EFFECTS OF COLD-EXPOSURE ON RAT ADRENAL TYROSINE-HYDROXYLASE - AN ANALYSIS OF RNA, PROTEIN, ENZYME-ACTIVITY, AND COFACTOR LEVELS
EFFECTS OF COLD-EXPOSURE ON RAT ADRENAL TYROSINE-HYDROXYLASE - AN ANALYSIS OF RNA, PROTEIN, ENZYME-ACTIVITY, AND COFACTOR LEVELS
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DOI：
10.1111/j.1471-4159.1990.tb01232.x
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发表时间：
1990-05-01
影响因子：
4.7
通讯作者：
KAPLAN, BB
中科院分区：
文献类型：
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作者：
BARUCHIN, A;WEISBERG, EP;KAPLAN, BB
众所周知，长期冷暴露(5-7天)会导致肾上腺髓质酪氨酸羟基酶(TH)RNA、蛋白质和酶活性的相应增加。在这份报告中，我们比较了这些变化的时间进程，并调查了寒冷暴露对生物蝶呤水平的影响，生物蝶呤是酪氨酸羟化所需的辅因子。冷暴露仅1h，TH基因丰度较非应激对照组增加71%。细胞总TH RNA水平在冷暴露后3-6小时内最高(是对照的3倍)，并在整个实验期间(72小时)保持在较高水平。冷暴露24小时后，TH蛋白水平迅速升高，48-72小时达到最大值，是对照的3倍。肾上腺髓质生物蝶呤在冷暴露开始后迅速增加，在24小时时上升到非应激对照组的两倍左右，并在应激期间一直保持在这个水平。综上所述，这一时程研究的结果表明，寒冷诱导的肾上腺TH活性的变化是由多种细胞控制机制介导的，其中可能包括翻译前和翻译后的调节。我们的发现还表明，冷应激诱导的TH辅因子水平的增加可能是交感肾上腺系统对冷应激反应的另一个关键事件。
Long-term cold exposure (5-7 days) is known to induce concomitant increases in the levels of adrenomedullary tyrosine hydroxylase (TH) RNA, protein, and enzyme activity. In this report, we compare the time courses of these changes and investigate the effects of cold exposure on the levels of biopterin, the cofactor required for tyrosine hydroxylation. After only 1 h of cold exposure, TH mRNA abundance increased 71% compared with nonstressed controls. Increases in total cellular TH RNA levels were maximal (threefold over control values) within 3-6 of cold exposure and remained elevated throughout the duration of the experiment (72 h) TH protein levels increased rapidly after 24 h of cold exposure and reached a maximal value threefold above that of controls at 48-72 h. Despite the relatively rapid and large elevations in TH RNA and protein content, only modest increases in TH activity were detected during the initial 48 h of cold exposure. Adrenomedullary biopterin increased rapidly after the onset of cold exposure, rising to a level approximately twofold that of the nonstressed controls at 24 h, and remained at this level throughout the duration of the stress period. Taken together, the results of this time course study indicate that cold-induced alterations in adrenal TH activity are mediated by multiple cellular control mechanisms, which may include pre- and posttranslational regulation. Our findings also suggest that cold stress-induced increases in the levels of TH cofactor may represent another key event in the sympathoadrenal system''s response to cold stress.