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致畸剂量的汞和镉对孕鼠某些生化效应的比较。

Comparison of some biochemical effects of teratogenic doses of mercuric mercury and cadmium in the pregnant rat.

作者信息

Holt D, Webb M

出版信息

Arch Toxicol. 1986 Apr;58(4):249-54. doi: 10.1007/BF00297115.

Abstract

Mercuric mercury (Hg2+), like cadmium (Cd2+), interferes with the transport of certain essential metals to the conceptus in the pregnant Wistar rat and, at 48 h after the IV injection of a teratogenic dose (0.79 mg Hg2+/kg body weight) on day 12 of gestation, the foetal concentrations of Zn2+, Cu2+ and Fe3+, but not of Mg2+, are reduced significantly. Both Hg2+ and Cd2+, at teratogenic dose levels, inhibit the placental and foetal uptake of 65Zn2+ and 67Cu2+, but possibly by different mechanisms. In addition, the effects of Hg2+, at different times after dosing, on the uptake of these labelled tracers and of 59Fe3+, administered as 15-min pulses, do not parallel the changes in the placental and foetal concentrations and contents of the endogenous, stable metallic ions. The teratogenic dose of Hg2+ inhibits the placental and foetal uptake of L-[4,5-3H]-leucine, but not the incorporation of the labelled amino acid into foetal protein. In contrast, the corresponding dose of Cd2+ inhibits both leucine uptake and protein synthesis in the placenta and foetus. Similarly, Cd2+ inhibits the uptake of [2-14C]-thymidine and its incorporation into foetal DNA, whereas Hg2+ reduces the placental and foetal uptake, but has little or no effect on the utilization of the nucleoside. Since both Cd2+ and Hg2+ reduce the foetal uptake of 65Zn and the foetal concentration of Zn, but only Cd2+ interferes with DNA synthesis, it is unlikely that the inhibition of the metabolism of thymidine can be attributed to reduction in thymidine kinase activity in consequence of foetal Zn deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

汞离子(Hg2+)与镉离子(Cd2+)一样,会干扰特定必需金属向怀孕的Wistar大鼠体内胚胎的转运。在妊娠第12天静脉注射致畸剂量(0.79毫克Hg2+/千克体重)48小时后,胚胎中锌离子(Zn2+)、铜离子(Cu2+)和铁离子(Fe3+)的浓度显著降低,但镁离子(Mg2+)的浓度未受影响。致畸剂量水平的Hg2+和Cd2+均会抑制胎盘和胚胎对65Zn2+和67Cu2+的摄取,但可能通过不同机制。此外,给药后不同时间Hg2+对这些标记示踪剂以及以15分钟脉冲形式给药的59Fe3+摄取的影响,与胎盘和胚胎中内源性稳定金属离子的浓度及含量变化并不平行。致畸剂量的Hg2+会抑制胎盘和胚胎对L-[4,5-3H]-亮氨酸的摄取,但不会抑制标记氨基酸掺入胚胎蛋白质。相比之下,相应剂量的Cd2+会抑制胎盘和胚胎中亮氨酸的摄取以及蛋白质合成。同样,Cd2+会抑制[2-14C]-胸腺嘧啶核苷的摄取及其掺入胚胎DNA,而Hg2+会降低胎盘和胚胎的摄取,但对该核苷的利用影响很小或没有影响。由于Cd2+和Hg2+都会降低胚胎对65Zn的摄取以及胚胎中Zn的浓度,但只有Cd2+会干扰DNA合成,因此胸腺嘧啶核苷代谢的抑制不太可能归因于胚胎锌缺乏导致的胸腺嘧啶激酶活性降低。(摘要截选至250词)

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