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孕前哺乳动物卵子的X射线辐射会导致不育和/或先天性异常吗?

Does x-radiation of the preconceptional mammalian ovum lead to sterility and/or congenital anomalies?

作者信息

Rugh R, Budd R A

出版信息

Fertil Steril. 1975 Jun;26(6):560-72. doi: 10.1016/s0015-0282(16)41176-3.

Abstract

Sexually mature CF1 female mice were x-radiated with 10 to 500 R prior to mating with normal males of the same strain, and no exposure rendered the mice sterile immediately; estrous was not altered, so that normal matings occurred; the litter size of females exposed to the 500-R dose was reduced, possibly due to induction of dominant lethal genes. The second and third meiotic maturations following x-radiation gave rise to fertilizable ova which resulted in offspring that did not show any increase in the incidence of congenital anomalies. With increasing levels of exposure to x-rays, there was a decrease in the reproductive live-span. If the interval between x-radiation and mating was lengthened to 60 days, none of those exposed to 300 R or more was fertile; those exposed to 100 R showed variable fertility, evidenced by reduced litter sizes, but there were no anomalies. None of the offspring of the x-radiated females showed a significant weight loss, even to 2 months of age. Thus, when ova were x-rayed before fertilization with normal sperm, normal fertilization occurred and normal offspring were produced from at least the first three successive estrous cycles; after that, various degrees of sterility were evident, depending upon the dose level of the original exposure. Since resorptions (but not anomalies) were increased with the higher doses, dominant lethal and recessive mutatuions may have been obscured by the normal alleles of the unirradiated male mates. The ovarian ovum could not readily be sterilized by x-rays, nor could it be so damaged as to cause congenital anomalies. Nevertheless, one must be aware that all x-rayed ova may carry recessive mutatuions which might be phenotypically evident if they are on the female sex (X) chromosome, unmasked by an allelomorph on the male (Y) chromosome, or might even surface in future generations, if chance combines them with similar genes.

摘要

性成熟的CF1雌性小鼠在与同品系正常雄性小鼠交配前接受10至500伦琴的X射线照射,未照射的小鼠不会立即不育;发情期未改变,因此能正常交配;接受500伦琴剂量照射的雌性小鼠产仔数减少,可能是由于显性致死基因的诱导。X射线照射后的第二次和第三次减数分裂成熟产生了可受精的卵子,这些卵子产生的后代先天性异常发生率没有增加。随着X射线照射水平的提高,生殖寿命缩短。如果X射线照射与交配之间的间隔延长至60天,接受300伦琴或更高剂量照射的小鼠无一能生育;接受100伦琴照射的小鼠生育能力不一,表现为产仔数减少,但没有异常。接受X射线照射的雌性小鼠的后代即使到2月龄也没有明显体重减轻。因此,当卵子在与正常精子受精前接受X射线照射时,至少在连续的前三个发情周期能正常受精并产生正常后代;此后,根据最初照射的剂量水平,会出现不同程度的不育。由于高剂量照射会增加吸收(但不是异常),显性致死和隐性突变可能被未照射的雄性配偶的正常等位基因掩盖。卵巢卵子不容易被X射线绝育,也不会被损伤到导致先天性异常的程度。然而,必须意识到所有接受X射线照射的卵子可能携带隐性突变,如果这些突变位于雌性(X)染色体上,可能会因雄性(Y)染色体上的等位基因而在表型上显现出来,或者如果偶然与相似基因结合,甚至可能在后代中显现出来。

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