Inactivation of the human CuZn superoxide dismutase during exposure to O2− and H2O2

Sinet, P.-M.; Garber, Pascale

doi:10.1016/0003-9861(81)90382-9

Cited by 166 publications

(62 citation statements)

References 27 publications

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“…The most probable explanation for decreased SOD activity is a possible direct inactivation of the enzyme by its product hydrogen peroxide, or by superoxide anion itself (16,17). Decreased SOD activity could also be related to trace element deficiencies in hemodialyzed patients (18).…”

Section: Resultsmentioning

confidence: 99%

Effect of vitamin E supplementation on oxidative stress in hemodialysis patients

Bhogade

Suryakar

Joshi

et al. 2008

Indian J Clin Biochem

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Section: Resultsmentioning

confidence: 99%

Effect of vitamin E supplementation on oxidative stress in hemodialysis patients

Bhogade

Suryakar

Joshi

et al. 2008

Indian J Clin Biochem

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“…The H202-induced decreases in both GSHpx and SOD activities were also inhibited by pretreatment with rebamipide. Because Cu,Zn-SOD activity has been reported to be inhibited by the hydroxyl radical (25), the scavenging effect of rebamipide on the hydroxyl radical may be related to the protection of SOD activity.…”

Section: Resultsmentioning

confidence: 99%

Protective Effect of Rebamipide against Hydrogen Peroxide-Induced Hemorrhagic Mucosal Lesions in Rat Stomach

Sakurai

Yamasaki

1994

Japanese Journal of Pharmacology

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ABSTRACT-Intragastric administration of 6°1o H202 induces gastric mucosal hemorrhagic lesions in rats. Intraperitoneal administration of rebamipide at 10 to 100 mg/kg dose-dependently prevented the H202 induced mucosal lesions. The fact that cimetidine, ranitidine and omeprazole could not prevent the gastric mucosa from developing H202-induced lesions indicates that acid secretion might not be the main cause of these lesions. The protective effect of rebamipide was partially reduced by indomethacin and completely blocked by diethyl maleate, a glutathione depressor. Gastric mucosal glutathione level and glutathione peroxidase and superoxide dismutase (SOD) activities were significantly decreased by 6% H202 instillation. Rebamipide at 100 mg/kg significantly inhibited the decreases in gastric mucosal glutathione level and SOD activity. These results suggest that H202-induced gastric mucosal lesions might partially involve a decrease in defense activities against reactive oxygen species and that the protective effect of rebamipide might be related to its ability to improve oxidative stress in gastric mucosa.

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“…The latter are produced by the reaction between superoxide anions and hydroperoxide [28]. In our study, the decreased activity of catalase and GPx in kidney after cisplatin administration could be due to enhanced production of hydroperoxide.…”

Section: Discussionmentioning

confidence: 46%

Protective Role of Vitamin E and Acetazolamide in Cisplatin-Induced Changes in Lipid Peroxidation and Antioxidant Enzyme Levels in Albino Rats.

Gopalakrishnan

Murugesan

Babu

et al. 1996

J. Clin. Biochem. Nutr.

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SummaryCisplatin, an antitumor chemotherapeutic agent with doselimiting nephrotoxic side effects, was administered i.p, to male albino rats at a concentration of 6 mg/kg body wt. The antioxidant vitamin E (400 mg/kg body wt., orally) and the diuretic acetazolamide (ACZ) (20 mg/ kg body wt., i.p.) were co-administered as modulators. The effect of cisplatin on lipid peroxidation and antioxidant enzyme levels was then examined. The agent increased the level of lipid peroxidation and significantly decreased the activities of antioxidant enzymes. These effects may have been due to the formation of free radicals and were considered to be one of the reasons for cisplatin-induced nephrotoxicity. Interestingly, these changes were found to be very much counteracted by vitamin E and acetazolamide when they were co-administered along with the cisplatin. Hence, we suggest that co-administration of vitamin E and acetazolamide along with cisplatin will be clinically advantageous in attenuating cisplatin-induced nephrotoxicity during chemotherapy. Cisplatin (cis-diammine dichloro platinum-II), a platinum containing coordination complex, is an antitumor agent with proven efficacy as a single agent against a wide spectrum of malignancies [1]. Toxicological studies in humans and animals indicate that higher doses produce enzyme inhibition and histological changes in liver, kidney, gastrointestinal tract, and bone marrow [2]. However, the chief dose-limiting side effect of cisplatin is its pronounced nephrotoxicity, which occurs at doses lower than those that damage other organs [3]. The underlying molecular mechanism of the nephrotoxicity induced by cisplatin remains unclear

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Inactivation of the human CuZn superoxide dismutase during exposure to O2− and H2O2

Cited by 166 publications

References 27 publications

Effect of vitamin E supplementation on oxidative stress in hemodialysis patients

Effect of vitamin E supplementation on oxidative stress in hemodialysis patients

Protective Effect of Rebamipide against Hydrogen Peroxide-Induced Hemorrhagic Mucosal Lesions in Rat Stomach

Protective Role of Vitamin E and Acetazolamide in Cisplatin-Induced Changes in Lipid Peroxidation and Antioxidant Enzyme Levels in Albino Rats.

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