Literature DB >> 8672172

Thiamine administration during chronic alcohol intake in pregnant and lactating rats: effects on the offspring neurobehavioural development.

A Bâ1, B V Seri, S H Han.   

Abstract

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).

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Year:  1996        PMID: 8672172     DOI: 10.1093/oxfordjournals.alcalc.a008113

Source DB:  PubMed          Journal:  Alcohol Alcohol        ISSN: 0735-0414            Impact factor:   2.826


  6 in total

1.  Choline supplementation and DNA methylation in the hippocampus and prefrontal cortex of rats exposed to alcohol during development.

Authors:  Nicha K H Otero; Jennifer D Thomas; Christopher A Saski; Xiaoxia Xia; Sandra J Kelly
Journal:  Alcohol Clin Exp Res       Date:  2012-04-17       Impact factor: 3.455

Review 2.  Metabolic and structural role of thiamine in nervous tissues.

Authors:  Abdoulaye Bâ
Journal:  Cell Mol Neurobiol       Date:  2008-07-19       Impact factor: 5.046

3.  A Pivotal Role for Thiamine Deficiency in the Expression of Neuroinflammation Markers in Models of Alcohol-Related Brain Damage.

Authors:  Polliana Toledo Nunes; Lindsey C Vedder; Terrence Deak; Lisa M Savage
Journal:  Alcohol Clin Exp Res       Date:  2019-01-20       Impact factor: 3.455

4.  Prenatal Ethanol Exposure Leads to Attention Deficits in Both Male and Female Rats.

Authors:  Ruixiang Wang; Connor D Martin; Anna L Lei; Kathryn A Hausknecht; Keita Ishiwari; Jerry B Richards; Samir Haj-Dahmane; Roh-Yu Shen
Journal:  Front Neurosci       Date:  2020-01-24       Impact factor: 4.677

5.  Disinhibition-Like Behavior Correlates with Frontal Cortex Damage in an Animal Model of Chronic Alcohol Consumption and Thiamine Deficiency.

Authors:  Marta Moya; Leticia López-Valencia; Borja García-Bueno; Laura Orio
Journal:  Biomedicines       Date:  2022-01-25

Review 6.  Effects of nutrition and gestational alcohol consumption on fetal growth and development.

Authors:  Vishal D Naik; Jehoon Lee; Guoyao Wu; Shannon Washburn; Jayanth Ramadoss
Journal:  Nutr Rev       Date:  2022-05-09       Impact factor: 6.846

  6 in total

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