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硒和碘缺乏:对大脑和棕色脂肪组织硒酶活性及表达的影响。

Selenium and iodine deficiencies: effects on brain and brown adipose tissue selenoenzyme activity and expression.

作者信息

Mitchell J H, Nicol F, Beckett G J, Arthur J R

机构信息

Rowett Research Institute, Bucksburn, Aberdeen, UK.

出版信息

J Endocrinol. 1997 Nov;155(2):255-63. doi: 10.1677/joe.0.1550255.

Abstract

Adequate dietary iodine supplies and thyroid hormones are needed for the development of the central nervous system (CNS) and brown adipose tissue (BAT) function. Decreases in plasma thyroxine (T4) concentrations may increase the requirement for the selenoenzymes types I and II iodothyronine deiodinase (ID-I and ID-II) in the brain and ID-II in BAT to protect against any fall in intracellular 3,3',5 tri-iodothyronine (T3) concentrations in these organs. We have therefore investigated selenoenzyme activity and expression and some developmental markers in brain and BAT of second generation selenium- and iodine-deficient rats. Despite substantial alterations in plasma thyroid hormone concentrations and thyroidal and hepatic selenoprotein expression in selenium and iodine deficiencies, ID-I, cytosolic glutathione peroxidase (cGSHPx) and phospholipid hydroperoxide glutathione peroxidase (phGSHPx) activities and expression remained relatively constant in most brain regions studied. Additionally, brain and pituitary ID-II activities were increased in iodine deficiency regardless of selenium status. This can help maintain tissue T3 concentrations in hypothyroidism. Consistent with this, no significant effects of iodine or selenium deficiency on the development of the brain were observed, as assessed by the activities of marker enzymes. In contrast, BAT from selenium- and iodine deficient rats had impaired thyroid hormone metabolism and less uncoupling protein than in tissue from selenium- and iodine-supplemented animals. Thus, the effects of selenium and iodine deficiency on the brain are limited due to the activation of the compensatory mechanisms but these mechanisms are less effective in BAT.

摘要

中枢神经系统(CNS)的发育和棕色脂肪组织(BAT)的功能需要充足的膳食碘供应和甲状腺激素。血浆甲状腺素(T4)浓度降低可能会增加大脑中I型和II型碘甲状腺原氨酸脱碘酶(ID-I和ID-II)以及BAT中ID-II对硒酶的需求,以防止这些器官细胞内3,3',5-三碘甲状腺原氨酸(T3)浓度下降。因此,我们研究了第二代缺硒和缺碘大鼠大脑和BAT中的硒酶活性、表达以及一些发育标志物。尽管缺硒和缺碘会使血浆甲状腺激素浓度以及甲状腺和肝脏硒蛋白表达发生显著变化,但在所研究的大多数脑区中,ID-I、胞质谷胱甘肽过氧化物酶(cGSHPx)和磷脂氢过氧化物谷胱甘肽过氧化物酶(phGSHPx)的活性和表达仍保持相对稳定。此外,无论硒状态如何,缺碘时大脑和垂体中的ID-II活性都会增加。这有助于维持甲状腺功能减退时的组织T3浓度。与此一致的是,通过标记酶的活性评估,未观察到缺碘或缺硒对大脑发育有显著影响。相比之下,缺硒和缺碘大鼠的BAT甲状腺激素代谢受损,解偶联蛋白比补充硒和碘的动物组织中的少。因此,由于补偿机制的激活,缺硒和缺碘对大脑的影响有限,但这些机制在BAT中效果较差。

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