Bâ A, Seri B V, Han S H
Département de Biologie et Physiologie Animale, Faculté des Sciences et Techniques, Université Nationale, Abidjan, Côte d'Ivoire.
Alcohol Alcohol. 1996 Jan;31(1):27-40. doi: 10.1093/oxfordjournals.alcalc.a008113.
A number of mechanisms may be involved in the pathogenesis of thiamine deficiency in the alcoholic. Among these mechanisms are inadequate dietary intake of thiamine, impaired intestinal transport of the vitamin and decreased conversion of thiamine to the active coenzyme. The present study was undertaken to further investigate the mechanism by which alcohol can interfere with thiamine deficiency in the brain. Thus, the neurobehavioural development of rat pups (E) nursed by 12% ethanol/water-drinking mothers, or pups (E-T) nursed by mothers drinking 12% ethanol/water + thiamine hydrochloride mixture, was monitored from the 1st to 45th postnatal days. Appropriate pair-fed saccharose (S) and ad libitum controls (C) were assessed. Histological studies were performed at the age of 45 days on the hippocampal CA3 pyramidal neurons of the offspring from each treatment. Exposing rat pups to ethanol during pregnancy and lactation showed a significant impairment of neurobehavioural development, more cornered pyramidal cells in the hippocampal field CA3, reduced cell number and cell size. The results point out long-lasting effects of maternal alcohol exposure in the offspring. Both functional and structural studies showed that neurotoxic effects of developmental alcohol exposure were not reversed by thiamine administration. However, adverse effects of undernutrition following developmental alcohol exposure were suppressed by thiamine administration. From this work, we suggest that inadequate dietary intake of thiamine and impaired intestinal transport of the vitamin are not critical mechanisms leading to thiamine deficiency in chronic alcoholism. The most prevalent mechanism contributing to ethanol-induced thiamine deficiency in chronic alcoholics would be the alteration of thiamine metabolism, and particularly the reduction of the vitamin conversion to its metabolically active form TPP (thiamine pyrophosphate).
酒精性患者硫胺素缺乏的发病机制可能涉及多种机制。这些机制包括硫胺素饮食摄入不足、维生素肠道转运受损以及硫胺素向活性辅酶的转化减少。本研究旨在进一步探讨酒精干扰大脑硫胺素缺乏的机制。因此,监测了由饮用12%乙醇/水的母鼠哺育的幼鼠(E组)以及由饮用12%乙醇/水+盐酸硫胺混合物的母鼠哺育的幼鼠(E-T组)从出生后第1天到第45天的神经行为发育情况。对适当的配对喂食蔗糖组(S组)和自由摄食对照组(C组)进行了评估。在45日龄时对各处理组后代的海马CA3锥体神经元进行了组织学研究。孕期和哺乳期将幼鼠暴露于乙醇中会导致神经行为发育显著受损,海马CA3区的锥体细胞更加扭曲,细胞数量和细胞大小减少。结果指出母体酒精暴露对后代有长期影响。功能和结构研究均表明,发育性酒精暴露的神经毒性作用不会因给予硫胺素而逆转。然而,发育性酒精暴露后营养不良的不良影响可通过给予硫胺素得到抑制。从这项研究中,我们认为硫胺素饮食摄入不足和维生素肠道转运受损并非导致慢性酒精中毒患者硫胺素缺乏的关键机制。导致慢性酒精中毒患者乙醇诱导的硫胺素缺乏的最普遍机制可能是硫胺素代谢的改变,尤其是维生素向其代谢活性形式焦磷酸硫胺素(TPP)的转化减少。