GSH‐dependent inhibition of lipid peroxidation: Properties of a potent cytosolic system which protects cell membranes

Gibson, Donald D.; Hawrylko, Josephine; McCay, Paul B.

doi:10.1007/bf02534391

Cited by 66 publications

(20 citation statements)

References 29 publications

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“…An important consideration is that activity of these enzymes is dependent on the availability of reduced glutathione, which in turn depends on the activity of glutathione reductase and g-glutamyl cysteine synthase, the rate-limiting enzyme for reduced glutathione (GSH) synthesis [68]. Consistent with these observations, glutathione reductase has a similar distribution to that of GPX [69].…”

Section: Other Oxidasessupporting

confidence: 67%

Role of hydrogen peroxide and oxidative stress in healing responses

Rojkind¹,

Domínguez-Rosales²,

Nieto

et al. 2002

CMLS, Cell. Mol. Life Sci.

228

153

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Oxidative stress is a host defense mechanism whose involvement in maintaining homeostasis and/or inducing disease has been widely investigated over the past decade. Various reactive oxygen species (ROS) have been defined and the enzymes involved in generating and/or eliminating them have been widely studied. In this review we briefly discuss general mechanisms of oxidative stress and the oxidative stress response of the host. We focus primarily on hydrogen peroxide and summarize the systems involved in its formation and elimination. We describe mechanisms whereby hydrogen peroxide and other ROS can modify protein conformation and, thus, alter protein function, and describe a group of transcription factors whose biological activity is modulated by the redox state of cells. These basic aspects of oxidative stress are followed by a discussion of mechanisms whereby hydrogen peroxide and other ROS can modulate some physiological and pathological processes, with special emphasis on wound healing and scarring of the liver.

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Section: Other Oxidasessupporting

confidence: 67%

Role of hydrogen peroxide and oxidative stress in healing responses

Rojkind¹,

Domínguez-Rosales²,

Nieto

et al. 2002

CMLS, Cell. Mol. Life Sci.

228

153

View full text Add to dashboard Cite

show abstract

“…Mongrel dogs of either sex weighing [17][18][19][20][21][22][23][24][25] kg were quarantined for 2 weeks to ensure that they were free of canine diseases. Dogs were prepared approximately 1 week before the experiment under general anesthesia [sodium pentobarbital (30 mg/kg)] via left thoracotomy.…”

Section: Surgical Preparationmentioning

confidence: 99%

“…[18][19][20][21] N-Acetylcysteine is a precursor of glutathione and has been used effectively to replenish intracellular glutathione stores in several disease processes.22-24 Therefore, the aim of the present study was to assess the effect of N-acetylcysteine on infarct size, left ventricular function, and cellular ultrastructure in a 90-minute canine occlusionreperfusion model. Because N-acetylcysteine has been shown to increase superoxide dismutase activity, levels of this enzyme as well as total glutathione and glutathione peroxidase activity were measured in treated and control animals.…”

mentioning

confidence: 99%

Glutathione redox pathway and reperfusion injury. Effect of N-acetylcysteine on infarct size and ventricular function.

et al. 1988

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Glutathione peroxidase is an important enzyme in the degradative cascade of reactive oxygen free radicals. N-Acetylcysteine (NAC) is a low molecular weight compound that has been used clinically to replenish glutathione. To assess the role of the glutathione redox pathway on reperfusion injury, 23 animals underwent 90 minutes of proximal left anterior descending coronary artery occlusion followed by 24 hours of reperfusion with the administration of NAC (n = 11) or saline (n = 12) beginning 30 minutes into occlusion and continuing for 3 hours after reperfusion. Regional ventricular function was measured with contrast ventriculography, and regional myocardial blood flow was determined with microspheres. At 24 hours, the area at risk was defined in vivo with Monastral Blue, and the area of necrosis was defined by incubation in triphenyltetrazolium. Biopsies were taken from the ischemic and nonischemic zones to determine levels of total glutathione, superoxide dismutase and glutathione peroxidase activity, and reactivity to thiobarbituric acid, an index of lipid peroxidation. The rate-pressure product and myocardial blood flow were similar in the two groups throughout the study. No significant differences were noted in infarct size expressed as a percentage of the area at risk (28.6 5.3% vs. 36.6 6.0%) and of the total left ventricle (14.4 3.2% vs. 16.5 + 3.1%), and no differences were noted between the two groups on examination of the ischemic subendocardium by light and electron microscopy. Both groups exhibited similar degrees of dyskinesis during occlusion; however, treated animals showed significant improvement in regional radial shortening at 3 hours (3.4+2.4% vs. -2.4±2.1%, p<0.02) and 24 hours (9.2±2.2% vs. -2.5 ±6.3%, p

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“…Among various antioxidant systems, the glutathione / glutathione peroxidase system seems more important in the myocardium (2). Glutathione peroxidase reduces reactive oxygen intermediates, hydrogen peroxide, and other glutathionedependent enzymes, including glutaredoxin and glutathione S-transferase, inhibit lipid peroxidation (3).…”

Section: Introductionmentioning

confidence: 99%

Comparison of the Protective Effect of N-Acetylcysteine by Different Treatments on Rat Myocardial Ischemia-Reperfusion Injury

et al. 2008

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Abstract. Reactive oxygen species have been known as important contributors to ischemia / reperfusion (I / R) injury. Studies on the beneficial effect of N-acetylcysteine (NAC), a potent antioxidant, on limiting infarct size induced by I / R yielded contrasting results. The present study was undertaken to compare the effect of NAC by different administration methods on infarct size in a rat myocardial I/ R model. Rats underwent 30 min of left coronary occlusion followed by 4 h of reperfusion. Treatment with continuous infusion of NAC (150 mg / kg per hour) from 30 min before occlusion for 2 h (until 1 h after the start of reperfusion) produced a significant limitation of the infarct size as a percentage of the ischemic area (8%) compared to the non-treated control (60%). However, bolus injection of 150 mg / kg at 30 min prior to occlusion and 5 min prior to reperfusion failed to reduce it (56%) although the total dose is the same. The decreased total glutathione content and glutathione peroxidase activity in the ischemic region were recovered in the continuous infusion group, but not in the bolus injection group. The increased myeloperoxidase activity and phosphorylation of inhibitor κB after I / R were inhibited by the continuous treatment. These results indicate that the protective effect of NAC on myocardial infarction induced by I / R was different depending on the administration method. It is necessary to maintain blood concentration during the early period of reperfusion to obtain the beneficial effect of NAC.

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GSH‐dependent inhibition of lipid peroxidation: Properties of a potent cytosolic system which protects cell membranes

Cited by 66 publications

References 29 publications

Role of hydrogen peroxide and oxidative stress in healing responses

Role of hydrogen peroxide and oxidative stress in healing responses

Glutathione redox pathway and reperfusion injury. Effect of N-acetylcysteine on infarct size and ventricular function.

Comparison of the Protective Effect of N-Acetylcysteine by Different Treatments on Rat Myocardial Ischemia-Reperfusion Injury

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