Astancolle S, Davalli P, Corti A
Istituto di Chimica Biologica, Modena, Italy.
Biochem Biophys Res Commun. 1991 Jan 31;174(2):915-21. doi: 10.1016/0006-291x(91)91505-7.
Rat liver ornithine decarboxylase induction by dexamethasone or laparatomy, which is dramatically impaired by catecholamine depletion, is not affected by alpha-and beta -adrenergic blockers administered simultaneously 1 h prior to steroid injection or operation. However, if blockade is maintained for 24 h, an effect comparable to that of catecholamine depletion is obtained. Reciprocally, the response of the decarboxylase to catecholamines is severely compromised in adrenalectomized rats. Under the same conditions, induction of tyrosine aminotransferase by dexamethasone is not significantly affected by catecholamine availability, which altogether demonstrates that rat liver ornithine decarboxylase activity is specifically governed by the interaction between glucocorticoids and catecholamines.
地塞米松或剖腹术诱导大鼠肝脏鸟氨酸脱羧酶,这一过程会因儿茶酚胺耗竭而显著受损,在注射类固醇或手术前1小时同时给予α和β肾上腺素能阻滞剂则不会产生影响。然而,如果持续阻断24小时,则会产生与儿茶酚胺耗竭相当的效果。相反,在肾上腺切除的大鼠中,脱羧酶对儿茶酚胺的反应严重受损。在相同条件下,地塞米松诱导酪氨酸转氨酶不受儿茶酚胺可用性的显著影响,这充分表明大鼠肝脏鸟氨酸脱羧酶活性受糖皮质激素和儿茶酚胺之间相互作用的特异性调控。