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Effects of Cold Exposure on Rat Adrenal Tyrosine Hydroxylase: An Analysis of RNA, Protein, Enzyme Activity, and Cofactor Levels
Author(s) -
Baruchin Andrea,
Weisberg Edward P.,
Miner Lucinda L.,
Ennis David,
Nisenbaum Laura K.,
Naylor Edwin,
Stricker Edward M.,
Zigmond Michael J.,
Kaplan Barry B.
Publication year - 1990
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1990.tb01232.x
Subject(s) - tyrosine hydroxylase , endocrinology , medicine , cold stress , biopterin , enzyme assay , cofactor , chemistry , enzyme , tyrosine , biology , biochemistry , tetrahydrobiopterin , gene
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 h 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 the TH cofactor may represent another key event in the sympathoadrenal system's response to cold stress.