Zinc deficiency, ethanol, and myocardial ischemia affect lipoperoxidation in rats View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1991-08

AUTHORS

Charles Coudray, François Boucher, Marie J. Richard, Josiane Arnaud, Joel De Leiris, Alain Favier

ABSTRACT

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. More... »

PAGES

103-118

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf02990347

DOI

http://dx.doi.org/10.1007/bf02990347

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1040721416

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/1723883


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