidence: 98%

mentioning

confidence: 99%

Oxygen toxicity in the perfused rat liver and lung under hyperbaric conditions

Nishiki

Jamieson

Oshino

et al. 1976

Biochemical Journal

119

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“…Similarly H202 has been implicated in the enhancement of lipid peroxidation in tissues of animals exposed to hyperbaric 02-For instance, Jerrett et al (1973) found increased amounts of H202 and a corresponding increase in lipid peroxidation after approx. 1 h of pressurization of rats to 4 x I05 Pa and Johnson et al (1972) demon-stratedhaemolysis and increased H202 production and lipid peroxidation in erythrocytes of rats exposed to hyperbaric 2. However, such increased amounts of H202 in these studies were observed in tocopheroldeficient animals only.…”

Section: H202 Production Under Hyperbaric Oxygenmentioning

confidence: 94%

Optical measurement of the catalase-hydrogen peroxide intermediate (Compound I) in the liver of anaesthetized rats and its implication to hydrogen peroxide production in situ

Oshino

Jamieson

Sugano

et al. 1975

Biochemical Journal

110

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The spectrophotometric determination of the catalase-H2O2 intermediate (Compound I) was extended to the liver in situ in anaesthetized rats. The rate of H2O2 production was determined for the liver in situ with endogenous substrates, and in the presence of excess of glycollate. Glycollate infusion doubled H2O2 production rate in the liver of air-breathing rats, and caused a fourfold increase when rats breathed O2 at 1 times 10(5) Pa. Hyperbaric O2 up to 6 times 10(5) Pa did not increase H2O2 generation supported by endogenous substrates, nor did it increase H2O2 production above that produced by 1 times 10(5) Pa O2 in glycollate-supplemented rats. The rates of ethanol oxidation via hepatic catalase and via alcohol dehydrogenase in the whole body were separately measured. The contribution of hepatic catalase to ethanol oxidation was found to be approx. 10 percent in endogenous conditions and increased to 30 percent or more of the total ethanol oxidation in rats supplemented with glycolate.

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“…In this study, in order to determine whether the oxidative damage of nerve terminals lowers fusion of synaptic plasma membrane with synaptic vesicles in neurotransmission, the influence of oxidative damage in synaptic plasma membranes from rat brains subjected to hyperoxia on membrane fusion with bilayer PC liposomes as a model of synaptic vesicles has been investigated. Although it has been questioned whether hyperoxia induces ROS in living tissues, there are several evidences that ROS, such as hydrogen peroxide and supeoxide, are generated by hyperoxia in the lungs, heart muscle, brain and erythrocytes of several animals (25)(26)(27), and that the rate of ROS generation in the lung is proportional to the concentration of oxygen inhaled (28).…”

Section: Discussionmentioning

confidence: 99%

Influence of Oxidative Stress on Fusion of Pre-Synaptic Plasma Membranes of the Rat Brain with Phosphatidyl Choline Liposomes, and Protective Effect of Vitamin E

Omoi

Arai

Saito

et al. 2006

J Nutr Sci Vitaminol

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Summary Influence of oxidative stress on fusion of pre-synaptic plasma membranes with phosphatidylcholine (PC) liposomes as a model of synaptic vesicle was investigated. The inhibitory effect of vitamin E on the decline in the fusion caused by oxidative stress was also assessed. Rats subjected to hyperoxia as oxidative stress showed significant increases in the levels of lipid hydroperoxides and protein carbonyl moieties in pre-synaptic plasma membranes in the brain. The potential of pre-synaptic membrane surface was decreased markedly. When synaptosomes were incubated with PC liposomes labeled by either rhodamine B or calcein as a fluorescence probe, or 12-doxyl stearic acid as an ESR spin trapping agent, translocation of each probe into oxidatively damaged pre-synaptic membranes was decreased significantly. Fatty acid composition analysis in pre-synaptic membranes obtained from normal rats revealed a marked increase in linoleic acid and a moderate decrease in docosahexaenoic content after the incubation with liposomes. However, rats subjected to hyperoxia did not show marked changes in these fatty acid contents in their pre-synaptic membranes after the incubation. Such changes caused by hyperoxia were inhibited by vitamin E treatment of rats. These results suggest that oxidative damage of pre-synaptic membranes caused by oxidative stress lowers the lipid-mixing for the membrane fusion. The results of this study imply that vitamin E prevents the deficit in neurotransmission at nerve terminals due to the decline in fusion between pre-synaptic membrane and synaptic vesicles caused by oxidative membrane damage. Key Words vitamin E, neurotransmission, synaptic membrane fusion, oxidative damage, lipid-mixing Neurodegenerative diseases such as senile dementia including Alzheimer's disease have been characterized by progressive deterioration of cognitive function ( 1 ). Previous studies on brain aging revealed the high level of oxidative damage in the brain during normal aging, as well as in dementia ( 2 -4 ). Dementia is considered to be an acceleration of normal aging in affected brain regions which undergo progressive damage from reactive oxygen species (ROS) ( 5 ). It is, therefore, reasonable to assume that the deficit in neurotransmission is caused by oxidative damage to nerve terminals through chronic oxidative stress experienced over a long time, resulting in a cognitive dysfunction. In terms of neurodegeneration, the amount of oxidative damage to synapses in the brain regions, which modulate cognitive and motor functions, seems to depend on the protection afforded by several antioxidants ( 6 ). Accordingly, it seems that long-term vitamin E supplementation may prevent the oxidative damage of the nervous system during aging. In fact, a previous report revealed that long-term high-dose supplementation of vitamin E to aged individuals provides significant enhancement in cognitive function ( 7 ). A clinical trial on vitamin E supplementation in patients with moderately severe Alzheimer's disease showed delays in ...

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In vivo formation of H2O2 in red cells during exposure to hyperoxia

Cited by 12 publications

References 6 publications

Oxygen toxicity in the perfused rat liver and lung under hyperbaric conditions

Oxygen toxicity in the perfused rat liver and lung under hyperbaric conditions

Optical measurement of the catalase-hydrogen peroxide intermediate (Compound I) in the liver of anaesthetized rats and its implication to hydrogen peroxide production in situ

Influence of Oxidative Stress on Fusion of Pre-Synaptic Plasma Membranes of the Rat Brain with Phosphatidyl Choline Liposomes, and Protective Effect of Vitamin E

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