Coudray C, Boucher F, Richard M J, Arnaud J, De Leiris J, Favier A
Laboratoire de Biochimie C, Centre Hospitalier Régional de Grenoble, France.
Biol Trace Elem Res. 1991 Aug;30(2):103-18. doi: 10.1007/BF02990347.
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.
过量的铁、镉、镍等可刺激氧自由基的产生。相反，铜、锌和硒可通过自身作用或抗自由基金属酶抑制其产生。该研究旨在确定锌缺乏与慢性乙醇给药相结合对血液和组织自由基状态以及对离体灌注大鼠心脏心脏功能的影响。给动物喂食含锌量为0.2 - 0.3 ppm的基础饮食。在持续5周的锌缺乏后，在最后4周伴有慢性乙醇给药，然后将心脏在体外进行30分钟的缺血，随后再灌注。对血液和不同器官的匀浆进行生化分析（锌、超氧化物歧化酶、丙二醛、共轭二烯等）。实验性锌缺乏导致超氧化物歧化酶活性略有下降，同时过氧化脂质的产生增加。乙醇给药似乎会增加心脏中过氧化脂质的水平。最后，锌缺乏和乙醇给药的组合具有非常有害的影响，尤其是对缺血前条件下离体灌注心脏的脂质过氧化和收缩功能。
