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小鼠胎儿期锌缺乏后发育迟缓的可逆性

Reversibility of development retardation following murine fetal zinc deprivation.

作者信息

Beach R S, Gershwin M E, Hurley L S

出版信息

J Nutr. 1982 Jun;112(6):1169-81. doi: 10.1093/jn/112.6.1169.

Abstract

To investigate the effects and reversibility of moderate prenatal zinc deprivation, pregnant mice were fed, beginning on day 7 of gestation, a diet containing either 100 ppm (control) or 5 ppm zinc; pair-fed controls were also studied. Nutritional manipulation was limited to the prenatal period. Zinc-deprived dams had significantly smaller litters than did controls, and postnatal survival was markedly compromised. Progeny of zinc-deprived dams displayed significant growth retardation, as reflected by lower body weight and length than controls, whether ad libitum-fed or pair-fed. Growth of spleen and thymus was affected by zinc deprivation to a significantly greater extent than was growth of heart, kidney or brain. Cross-fostering of control pups to zinc-deprived dams resulted in delayed growth; however, retardation was not as great as that observed in deprived pups allowed to suckle their natural mothers. Cross-fostering of zinc-deprived pups to control dams improved growth of most organs, but did little to improve growth of spleen and, most notably, thymus. Zinc-deprived pups exhibited considerable "catch up" growth following neonatal zinc repletion, and by 6-8 weeks of age, no significant differences between control and deprived offspring were observed.

摘要

为研究孕期适度缺锌的影响及可逆性,从妊娠第7天开始,给怀孕小鼠喂食含100 ppm(对照)或5 ppm锌的饲料;同时也研究了配对喂养的对照组。营养干预仅限于孕期。缺锌母鼠的产仔数明显少于对照组,且产后存活率显著降低。无论自由采食还是配对喂养,缺锌母鼠的后代均表现出明显的生长迟缓,表现为体重和体长低于对照组。锌缺乏对脾脏和胸腺生长的影响程度明显大于对心脏、肾脏或大脑生长的影响。将对照幼崽寄养给缺锌母鼠会导致生长延迟;然而,生长迟缓程度不如由亲生母亲哺乳的缺锌幼崽严重。将缺锌幼崽寄养给对照母鼠可改善大多数器官的生长,但对脾脏尤其是胸腺的生长改善作用不大。缺锌幼崽在新生期补锌后表现出相当程度的“追赶”生长,到6 - 8周龄时,对照后代和缺锌后代之间未观察到显著差异。

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