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次黄嘌呤维持小鼠胚胎的二细胞阻滞:对葡萄糖的依赖性及次黄嘌呤磷酸核糖基转移酶抑制剂的作用

Hypoxanthine-maintained two-cell block in mouse embryos: dependence on glucose and effect of hypoxanthine phosphoribosyltransferase inhibitors.

作者信息

Downs S M, Dow M P

机构信息

Biology Department, Marquette University, Milwaukee, Wisconsin 53233.

出版信息

Biol Reprod. 1991 Jun;44(6):1025-39. doi: 10.1095/biolreprod44.6.1025.

Abstract

The culture conditions under which hypoxanthine maintains a two-cell block in preimplantation mouse embryos were assessed. Hypoxanthine prevented embryo development past the two-cell stage at concentrations as low as 30 nM, and this inhibitory activity required the presence of D-glucose. The action of hypoxanthine plus D-glucose was reversed by glutamine and higher lactate. D-mannose substituted for D-glucose in supporting the inhibitory action of hypoxanthine, but L-glucose, D-fructose, and 2-deoxyglucose were much less effective. Other purine derivatives such as inosine and adenosine, but not xanthosine or uric acid, also blocked development at the two-cell stage at a concentration of 30 microM, and guanosine was inhibitory at higher doses. Assays of hypoxanthine phosphoribosyltransferase (HPRT) activity in lysates of four-cell embryos determined that the drugs 6-mercapto-9-(tetrahydro-2-furyl)-purine (MPTF) and 6-mercaptopurine (6-MP), but not 6-azauridine (6-AzaU), prevented salvage of hypoxanthine. In addition, MPTF and 6-MP produced a significant two-cell block, which did not depend upon the presence of hypoxanthine or D-glucose; whereas 6-AzaU was without effect. When embryos were cultured 2 days in the presence or absence of D-glucose, hypoxanthine salvage was significantly reduced in lysates of four-cell embryos exposed to D-glucose. D-glucose had no effect when added directly to the assay mixture. These data demonstrate that the ability of hypoxanthine to block embryo development at the two-cell stage depends on the presence of D-glucose or other glycolyzable sugars and suggest that inhibition of the purine salvage pathway promotes the two-cell block.

摘要

评估了次黄嘌呤在植入前小鼠胚胎中维持二细胞阻滞的培养条件。次黄嘌呤在低至30 nM的浓度下就能阻止胚胎发育超过二细胞阶段,且这种抑制活性需要D - 葡萄糖的存在。谷氨酰胺和较高浓度的乳酸可逆转次黄嘌呤加D - 葡萄糖的作用。D - 甘露糖在支持次黄嘌呤的抑制作用方面可替代D - 葡萄糖,但L - 葡萄糖、D - 果糖和2 - 脱氧葡萄糖的效果则差得多。其他嘌呤衍生物,如肌苷和腺苷,但黄苷或尿酸则不然,在30 μM的浓度下也会在二细胞阶段阻滞发育,而鸟苷在较高剂量时具有抑制作用。对四细胞胚胎裂解物中的次黄嘌呤磷酸核糖转移酶(HPRT)活性进行测定发现,药物6 - 巯基 - 9 -(四氢 - 2 - 呋喃基)嘌呤(MPTF)和6 - 巯基嘌呤(6 - MP),但不是6 - 氮杂尿苷(6 - AzaU),可阻止次黄嘌呤的补救。此外,MPTF和6 - MP产生了显著的二细胞阻滞,这并不依赖于次黄嘌呤或D - 葡萄糖的存在;而6 - AzaU则没有效果。当胚胎在有或没有D - 葡萄糖的情况下培养2天时,暴露于D - 葡萄糖的四细胞胚胎裂解物中的次黄嘌呤补救显著减少。直接添加到测定混合物中时,D - 葡萄糖没有作用。这些数据表明,次黄嘌呤在二细胞阶段阻滞胚胎发育的能力取决于D - 葡萄糖或其他可糖酵解糖的存在,并表明嘌呤补救途径的抑制促进了二细胞阻滞。

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