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缺锌大鼠胚胎中的细胞坏死。

Cellular necrosis in zinc-deficient rat embryos.

作者信息

Record I R, Tulsi R S, Dreosti I E, Fraser F J

出版信息

Teratology. 1985 Dec;32(3):397-405. doi: 10.1002/tera.1420320310.

Abstract

Abnormal cellular necrosis was studied in 9.5-11.5-day embryos obtained from zinc-deficient rats. At periods of low maternal zinc status induced by a high intake of a zinc-deficient diet, cell death was observed in those regions of the embryo that were most sensitive to teratogenic insult at that time. As the maternal serum zinc level increased during the fasting phase of the feeding cycle, the degree of necrosis decreased, leaving the tissue histologically more normal even though the embryos were grossly malformed. The mitotic index of cells in the neural epithelium and limb buds of zinc-deficient, non-necrotic embryos was found to be elevated, but there was no evidence of blockage at any particular stage of mitosis. It can be hypothesised that during the early stages of organogenesis, periods of low maternal zinc status initiate unscheduled cell death by some as yet undefined mechanism that in turn, gives rise to the morphological anomalies observed later.

摘要

对从缺锌大鼠获得的9.5至11.5天胚胎中的异常细胞坏死进行了研究。在因高摄入缺锌饮食而导致母体锌状态较低的时期,在胚胎中对致畸性损伤最敏感的那些区域观察到了细胞死亡。随着母体血清锌水平在喂养周期的禁食阶段升高,坏死程度降低,尽管胚胎严重畸形,但组织学上组织变得更正常。发现缺锌、无坏死的胚胎神经上皮和肢芽中的细胞有丝分裂指数升高,但没有证据表明在有丝分裂的任何特定阶段存在阻滞。可以推测,在器官发生的早期阶段,母体锌状态较低的时期通过某种尚未明确的机制引发了非程序性细胞死亡,而这种机制反过来又导致了后来观察到的形态异常。

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