Ethanol-induced stimulation of hepatic ornithine decarboxylase activity in the rat.
Ethanol-induced stimulation of hepatic ornithine decarboxylase activity in the rat.
复制标题
乙醇诱导的大鼠肝脏鸟氨酸脱羧酶活性的刺激。
DOI：
10.1111/j.1530-0277.1982.tb05384.x
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Sidransky,H
中科院分区：
文献类型：
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作者：
Murty,CN;Hornseth,R;Verney,E;Sidransky,H
研究了单次饲喂乙醇对大鼠肝脏鸟氨酸脱羧酶(ODC)活性的影响。在处死前1、2、3、4、8、12或24小时，将乙醇(7.5g/kg体重)以50%(v/v)水溶液管饲给禁食过夜的大鼠。通过测定0L-1-14C-鸟氨酸释放14C02来检测肝脏中ODC的活性水平。乙醇(7.5g/kg体重)显著刺激肝脏ODC活性，从1小时开始，4小时达到峰值(比零时间对照组增加16倍以上)。不同剂量的乙醇(2.5、5.0或7.5g/kg体重)在牺牲前3小时给隔夜禁食的大鼠一次喂养也显示肝脏ODC活性显著增加(3-13倍)。在体外实验中，与对照组相比，乙醇处理的大鼠肝微粒体14C-Leucir&Gt；e掺入蛋白质的量减少。乙醇代谢抑制剂吡喃吡啶不能阻断乙醇对肝脏ODC活性的刺激作用。而乙醇对肝脏ODC活性的刺激作用可被放线菌素D或放线菌亚胺抑制，提示这种增强作用与新的酶蛋白的合成有关。此外，先前肾上腺切除取消了乙醇对肝脏ODC活性的刺激，这表明诱导的增加可能是通过刺激肾上腺激素来调节的。这些研究表明，口服单剂量乙醇可以显著提高大鼠肝脏ODC的活性，ODC是多胺生物合成的关键酶，这种影响是通过肾上腺激素间接实现的。
The effect of a single feeding of ethanol on hepatic ornithine decarboxylase (ODC) activity in rats was investigated. Ethanol (7.5 g/kg body weight) was tube‐fed to overnight‐fasted rats as a 50% (v/v) solution in water 1, 2, 3, 4, 8, 12, or 24 hr before sacrifice. The levels of ODC activity in the livers were assayed in vitro by measuring the release of14C02from 0L‐1‐14C‐ornithine. Hepatic ODC activities were significantly stimulated by ethanol (7.5 g/kg body weight) beginning at 1 hr and reaching a peak at 4 hr (more than a 16‐fold increase over zero time controls). Single feedings of varying doses of ethanol (2.5, 5.0, or 7.5 g/kg body weight) to overnight‐fasted rats 3 hr before sacrifice also exhibited significant increases (3 to 13‐fold) in the hepatic ODC activities. In vitro14C‐leucir>e incorporation into protein using hepatic microsomes of ethanol‐treated rats was decreased in comparison with that of controls. The ethanoMnduced stimulation of hepatic ODC activity was not abolished by pretreatment with pyrazoie, an inhibitor of ethanol metabolism. However, the stimulation of hepatic ODC activity by ethanol was suppressed by actinomycin D or cycloheximide, indicating that the enhancement is attributable to the synthesis of new enzyme protein. Furthermore, abolition of the stimulation of hepatic ODC activity due to ethanol by prior adrenalectomy suggests that the induced increase is probably mediated through stimulation of adrenal hormones. These studies demonstrate that a single dose of ethanol per os can significantly enhance in the rat the activity of hepatic ODC, a key enzyyme in the biosynthesis of polyamines, and that the effect is indirect, via adrenal hormones.