Susceptibility of glutathione peroxidase to proteolysis after oxidative alteration by peroxides and hydroxyl radicals

Pigeolet, Etienne; Remacle, José

doi:10.1016/0891-5849(91)90171-x

Cited by 72 publications

(30 citation statements)

References 19 publications

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“…Glutathione acts synergistically with zinc in protecting sulfhydryl groups, the reason for depletion of glutathione might have contributed to the higher consumption of glutathione and higher oxidative damage in zinc deficient rats [52]. The observed decline in GSH-Px and GST activities probably due to modification of the sulfhydryl groups in these enzymes by oxygen free radicals [53]. Elevated glucose and hydrogen peroxide levels have also been found to inactivate GST and GSH-Px [54].…”

Section: Discussionmentioning

confidence: 99%

Chard (Beta Vulgaris Var. Cicla) Extract Modulates Zinc Status, Glucose Level and Antioxydant Values in Diabetic Rats Fed Zinc Deficiency Diet

Hamdiken

Kechrid

2017

Int J Pharm Pharm Sci

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Objective: Oxidative stress which comes from hyperglycemia, it accelerates the development of cellular and vascular damage complications in diabetes, but the antioxidants may play a beneficial role in its prevention. Several plants extracts have an antioxidant activity and the ability to reduce oxidative stress in diabetes. Thus this study was conducted to investigate the effect of Beta vulgaris var cicla extract on zinc status, glucose concentration and antioxidant parameters in streptozotocin-diabetic rats fed zinc deficiency diet.Methods: Twenty-eight male albino (Wistar) rats were divided into four groups:Results: Body weight gain of zinc-deficient diabetic animals was lower than that of zinc-adequate diabetic animals. It was noticed also that inadequate dietary zinc intake increased glucose and MDA levels. In addition, zinc deficiency diet led to a decrease in zinc tissues, GSH concentration both GST and GSH-Px activities. However, Oral administration of Beta vulgaris extract significantly decreased both serum glucose and MDA (p<0.001) levels, with a significant increase in body weight gain (p<0.001), GSH concentration (p<0.05, P<0.001), GST (p<0.05, p<0.001) and GSHPx (p<0.001) activities.two groups fed a zinc-sufficient diet one non-diabetic and the other diabetic, while the others two diabetic groups were fed a zinc-deficient diet, one non-treated group and the other treated with the extract of Beta vulgaris var cicla. After 21 d of dietary manipulation, fasting animals were scarified. Blood glucose, tissues zinc (femur, liver, kidney), malondialdehyde (MDA), reduced glutathione (GSH), glutathione peroxidase (GSH-Px) and glutathione-S-transferase (GST) were evaluated. Conclusion:The present study showed that Beta vulgaris var cicla supplementation presumably acting as an antioxidant, and it can be a natural Keywords: Diabetes, Rat, Zinc deficiency, Beta vulgaris var cicla, Antioxidant source for the reduction of diabetes development caused by zinc deficiency.

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Section: Discussionmentioning

confidence: 99%

Chard (Beta Vulgaris Var. Cicla) Extract Modulates Zinc Status, Glucose Level and Antioxydant Values in Diabetic Rats Fed Zinc Deficiency Diet

Hamdiken

Kechrid

2017

Int J Pharm Pharm Sci

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“…Every one of the antioxidant enzymes is susceptible to ROS inactivation and their oxidation leads to the degradation of enzymes by proteosome at a high ratio. [29][30][31] The next comment is on the absence of a further increment in OX after the addition of one, two, three or four components of the MS to the basic one, hypertension, was analyzed. Likewise, the addition of the individual components, low HDL, high triglycerides, abdominal obesity or impaired fasting glucose, separately, did not increase the OX level.…”

Section: Discussionmentioning

confidence: 99%

Impact of the components of metabolic syndrome on oxidative stress and enzymatic antioxidant activity in essential hypertension

et al. 2006

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The objective of the present study was to analyze the impact of metabolic syndrome (MS) and its individual components on oxidative stress (OX) and on the activity of antioxidant enzymes of patients with essential hypertension. One hundred and eighty-seven hypertensives, 127 (61.9%) of them having criteria for MS according to the International Diabetes Federation criteria and 30 healthy normotensive subjects were included. OX status was assessed by measuring glutathione oxidized/glutathione reduced and reactive oxygen species-induced byproducts of lipid peroxidation, malondialdehide, and DNA damage, 8-oxo-dG genomic and mitochondrial. Antioxidant enzymatic activity of Cu/Zn extracellular-superoxide dismutase (SOD) and catalase (CAT) was measured in plasma and glutathione peroxidase 1 in hemolysad erythrocytes. In mononuclear cells, total-SOD activity, CAT and glutathione peroxidase 1, were assessed as well. The OX state in both blood and peripheral mononuclear cells observed in hypertensives were not enhanced by the addition of components of the so-called MS. Likewise, the reduction in the activity of antioxidant enzymes, both extracellular and cytoplasmic, was not affected by the presence of additional components of the MS. Neither the number of components nor the individual addition of each of them, low high-density lipoprotein, triglycerides, abdominal obesity or fasting glucose, further impact in the OX abnormalities observed in those with only hypertension in absence of other components. In conclusion, the present data indicates that contribution of MS components to the OX burden generated by high blood pressure is minimal.

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“…Oxygen radicals have been reported to inactivate GR (Huang and Philbert, 1996) and GPx (Pigeolet and Remacle, 1991). In addition, depletion of brain GSH results in a decrease of GR activity, an enzyme susceptible to oxidative injury (Barker et al, 1996).…”

Section: Effects Of Ischemia On Hippocampal Antioxidant Defensesmentioning

confidence: 99%

Time course of oxidative damage in different brain regions following transient cerebral ischemia in gerbils

Candelario‐Jalil

Mhadu

Al-Dalain

et al. 2001

Neuroscience Research

163

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The time course of oxidative damage in different brain regions was investigated in the gerbil model of transient cerebral ischemia. Animals were subjected to both common carotid arteries occlusion for 5 min. After the end of ischemia and at different reperfusion times (2,6,12,24,48, 72, 96 hr and 7 days), markers of lipid peroxidation, reduced and oxidized glutathione levels, glutathione peroxidase, glutathione reductase, manganese-dependent superoxide dismutase (MnSOD) and copper/zinc containing SOD (Cu/ZnSOD) activities were measured in hippocampus, cortex and striatum. Oxidative damage in hippocampus was maximal at late stages after ischemia (48 to 96 h) coincident with a significant impairment in glutathione homeostasis. MnSOD increased in hippocampus at 24, 48 and 72 h after ischemia, coincident with the marked reduction in the activity of glutathione-related enzymes. The late disturbance in oxidant-antioxidant balance corresponds with the time course of delayed neuronal loss in the hippocampal CA1 sector. Cerebral cortex showed early changes in oxidative damage with no significant impairment in antioxidant capacity. Striatal lipid peroxidation significantly increased as early as 2 h after ischemia and persisted until 48 h with respect to the sham-operated group. These results contribute significant information on the timing and factors that influence free radical formation following ischemic brain injury, an essential step in determining effective antioxidant intervention.

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Susceptibility of glutathione peroxidase to proteolysis after oxidative alteration by peroxides and hydroxyl radicals

Cited by 72 publications

References 19 publications

Chard (Beta Vulgaris Var. Cicla) Extract Modulates Zinc Status, Glucose Level and Antioxydant Values in Diabetic Rats Fed Zinc Deficiency Diet

Chard (Beta Vulgaris Var. Cicla) Extract Modulates Zinc Status, Glucose Level and Antioxydant Values in Diabetic Rats Fed Zinc Deficiency Diet

Impact of the components of metabolic syndrome on oxidative stress and enzymatic antioxidant activity in essential hypertension

Time course of oxidative damage in different brain regions following transient cerebral ischemia in gerbils

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