Quik M, Sourkes T L
Can J Biochem. 1977 Jan;55(1):60-5. doi: 10.1139/o77-011.
Chronic nutritional iron deficiency of 2 to 5 weeks duration reduced the blood hemoglobin content to 30-50% of control values and resulted in an increase in rat adrenal tyrosine hydroxylase (TH) (EC 1.14.16.2) activity. Kinetic and mixing experiments indicated that this increase was due to an increase in enzyme protein. The body weight of iron-deficient rats ranged from 60 to 80% of control; this factor, however, was not responsible for the increase in adrenal TH as enzyme activity was directly proportional to final body weight. To determine whether the increase in adrenal TH in iron-deficient rats was due to increased sympathetic activity to the adrenal medulla, the splanchnic nerve was cut. The increased TH was still observed after adrenal denervation; this indicates that the mechanism of response to iron deficiency lies within the adrenal itself. Age of the rats is important in determining whether the increase in TH activity will occur.
持续2至5周的慢性营养性缺铁使大鼠血液血红蛋白含量降至对照值的30 - 50%,并导致大鼠肾上腺酪氨酸羟化酶(TH)(EC 1.14.16.2)活性增加。动力学和混合实验表明,这种增加是由于酶蛋白增加所致。缺铁大鼠的体重为对照大鼠的60%至80%;然而,该因素并非肾上腺TH活性增加的原因,因为酶活性与最终体重直接相关。为了确定缺铁大鼠肾上腺TH的增加是否由于对肾上腺髓质交感神经活动增加所致,切断了内脏神经。肾上腺去神经支配后仍观察到TH增加;这表明对缺铁的反应机制存在于肾上腺本身。大鼠的年龄对于确定是否会发生TH活性增加很重要。