Effects of Acute Ethanol Exposure upon In Vivo Leucine Uptake and Protein Synthesis in the Fetal Rat
Effects of Acute Ethanol Exposure upon In Vivo Leucine Uptake and Protein Synthesis in the Fetal Rat
复制标题
急性乙醇暴露对胎鼠体内亮氨酸摄取和蛋白质合成的影响
作者：
S. Fisher;Mary Anne Barnicle;Becky Steis;I. Holzman;D. H.;V. Thiel
总结：将氚标记的L-亮氨酸（13 H1 L-Leu）注入孕19天的大鼠胎儿羊膜腔，在短暂的（4小时）母体血清乙醇升高期间。孕鼠腹腔注射47.5%乙醇，高剂量（0.29 ~ 0.33g/100 g体重）或低剂量（0.12 ~ 0.14g/100 g体重）。取出胎脑和肝脏，分析[3 H]l-leu的组织摄取（TU）和蛋白掺入（PI）。相对蛋白质合成（与TU的变化无关）用PI/TU × 100的比值表示。通过在母体给予乙醇24小时后向胎儿羊水囊注射[3 H] l-leu来研究母体急性乙醇暴露对胎儿的延迟影响，发现高剂量胎儿脑中TU和PI均降低。肝脏PI（而非TU）被抑制。高剂量乙醇处理导致胎脑蛋白质合成减少（PI/TU × 100），但不影响肝脏。低剂量乙醇使脑PI及肝、脑PI/TU增加× 100。[3 H]L-leu的利用率与第4小时（处死）母体血清乙醇水平有关。胎脑比肝脏受影响更显著。乙醇浓度>200 mg/dl导致脑TU（对照，1879 ± 185，乙醇，1219 ± 123 dpm/mg蛋白）和PI/TU × 100（对照，48.9 ± 3.3，乙醇，31.5 ± 2.9）降低。在水平<100时（对照，48.9 ± 3.3，乙醇，31.5 ± 2.9）。在<100 mg/dl的水平下，脑（对照组，48.9 ± 3.3 vs乙醇，67.3 ± 2.8）和肝脏（对照组，45.3 ± 4.2 vs乙醇，62.3 ± 1.7）中的PI/TU × 100均增强。[3 H]L.-的组织摄取Leu 24小时后，高剂量的母亲乙醇暴露在胎儿brain.The结果支持的假设，即母亲/胎儿的乙醇暴露，类似于发现在“社会”饮酒humans，改变正常的胎儿metabolics.Speculation：母亲慢性乙醇滥用是有害的人类胎儿，但胎儿的风险急性或“社会”乙醇消费是不确定的。在急性母体乙醇给药期间和给药后24小时，观察到大鼠胎儿对亮氨酸的利用率发生变化，表明即使是短暂的乙醇暴露也可能对胎儿有害。这种接触对胎儿和新生儿生长发育的长期影响仍有待确定。
Summary: Tritiated L-leucine (l3HlL-leu) was injected into the amniotic saes of 19-day gestation rat fetuses during a brief (4-hr) period of elevation in maternal serum ethanol. The pregnant rats received 47.5% ethanol at “high dose” (0.29 to 0.33g/100g body weight) or “low dose” (0.12 to 0.14 g/100gm body weight) by intraperitoneal injection. Fetal brain and liver were removed and analyzed for tissue uptake (TU) and protein incorporation (PI) of [3H]l-leu. Relative protein synthesis, independent of alterations in TU, was expressed by the ratio Pl/TU × 100. Delayed fetal effects of acute maternal ethanol exposure were studied by injecting the fetal amniotic sacs with [3H]l-leu 24 hr after maternal ethanol administration.Both TU and PI were decreased in bigh dose fetal brain. Liver PI, but not TU, was depressed. High dose ethanol treatment caused a reduction in protein synthesis (PI/TU × 100) in fetal brain, but not liver. Low dose ethanol enhanced brain PI and both liver and brain PI/TU × 100. Utilization of [3H]L-leu was related to fourth-hour (sacrifice) maternal serum ethanol levels. Fetal brain was more strikingly affected than liver. Ethanol concentrations >200 mg/dl caused a decrease in brain TU (control, 1879 ± 185 versus ethanol, 1219 ± 123 dpm/mg protein) and PI/TU × 100 (control, 48.9 ± 3.3 versus ethanol, 31.5 ± 2.9). At levels <100 (control, 48.9 ± 3.3 versus ethanol, 31.5 ± 2.9). At levels <100 mg/dl, PI/TU × 100 was enhanced in both brain (control, 48.9 ± 3.3 versus ethanol, 67.3 ± 2.8) and liver (control, 45.3 ± 4.2 versus ethanol, 62.3 ± 1.7). Tissue uptake of [3H]L.-leu 24 hr after high dose maternal ethanol exposure was increased in fetal brain.The results support the hypothesis that a brief period of maternal/fetal ethanol exposure, similar to that found in “social” drinking humans, alters normal fetal metabolism.Speculation: Chronic maternal ethanol abuse is harmful to the human fetus, but the fetal risks of acute or “social” ethanol consumption are undefined. The observation of altered rat fetal utilization of leucine both during and 24 hr after acute maternal ethanol administration suggests that even a brief period of ethanol exposure is potentially harmful to the fetus. The long-term effects of such exposure upon fetal and neonatal growth and development remain to be determined.