The Effect of Dietary Selenium on Cadmium Cardiotoxicity

Jamall, Ijaz S.; Smith, J. C.

doi:10.1007/978-3-642-70856-5_10

Cited by 6 publications

(4 citation statements)

References 30 publications

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“…The primacy of GSH-Px compared with other cellular antioxidant enzymes, as demonstrated in the present study, substantiates previous findings in our laboratory (Jamall & Smith, 1985a;Jamall & Smith, 1986;Jamall & Sprowls, 1987) as well as in other laboratories in both in vivo (Doroshow et al, 1980;Lal et al, 1980) and in vitro studies (Cohen & Hochstein, 1963;Jones et al, 1981;Jones & Kennedy, 1983;Suttorp et al, 1986;Raes et al, 1987). Empirical data from these studies can be explained by the fact that (1) the selenoenzyme, GSH-Px, has a much lower Km for H202 (in the micromolar range) as compared with catalase which has a Km for H202 in the millimolar range and (2) catalase is localized in peroxisomes whereas GSH-Px is present in both cytosol and mitochondria (Flohe, 1971;Flohe et al, 1979).…”

Section: Discussionsupporting

confidence: 82%

Significance of alterations in hepatic antioxidant enzymes. Primacy of glutathione peroxidase

Simmons

Jamall

1988

Biochemical Journal

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The relative contributions of catalase and the selenoenzyme glutathione peroxidase (GSH-Px) were elucidated in the rat liver by selectively modulating the activities of these enzymes using dietary selenium (Se) and the catalase inhibitor 3-amino-1,2,4-triazole (3-AT). Increased peroxidation occurred only in Sedeficient rats with markedly reduced cytosolic and mitochondrial GSH-Px activities. Although 3-AT treatment resulted in a 7500 reduction of hepatic catalase activity and also a 200% reduction of both cytosolic and mitochondrial superoxide dismutase (SOD) activity, no incremental increase in peroxidation was observed over that associated with Se deficiency. In Se-deficient animals, treatment with 3-AT resulted in a doubling of cytosolic GSH-Px. This was associated with a 49 % elevation in hepatic Se suggesting that increased Se may have contributed to the enhanced GSH-Px activity. These results suggest that GSH-Px plays the pivotal role in preventing hepatic peroxidation. Furthermore, the effects of 3-AT in vivo are not restricted to inhibition of catalase activity insofar as it also affects cytosolic GSH-Px activity and cytosolic and mitochondrial SOD activities.

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Section: Discussionsupporting

confidence: 82%

Significance of alterations in hepatic antioxidant enzymes. Primacy of glutathione peroxidase

Simmons

Jamall

1988

Biochemical Journal

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“…The reports by Jamall GSSG is reconverted into GSH through the action of glutathione reductase. Cadmium treatment in the and Smith, 20 Sidhu et al 21 and Ognjanovic et al 32 also suggest the same. The selenium which escaped the present experiment shows a significant increase in the GSSG level, concomitant with the decrease in GSH.…”

mentioning

confidence: 60%

“…These observations are also supported of this metal in the body. However, Behne and Wolters 34 also noticed that the high intake of selenium by Jamall and Smith 20 and Sidhu et al 21 Glutathione reductase is not affected by the cadmium treatment.…”

mentioning

confidence: 92%

Effect of Selenium Supplementation on the Glutathione Redox System in the Kidney of Mice after Chronic Cadmium Exposures

Nehru

Bansal

1997

J. Appl. Toxicol.

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“…Depressed cardiac contractility, following reperfusion injury in the isolated rabbit heart, has also been shown to involve significant reductions in myocardial GSH with no change in oxidized glutathione, glutathione reductase or glutathione peroxidase (GSH-Px) activities [3]. Work in our laboratory has demonstrated that cadmium cardiotoxicity is mediated by increased lipid peroxidation [4,5]. This peroxidative injury occurs only when the activity of the selenoenzyme, GSH-Px, is markedly reduced in cardiac cytosol and mitochondria [6].…”

Section: Introductionmentioning

confidence: 99%

Differential effects of cadmium on cytosolic and mitochondrial glutathione levels in the rat heart

Jamall

1987

FEBS Letters

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In rats fed a low-selenium diet, cytosolic GSH levels in the heart were significantly elevated when compared to rats fed a selenium-supplemented diet. Similar results were obtained in cardiac cytosol from rats treated with either parenteral or dietary Cd. Mitochondrial GSH was not affected by cadmium in selenium-deficient rats, However, significant elevations of mitochondrial GSH were seen in cadmium-treated rats fed either 0.1 or 0.5 ppm selenium. The alterations in cytosolic GSH levels correlate with reductions in GSH-Px activity reported earlier [( 1987) Toxicol. Appl. Pharmacol. 87, in press]. However, levels of mitochondrial GSH did not correlate with GSH-Px activity.

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The Effect of Dietary Selenium on Cadmium Cardiotoxicity

Cited by 6 publications

References 30 publications

Significance of alterations in hepatic antioxidant enzymes. Primacy of glutathione peroxidase

Significance of alterations in hepatic antioxidant enzymes. Primacy of glutathione peroxidase

Effect of Selenium Supplementation on the Glutathione Redox System in the Kidney of Mice after Chronic Cadmium Exposures

Differential effects of cadmium on cytosolic and mitochondrial glutathione levels in the rat heart

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