Effects of selenium on chromium (VI)-induced hepatotoxicity in adult rats

Soudani, Nejla; Amara, Ibtissem Ben; Sefi, Mediha; Boudawara, Tahia; Zeghal, Najiba

doi:10.1016/j.etp.2010.04.005

Cited by 66 publications

(47 citation statements)

References 57 publications

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“…Further in our study it was also seen that when alpha-tocopherol was given there were reversal of histological alteration in liver cell which is similar to finding of Da Silva etal. Soudani et al, [17] had shown that antioxidant supplement could protect the chromium induce liver tissue damage which in our present study was shown by supplementation of alpha-tocopherol along with chromium, where the reversal of the distorted changes of the liver cell occurred to large extent. Bursell.…”

Section: Discussionsupporting

confidence: 49%

“…Da Silva etal in his study of trivalent chromium found damage and distortion of liver hepatocytes. [17] Inpresent study the toxic effect of chromium led to damage of hepatocytes, dilatation of sinusoids. Further in our study it was also seen that when alpha-tocopherol was given there were reversal of histological alteration in liver cell which is similar to finding of Da Silva etal.…”

Section: Discussionmentioning

confidence: 99%

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Protective Role of Alpha-Tocopherol in Chromium Induced Toxicity in Albino Rat’s Liver: A Histopathological Study

Kausar¹,

Singh²,

Kaushik³

et al. 2017

AIMDR

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Section: Discussionsupporting

confidence: 49%

Section: Discussionmentioning

confidence: 99%

Protective Role of Alpha-Tocopherol in Chromium Induced Toxicity in Albino Rat’s Liver: A Histopathological Study

Kausar¹,

Singh²,

Kaushik³

et al. 2017

AIMDR

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“…Liver is an organ capable of being injured by Cr(VI), and it has been demonstrated that the exposition to K 2 Cr 2 O 7 induces hepatotoxicity associated to increased ROS levels [38], lipid peroxidation [39, 40], inhibition of antioxidant enzymes [41, 42], structural tissue injury [43, 44], and mitochondrial damage [45] including impaired mitochondrial bioenergetics [46, 47]. Natural and synthetic antioxidants have been reported to ameliorate or prevent K 2 Cr 2 O 7 -induced hepatotoxicity [42, 48, 49].…”

Section: Introductionmentioning

confidence: 99%

Curcumin Pretreatment Prevents Potassium Dichromate-Induced Hepatotoxicity, Oxidative Stress, Decreased Respiratory Complex I Activity, and Membrane Permeability Transition Pore Opening

García-Niño

Tapia

Zazueta

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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Curcumin is a polyphenol derived from turmeric with recognized antioxidant properties. Hexavalent chromium is an environmental toxic and carcinogen compound that induces oxidative stress. The objective of this study was to evaluate the potential protective effect of curcumin on the hepatic damage generated by potassium dichromate (K2Cr2O7) in rats. Animals were pretreated daily by 9-10 days with curcumin (400 mg/kg b.w.) before the injection of a single intraperitoneal of K2Cr2O7 (15 mg/kg b.w.). Groups of animals were sacrificed 24 and 48 h later. K2Cr2O7-induced damage to the liver was evident by histological alterations and increase in the liver weight and in the activity of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and alkaline phosphatase in plasma. In addition, K2Cr2O7 induced oxidative damage in liver and isolated mitochondria, which was evident by the increase in the content of malondialdehyde and protein carbonyl and decrease in the glutathione content and in the activity of several antioxidant enzymes. Moreover, K2Cr2O7 induced decrease in mitochondrial oxygen consumption, in the activity of respiratory complex I, and permeability transition pore opening. All the above-mentioned alterations were prevented by curcumin pretreatment. The beneficial effects of curcumin against K2Cr2O7-induced liver oxidative damage were associated with prevention of mitochondrial dysfunction.

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“…Earlier studies on fish model revealed hypoglycemic effect of chromium at a low dose of exposure for 2 months [38]. Experimental studies demonstrated that renal tubular damage and glycosuria are accompanied with the alteration in the activity of different enzymes and proteinuria, which could be the associated factors of hypoglycemia [14]. The decreased glucose may be due to nephritic tissue abnormality or may result from increased rate of glycolysis and excessive metabolism in various vital organs including liver to make up the high energy demand for attenuating the toxic effect of chromium.…”

Section: Shil and Palmentioning

confidence: 99%

“…The liver is the main organ responsible for the metabolism, detoxification and secretory function of the organism; it regulates plenty of metabolic pathways of mammalian systems [13]. Epidemiological studies show that Cr (VI) causes hepatotoxicity in human and laboratory animals primarily through oxidative stress-mediated mechanism [14]. Tubular necrosis occurs in the kidney due to the exposure of Cr (VI), acute exposure causes liver and kidney damage and also responsible for the deterioration of organ structure [15].…”

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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Effects of selenium on chromium (VI)-induced hepatotoxicity in adult rats

Cited by 66 publications

References 57 publications

Protective Role of Alpha-Tocopherol in Chromium Induced Toxicity in Albino Rat’s Liver: A Histopathological Study

Protective Role of Alpha-Tocopherol in Chromium Induced Toxicity in Albino Rat’s Liver: A Histopathological Study

Curcumin Pretreatment Prevents Potassium Dichromate-Induced Hepatotoxicity, Oxidative Stress, Decreased Respiratory Complex I Activity, and Membrane Permeability Transition Pore Opening

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

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