Rivkin I, Chasin M
Arch Int Pharmacodyn Ther. 1975 Oct;217(2):309-21.
Adrenal cell suspensions prepared from rats bearing the MtTF4 tumor failed to increase corticosterone production when exposed to adenosine 3', 5'-cyclic monophosphate (cyclic AMP) or ACTH, placing the defect in these adrenals beyond the ACTH receptor site. Adrenal cells from normal rats responded well to these stimuli. Adrenal cyclic AMP phosphodiesterase prepared from the tumor bearing rats appeared normal both with respect to its specific activity and inhibition profile with theophylline. Exposure of the MtTF4 adrenal cells to 1,2-3H-cholesterol in the presence of either cyclic AMP or ACTH did not result in an increase in radioactively labeled corticosterone, whereas increased label could be demonstrated in adrenal cells from normal rats similarly treated.
从患有MtTF4肿瘤的大鼠制备的肾上腺细胞悬液,在暴露于3',5'-环磷酸腺苷(环磷腺苷)或促肾上腺皮质激素(ACTH)时,皮质酮生成未能增加,表明这些肾上腺的缺陷位于ACTH受体位点之后。正常大鼠的肾上腺细胞对这些刺激反应良好。从荷瘤大鼠制备的肾上腺环磷腺苷磷酸二酯酶,其比活性和对茶碱的抑制谱看起来均正常。在存在环磷腺苷或ACTH的情况下,将MtTF4肾上腺细胞暴露于1,2-³H-胆固醇,并未导致放射性标记的皮质酮增加,而在同样处理的正常大鼠肾上腺细胞中可显示标记增加。