Saari J T, Dickerson F D, Habib M P
Human Nutrition Research Center, United States Department of Agriculture, Grand Forks, North Dakota 58202.
Proc Soc Exp Biol Med. 1990 Oct;195(1):30-3. doi: 10.3181/00379727-195-43114.
Evidence is accumulating which indicates that copper-deficient animals are prone to oxidative damage. To investigate this possibility further, we measured the production of breath ethane, a hydrocarbon by-product of lipid peroxidation, in copper-deficient rats. Male, weanling Sprague-Dawley rats were fed either a purified diet which was deficient in copper (CuD) or the same diet made sufficient with 5 ppm of copper (CuS). After 33 to 34 days the rats were placed individually in gastight metabolic cages through which ethane-free air or 100% O2 was passed. Expired ethane was absorbed onto cold, activated charcoal, liberated by heating, and measured by gas chromatography. Ethane production rates (pmoles/min/100 g +/- SD) were 3.3 +/- 0.8 (CuS-air), 4.3 +/- 1.4 (CuD-air), 8.3 +/- 2.5 (CuS-O2), and 12.2 +/- 4.3 (CuD-O2). Repeated measures analysis of variance indicated that both copper deficiency (P less than 0.01) and breathing 100% O2 (P less than 0.0001) enhanced ethane production, with no interaction between treatments. This finding complements previous evidence that increased lipid peroxidation occurs in copper-deficient rats.
越来越多的证据表明，缺铜动物容易受到氧化损伤。为了进一步研究这种可能性，我们测量了缺铜大鼠呼出气体中乙烷（脂质过氧化的一种碳氢化合物副产物）的生成量。将雄性断乳的斯普拉格-道利大鼠分别喂食缺乏铜的纯化饮食（CuD）或添加5 ppm铜使其充足的相同饮食（CuS）。33至34天后，将大鼠单独置于气密代谢笼中，向笼中通入无乙烷空气或100%氧气。呼出的乙烷被吸附到冷的活性炭上，通过加热释放出来，并用气相色谱法进行测量。乙烷生成率（皮摩尔/分钟/100克±标准差）分别为3.3±0.8（CuS-空气组）、4.3±1.4（CuD-空气组）、8.3±2.5（CuS-O₂组）和12.2±4.3（CuD-O₂组）。重复测量方差分析表明，缺铜（P<0.01）和呼吸100%氧气（P<0.0001）均会增加乙烷生成量，且各处理之间无相互作用。这一发现补充了先前关于缺铜大鼠脂质过氧化增加的证据。
