Interactions Between Trace Elements and Alcohol in Rats

Dreosti, Ivor E.

doi:10.1002/9780470720868.ch7

Cited by 5 publications

(1 citation statement)

References 46 publications

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“…While inadequate dietary intake is an obvious possible explanation for depressed red-cell concentrations, toxic influences--or oxidative stress itself--should not be discounted as modulaters of trace mineral levels. In fetal alcohol syndrome, for instance, excess free radical production increases demand for antioxidant enzyme production, resulting in a net deficit in selenium and zinc relative to requirements [26][27][28] .…”

Section: Resultsmentioning

confidence: 99%

Red-Cell Trace Minerals in Children with Autism

Jory¹,

McGinnis²

2008

American J. of Biochemistry and Biotechnology

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Abnormalities in mineral-dependent antioxidant enzymes in children with autism raise interest in the determination of trace mineral status in this population. A cross sectional investigation of red cell mineral levels was carried out among 20 children with autism and 15 controls. Children with autism demonstrated significantly lower red cell selenium (p<0.0006) and higher molybdenum (p<0.01) than the controls. There was a trend toward lower red cell zinc and higher cobalt and vanadium, among the children with autism. There were no differences in red cell levels of chromium, copper, manganese, or magnesium. These findings confirm an earlier report of low red cell selenium in autism and support a role for decreased trace mineral status in oxidative stress in autism through alteration of selenium-dependent antioxidant enzymes and increased lipid peroxidation

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Section: Resultsmentioning

confidence: 99%

Red-Cell Trace Minerals in Children with Autism

Jory¹,

McGinnis²

2008

American J. of Biochemistry and Biotechnology

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Zinc deficiency, ethanol, and myocardial ischemia affect lipoperoxidation in rats

Coudray

Boucher

et al. 1991

Biol Trace Elem Res

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The production of oxygen free radicals can be stimulated by excess iron, cadmium, nickel, and the like. Inversely, copper, zinc, and selenium inhibit production, either via their own action or via antiradical metalloenzymes. The study involved determining the effect of zinc deficiency combined with chronic ethanol administration on the status of blood and tissue free radicals, as well as on cardiac function in isolated, perfused rats' hearts. Animals were fed a basic diet containing residual zinc at 0.2-0.3 ppm. Following a zinc deficiency lasting 5 wk, which during the last 4 wk was accompanied by chronic ethanol administration, hearts were submitted to ischemia for 30 min in vitro, followed by reperfusion. Biochemical analyses (zinc, superoxide dismutase, malondialdehyde, conjugated dienes, and so on) were performed in the blood and in the homogenates of different organs. The experimental zinc deficiency caused a slight decrease of superoxide dismutase activity, accompanied by increased production of peroxidated lipids. Ethanol administration appeared to increase the levels of peroxidated lipids in the heart. Finally, the combination of zinc deficiency and ethanol administration had very harmful effects, especially on lipid peroxidation and contractile function of the isolated, perfused heart in preischemic conditions.

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