Cao G
Zhonghua Yi Xue Za Zhi. 1991 Nov;71(11):623-6, 44.
56 weanling Balb/c mice were assigned to Zn deficiency (ZD, n = 40), pair-fed (PF, n = 8) and fed ad libitum (AL, n = 8) groups according to their sex and weight, ZD mice were fed Zn-deficient (Zn: 1.6 ppm) diet, and PF and AL mice were fed control (Zn: 51.6 ppm) diet. After 6 weeks, 8 mice were taken out from ZD group and killed with all PF and AL mice. Blood and liver were sampled for the assays of Zn, Cu, malondialdehyde (MDA) and superoxide dismutase (SOD). The other 32 ZD mice were divided into four groups and supplemented with 0, 5, 50 and 500 ppm Zn in the Zn-deficient diet respectively. After another 3 weeks they were also killed and used for the measurements of Zn, Cu, MDA and SOD. The results showed that Zn deficiency increased MDA formation and decreased SOD activity in the liver of mice. Supplementation of 5 or 50 ppm Zn for 3 weeks enabled a satisfactory recovery of all the indices in ZD mice. But 500 ppm Zn increased MDA formation and decreased SOD activity further. This could be explained by the secondary Cu deficiency in mice.
56只断乳的Balb/c小鼠按性别和体重分为缺锌组(ZD,n = 40)、配对喂养组(PF,n = 8)和自由采食组(AL,n = 8)。ZD组小鼠喂饲缺锌(锌含量:1.6 ppm)饲料,PF组和AL组小鼠喂饲对照(锌含量:51.6 ppm)饲料。6周后,从ZD组取出8只小鼠并处死,所有PF组和AL组小鼠也被处死。采集血液和肝脏样本用于检测锌、铜、丙二醛(MDA)和超氧化物歧化酶(SOD)。其余32只ZD组小鼠分为四组,分别在缺锌饲料中补充0、5、50和500 ppm的锌。再过3周后,它们也被处死并用于检测锌、铜、MDA和SOD。结果表明,缺锌会增加小鼠肝脏中MDA的生成并降低SOD活性。在ZD组小鼠中补充5或50 ppm的锌3周可使所有指标得到满意的恢复。但500 ppm的锌会进一步增加MDA的生成并降低SOD活性。这可能是由小鼠继发性铜缺乏所解释的。