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肾上腺素预处理对大鼠肝脏制剂中3,5,3'-三碘甲状腺原氨酸和3,3',5'-三碘甲状腺原氨酸(反式T3)体外生成的影响。

The effect of adrenaline pretreatment on the in vitro generation of 3,5,3'-triiodothyronine and 3,3',5'-triiodothyronine (reverse T3) in rat liver preparation.

作者信息

Nauman A, Porta S, Bardowska U, Fiedorowicz K, Sadjak A, Korsatko W, Nauman J

出版信息

Horm Metab Res. 1984 Sep;16(9):471-4. doi: 10.1055/s-2007-1014822.

Abstract

The effects of adrenaline (A) on liver T3 and rT3 neogenesis from T4 were studied in Wistar rats. The animals were implanted subcutaneously either with A or placebo (P) especially coated tablets which linearly released the hormone. The serum A values 6 hrs after implantation of 7.5, 15.0 and 45.0 mg tablets were 6.5 +/- 1.31, 6.8 +/- 1.8 and 16.4 +/- 1.9 ng/ml, respectively vs 4.4 +/- 2.5 ng/ml seen in P pretreated group. The output rates of A were 0.11 (7.5 mg), 0.18 (15 mg) and 0.52 microgram/ml (45 mg). The pretreatment with A led to hyperglycemia and the "low T3 syndrome". Neogenesis of T3 from T4 in medium containing liver microsomes of P pretreated rats was 5.49 +/- 0.25 pmol of T3/mg protein/min and decreased in A pretreated rats to 3.82 +/- 0.17, 3.12 +/- 0.27 and 3.06 +/- 0.11 pmol of T3/mg of protein/min. Neogenesis of rT3 from T4 in microsomes from P group was 1.52 +/- 0.09 pmol rT3/mg protein/min and increased after A to 2.71 +/- 0.11, 2.60 +/- 0.21 and 2.21 +/- 0.34 pmol of rT3/mg protein/min thus showing no dose dependency. Enrichment of microsomes medium with cytosol either from P or A pretreated rats had no effect on T3 generation thus excluding effect of A on cytosolic cofactor. Although cytosol further increased rT3 neogenesis this was seen regardless of whether cytosol was obtained from A or P implanted rats. It is concluded that A decreases the activity of T4-5'-deiodinase in liver, and possibly increases the activity of T4-5-deiodinase.

摘要

在Wistar大鼠中研究了肾上腺素(A)对肝脏从T4生成T3和反式T3(rT3)的影响。给动物皮下植入A或安慰剂(P)的特殊包衣片,该片可线性释放激素。植入7.5、15.0和45.0mg片剂后6小时的血清A值分别为6.5±1.31、6.8±1.8和16.4±1.9ng/ml,而P预处理组为4.4±2.5ng/ml。A的释放速率分别为0.11(7.5mg)、0.18(15mg)和0.52μg/ml(45mg)。A预处理导致高血糖和“低T3综合征”。P预处理大鼠肝脏微粒体培养基中从T4生成T3的速率为5.49±0.25pmol T3/mg蛋白质/分钟,在A预处理大鼠中降至3.82±0.17、3.12±0.27和3.06±0.11pmol T3/mg蛋白质/分钟。P组微粒体中从T4生成rT3的速率为1.52±0.09pmol rT3/mg蛋白质/分钟,A处理后增加到2.71±0.11、2.60±0.21和2.21±0.34pmol rT3/mg蛋白质/分钟,因此未显示出剂量依赖性。用P或A预处理大鼠的细胞溶质富集微粒体培养基对T3生成没有影响,从而排除了A对细胞溶质辅因子的作用。尽管细胞溶质进一步增加了rT3的生成,但无论细胞溶质是从植入A还是P的大鼠中获得,均观察到这种情况。得出的结论是,A降低了肝脏中T4-5'-脱碘酶的活性,并可能增加了T4-5-脱碘酶的活性。

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