Protective effect of vitamin E on chromium (VI)-induced cytotoxicity and lipid peroxidation in primary cultures of rat Hepatocytes

Susa, Nobuyuki; Ueno, Shunji; Furukawa, Yoshinori; Sugiyama, Masayasu

doi:10.1007/s002040050353

Cited by 53 publications

(33 citation statements)

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“…The present study also showed that chromium (VI) treatment resulted in decreased levels of nonenzymatic antioxidants such as GSH, vitamins C and E, and inhibited activities of enzymatic antioxidants such as GR, GSH-Px and SOD in cultured rat hepatocytes. Similar results were observed in previous studies [40][41][42]. In the present study, pretreatment with DDTC had no effect on the reduction of GSH or vitamin C level or on inhibition of GR, GSH-Px or SOD activity induced by chromium (VI).…”

Section: Discussionsupporting

confidence: 93%

“…Concerning these antioxidants, our previous studies with cultured hepatocytes also showed that a metal chelator DFO had no influence on cellular levels of GSH and the activities of GR as well as SOD, however this chelator attenuated the suppression of cellular levels of vitamin C and vitamin E induced by chromium (VI), resulting in the suppression of chromium (VI)-induced DNA breaks, cytotoxicity and lipid peroxidation [41]. Similarly, treatment with vitamin E or melatonin inhibited chromium (VI)-induced cytotoxicity as well as lipid peroxidation, and normalized the levels of vitamins C and E suppressed by dichromate, without affecting such antioxidant enzymes as GSH-Px, SOD and CAT [40,42]. These and the present study suggest that the protective effect of DDTC against chromium (VI)-induced cytotoxicity and lipid peroxidation may be related more to the levels of nonenzymatic antioxidants such as vitamin E than to the enzymatic antioxidant activity within cells.…”

Section: Discussionmentioning

confidence: 99%

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Protective Effect of Diethyldithiocarbamate Pretreatment on Chromium(VI)-Induced Cytotoxicity and Lipid Peroxidation in Primary Cultures of Rat Hepatocytes.

Susa

Ueno

Furukawa

1998

The Journal of Veterinary Medical Science

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ABSTRACT. Pretreatment of primary cultures of rat hepatocytes with sodium diethyldithiocarbamate (DDTC) for 15 min prior to exposure to K 2 Cr 2 O 7 resulted in a marked decrease in dichromate-induced cytotoxicity, as evaluated by the leakage of lactate dehydrogenase, and in lipid peroxidation, as monitored by malondialdehyde formation. In addition, pretreatment with DDTC attenuated the suppression of the level of vitamin E attributed to K 2 Cr 2 O 7 . However, DDTC pretreatment had no effect on the cellular levels of glutathione or vitamin C or on the activity of the glutathione reductase, glutathione peroxidase, superoxide dismutase or alkaline phosphatase suppressed by dichromate. Under the same experimental conditions, cellular uptake or distribution of chromium was not affected by DDTC. These results indicate that the protective effect of DDTC on chromium (VI)-induced cytotoxicity as well as lipid peroxidation may be associated with the level of nonenzymatic antioxidants such as vitamin E. -KEY WORDS: chromium (VI), cytotoxicity, diethyldithiocarbamate, hepatocyte, lipid peroxidation.J. Vet. Med. Sci. 60(1): 71-76, 1998 associated in part with the production of active oxygen. Membrane-permeable metal-chelating agents such as deferoxamin (DFO) and o-phenanthroline (OP) have been reported to inhibit the DNA-strand breaks and cytotoxicity induced by hydrogen peroxide in cultured mammalian cells [8]. It is well known that these chelators form a complex with intracellular transition metals such as iron, preventing the occurrence of Fenton-type reaction of hydroxyl radical and protecting cells from the genetic and cytotoxic action of hydrogen peroxide [8]. With respect to chromium, recent studies showed that OP and DFO inhibited chromium (VI)-induced DNA breaks, cytotoxicity and lipid peroxidation in cultured cells [37,41] and that these chelators suppressed the formation of in vitro chromium (V) and chromium (V)-mediated hydroxyl radical [28,37].Diethyldithiocarbamate (DDTC) a metal chelator is used for the selective determination of chromium (VI) [30]. Furthermore, this chelator has also been shown to be an effecient inhibitor of Fe 2+ -and Cu 2+ -catalyzed hydroxyl radical formation, also protecting the cells from this toxic radical [46].In the present study, we using primary cultures of rat hepatocytes, to find examined whether DDTC has an effect on chromium (VI)-induced cytotoxicity and lipid Chromium (VI) compounds are potent toxic and carcinogenic metals [6]. With respect to their toxicity, hepatic and renal toxicities have been reported in workers and animals exposed to chromium (VI) [19]. Chromium (VI) compounds induced also DNA damage in vivo [5] and in cultured cells [36] as well as inhibition of the activity of such enzymes as glutathione peroxidase (GSH-Px), glutathione reductase (GR), glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) in mammalian cells [34].The biological effects of chromium (VI) are generally attributed to cellular uptake, since chromium (VI), in ...

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Protective Effect of Diethyldithiocarbamate Pretreatment on Chromium(VI)-Induced Cytotoxicity and Lipid Peroxidation in Primary Cultures of Rat Hepatocytes.

Susa

Ueno

Furukawa

1998

The Journal of Veterinary Medical Science

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“…These reactive intermediates are formed along with oxygen radicals generated via Fenton-like and other possible reactions that occur during intracellular reduction [9], which also intensively trigger the massive production of reactive oxygen species causing oxidative damage, protein cross-linkage, genomic instability and apoptosis, destruction of cellular protein, lipid and DNA [10,11].…”

Section: Introductionmentioning

confidence: 99%

Hexavalent Chromium Induced Alteration of Carbohydrate Bioenergetics: A Dose-dependent Study

Shil

Pal

2017

Asian J Pharm Clin Res

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Objective: This study was conducted to observe the dose-dependent effect of Cr (VI) on certain aspects of carbohydrate metabolism in mice with four different doses, viz., 5 mg/kg, 10 mg/kg, 15 mg/kg and 20 mg/kg b.w., respectively, for 30 days of exposure.Methods: Blood glucose, glycogen content, and pyruvic acid of liver tissue were determined to evaluate the glycolytic activity. Enzymes such as isocitrate dehydrogenase (IDH), succinate dehydrogenase, and malate dehydrogenase (MDH) activities were measured to determine the tricarboxylic acid cycle function. In addition, nicotinamide adenine dinucleotide (NADH) ubiquinone C oxidoreductase activity was estimated to evaluate the alteration in oxidative phosphorylation pathway with dose-dependent chromium exposure. Total protein, free amino acid nitrogen, and transaminase enzyme activity were also measured.Results: Chromium exposure caused marked depletion of blood glucose and liver glycogen contents in a dose-dependent manner. The activities of IDH, succinate dehydrogenase, and MDH were significantly altered in a dose-specific manner by chromium exposure. Relevant exhaustion of glycolytic substrates was noted in the form of reduced pyruvate content in hepatocytes following chromium exposure. In addition, the treatment caused elevation of free amino nitrogen associated with depletion of total protein content and elevated transaminase enzyme activities in hepatocytes. Significant alteration of mitochondrial NADH-ubiquinone C oxidoreductase activity was also noted. Conclusion:By analyzing the observed results, it can be suggested that Cr (VI) exerts hypoglycemic and glycogenolytic effects associated with alteration of citric acid cycle and electron transport pathways in hepatocytes in a dose-specific manner thus resulting in serious alteration in the carbohydrate bioenergetics and mitochondrial energy generation in hepatic cells.

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“…Although pretreatment of isolated rat hepatocytes with vitamin E or vitamin C protected the cells from chromium(VI)-induced lipid peroxidation , vitamin E had no effect on chromate-induced cytotoxicity . Moreover, pretreatment of primary cultures of rat hepatocytes with vitamin E (Susa et al, 1996) or deferoxamine (Susa et al, 1997) protected cells from both chromate-induced cytotoxicity and lipid peroxidation. In animals studies, it has been shown that dietary pretreatment of rats or guinea pigs with vitamin E (Chorvatovicová et al, 1991) or vitamin C (Ginter et al, 1989;Chorvatovicová et al, 1991) protected bone marrow cells from chromium(VI)-induced cytoxicity.…”

Section: Introductionmentioning

confidence: 97%

“…The role of physiological antioxidants, namely vitamin E and vitamin C, as well as the role of the membrane-permeable metal-chelating agent deferoxamine in chromium(VI)-induced cellular injury, including cytotoxicity, and lipid peroxidation has been studied in mammalian cells and experimental animals (Sugiyama, 1992;Susa et al, 1996Susa et al, , 1997. It has been shown that pretreatment of cultured Chinese hamster V-79 cells with vitamin E protected cells from chromate-induced cytotoxicity (Sugiyama et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Chromate-induced human erythrocytes haemoglobin oxidation and peroxidation: influence of vitamin E, vitamin C, salicylate, deferoxamine, and N-ethylmaleimide

Férnandes¹,

Geraldes²,

Oliveira³

et al. 2000

Toxicology Letters

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In order to attenuate or to prevent chromate-induced human erythrocytes injury, the influence of vitamin E, vitamin C, salicylate, deferoxamine, and N-ethylmaleimide on chromate-induced human erythrocytes haemoglobin oxidation and peroxidation were investigated. It was observed that pretreatment of human erythrocytes with vitamin E (20 mM), vitamin C (1 mM), salicylate (3 mM), and deferoxamine (4 mM) significantly increased (P =0.0001) chromate-induced human erythrocytes haemoglobin oxidation in a time dependent manner, while it was significantly decreased (P= 0.0001) by pretreatment with N-ethylmaleimide (1 mM). In contrast, pretreatment of human erythrocytes with deferoxamine (4 mM) immediately inhibited (P =0.0001) chromate-induced human erythrocytes peroxidation, while it was significantly increased (P= 0.0001) by pretreatment with N-ethylmaleimide (1 mM) during the first 4 h of cells exposition to chromate. For time periods superior to 6 h pretreatment with N-ethylmaleimide (1 mM) significantly decreased (P=0.0001) chromate-induced human erythrocytes peroxidation. It was concluded that care must be taken as these drugs are used to prevent against toxicity induced by chromium(VI) compounds.

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Protective effect of vitamin E on chromium (VI)-induced cytotoxicity and lipid peroxidation in primary cultures of rat Hepatocytes

Cited by 53 publications

References 25 publications

Protective Effect of Diethyldithiocarbamate Pretreatment on Chromium(VI)-Induced Cytotoxicity and Lipid Peroxidation in Primary Cultures of Rat Hepatocytes.

Protective Effect of Diethyldithiocarbamate Pretreatment on Chromium(VI)-Induced Cytotoxicity and Lipid Peroxidation in Primary Cultures of Rat Hepatocytes.

Hexavalent Chromium Induced Alteration of Carbohydrate Bioenergetics: A Dose-dependent Study

Chromate-induced human erythrocytes haemoglobin oxidation and peroxidation: influence of vitamin E, vitamin C, salicylate, deferoxamine, and N-ethylmaleimide

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