Kubow S, Bray T M, Bettger W J
Can J Physiol Pharmacol. 1986 Oct;64(10):1281-5. doi: 10.1139/y86-216.
The effects of dietary copper and zinc on free radical production in lung and liver microsomes were studied in male weanling rats. The rats were fed for 6 weeks on one of seven diets, with different copper and zinc concentrations representing low, adequate, and high dietary levels of copper and low and adequate levels of zinc. Rats were put on diets arranged in a 3 X 2 factorial design with copper and zinc supplementations of 0, 15, and 500 mg/kg and 0.5 or 100 mg/kg, respectively. The low copper diet depressed copper levels in both the lungs and liver, although zinc levels were unchanged in rats on the low zinc diets. Endogenous carbon-centered lipid radical production in microsomes induced by NADPH was measured using spin-trapping techniques. The low zinc diets increased free radical production in lung microsomes but not in liver microsomes. No change in free radical production was observed in lung or liver microsomes obtained from rats on low copper diets. The data indicate that endogenous free radical production is increased in lung microsomes as a function of dietary zinc deficiency but is not influenced by copper status.
在雄性断乳大鼠中研究了膳食铜和锌对肺和肝微粒体自由基产生的影响。将大鼠分为七组,分别喂食不同铜和锌浓度的七种饲料之一,这些浓度代表低、适宜和高膳食铜水平以及低和适宜膳食锌水平。大鼠采用3×2析因设计的饲料喂养,铜和锌的添加量分别为0、15和500mg/kg以及0.5或100mg/kg。低铜饲料降低了肺和肝中的铜水平,而低锌饲料喂养的大鼠锌水平未发生变化。使用自旋捕获技术测定由NADPH诱导的微粒体内源性以碳为中心的脂质自由基产生。低锌饲料增加了肺微粒体中的自由基产生,但未增加肝微粒体中的自由基产生。从低铜饲料喂养的大鼠获得的肺或肝微粒体中未观察到自由基产生的变化。数据表明,肺微粒体中的内源性自由基产生随膳食锌缺乏而增加,但不受铜状态的影响。