Yu H S, Chan S T
Teratology. 1986 Dec;34(3):313-9. doi: 10.1002/tera.1420340311.
A decline in LDH activity from four-cell to late blastocyst was demonstrated in pre-embryos from F1 (C57 female X A2G male) female mice. An exposure to 0.5 or 1 microgram/ml cadmium did not affect the in vitro development of the four-cell pre-embryos and morulae or their LDH activities. At 5 or 10 micrograms/ml cadmium, the in vitro development of the treated pre-embryos was affected. Although most of the treated four-cell pre-embryos had proceeded to compaction, they became degenerated 24 h after treatment. The LDH activity of these degenerated pre-embryos was higher than that in the control blastocysts. We propose that cadmium may interfere with the general energy metabolism of the cells. This causes a reduced rate of LDH degradation, leading to a slower decline in LDH activity in cadmium-treated pre-embryos. Failure of some critical biochemical processes after cadmium treatment may ultimately lead to the subsequent degeneration of the treated pre-embryos.
在F1(C57雌性×A2G雄性)雌性小鼠的胚胎前体中,已证实从四细胞期到晚期囊胚期乳酸脱氢酶(LDH)活性下降。暴露于0.5或1微克/毫升的镉不会影响四细胞胚胎前体和桑椹胚的体外发育及其LDH活性。在5或10微克/毫升的镉浓度下,经处理的胚胎前体的体外发育受到影响。虽然大多数经处理的四细胞胚胎前体已进入致密化阶段,但在处理后24小时它们开始退化。这些退化胚胎前体的LDH活性高于对照囊胚。我们认为镉可能会干扰细胞的一般能量代谢。这导致LDH降解速率降低,从而使经镉处理的胚胎前体中LDH活性下降更慢。镉处理后某些关键生化过程的失败可能最终导致经处理的胚胎前体随后发生退化。