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甲状腺素诱导的大鼠甲胎蛋白糖基化模式、脑和血清水平的变化。

Thyroxine-induced changes in the glycosylation pattern and in brain and serum levels of rat alpha-fetoprotein.

作者信息

Naval J, Calvo M, Lampreave F, Piñeiro A

出版信息

Int J Biochem. 1986;18(2):115-22. doi: 10.1016/0020-711x(86)90142-4.

Abstract

We have studied the effect of thyroid disfunction during the postnatal period, on the serum and brain levels of rat alpha-fetoprotein (AFP) and albumin. Hypothyroidism was induced by treatment of pregnant rats and their newborn pups with 2-mercapto-1-methylimidazole(methimazole). Hyperthyroidism was provoked in newborns by daily injections of thyroxine (0.25 micrograms/g body wt) from the 3rd postnatal day weaning. Impaired growth, lower brain size, altered behaviour and morphological features observed were according to an altered thyroid status. Hypothyroid rats showed a significantly reduction in serum AFP concentration (78% of control values at 8 days of age) and a slight increase in that of albumin. level could be appreciated. Thyroxine supplementation (0.2 micrograms/rat/day) corrected most of these alterations. Hyperthyroidism induced a drastic fall in both serum and brain AFP levels (about 48% of the corresponding control values). Albumin concentration in serum was augmented significantly from the 12th postnatal day, but its brain levels did not change significantly. In hyperthyroid rats, a significant reduction (37% relative to controls) in the concanavalin A-non reactive microform of AFP, was observed. This alteration of the glycosylation pattern of AFP could be due to the inhibition by thyroxine of the activity of the hepatic enzyme GlcNAc-transferase III.

摘要

我们研究了出生后甲状腺功能紊乱对大鼠血清和脑内甲胎蛋白(AFP)及白蛋白水平的影响。通过用2-巯基-1-甲基咪唑(甲巯咪唑)处理怀孕大鼠及其新生幼崽来诱发甲状腺功能减退。从出生后第3天断奶开始,每天给新生大鼠注射甲状腺素(0.25微克/克体重)来诱发甲状腺功能亢进。观察到的生长发育受损、脑体积变小、行为改变和形态特征均与甲状腺状态改变有关。甲状腺功能减退的大鼠血清AFP浓度显著降低(8日龄时为对照值的78%),白蛋白浓度略有升高。甲状腺素补充(0.2微克/只/天)纠正了这些改变中的大部分。甲状腺功能亢进导致血清和脑内AFP水平急剧下降(约为相应对照值的48%)。血清白蛋白浓度从出生后第12天开始显著升高,但其脑内水平无明显变化。在甲状腺功能亢进的大鼠中,观察到AFP的伴刀豆球蛋白A非反应性微形式显著减少(相对于对照降低37%)。AFP糖基化模式的这种改变可能是由于甲状腺素抑制了肝酶N-乙酰葡糖胺转移酶III的活性。

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