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Thiamine utilization in the pathogenesis of alcohol-induced brain damage.
Alcohol Alcohol Suppl. 1994; 2:273-9.AA

Abstract

There is increasing evidence for the role of thiamine deficiency in ethanol neurotoxicity and in development of alcoholic organic brain disorders other than Wernicke-Korsakoff syndrome [WKS] and cerebellar degeneration. Investigations in humans and in animal models have implicated a reduction in the activities of thiamine-utilizing enzymes as the metabolic basis of tissue injury due to thiamine deficiency. We have investigated the interactions of the thiamine-utilizing enzyme transketolase [Tk], derived from human fibroblasts, lymphoblasts, and various brain regions, with its cofactor, thiamine pyrophosphate [TPP], in an attempt to elucidate the molecular basis of selective brain damage in alcoholism-associated thiamine deficiency. There were no significant differences in the isoelectric pattern of Tk among the nine brain regions (white matter and grey matter) examined. However, Tk activity/mg protein, increase in Tk activity with addition of excess TPP (TPP effect), and TPP-dependent rate of formation of active Tk holoenzyme (tau) varied 2.5-, 6-, and 4-fold, respectively, among these brain regions. These differences in tissue requirements for TPP may contribute to the selective vulnerability of certain brain regions to alcoholism-associated thiamine deficiency, and may influence the pattern of clinical impairment in the individual patient.

Authors+Show Affiliations

Department of Psychiatry, Vanderbilt University School of Medicine, Nashville, TN 37240, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

Language

eng

PubMed ID

8974347

Citation

Martin, P R., et al. "Thiamine Utilization in the Pathogenesis of Alcohol-induced Brain Damage." Alcohol and Alcoholism (Oxford, Oxfordshire). Supplement, vol. 2, 1994, pp. 273-9.
Martin PR, Pekovich SR, McCool BA, et al. Thiamine utilization in the pathogenesis of alcohol-induced brain damage. Alcohol Alcohol Suppl. 1994;2:273-9.
Martin, P. R., Pekovich, S. R., McCool, B. A., Whetsell, W. O., & Singleton, C. K. (1994). Thiamine utilization in the pathogenesis of alcohol-induced brain damage. Alcohol and Alcoholism (Oxford, Oxfordshire). Supplement, 2, 273-9.
Martin PR, et al. Thiamine Utilization in the Pathogenesis of Alcohol-induced Brain Damage. Alcohol Alcohol Suppl. 1994;2:273-9. PubMed PMID: 8974347.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Thiamine utilization in the pathogenesis of alcohol-induced brain damage. AU - Martin,P R, AU - Pekovich,S R, AU - McCool,B A, AU - Whetsell,W O, AU - Singleton,C K, PY - 1994/1/1/pubmed PY - 1994/1/1/medline PY - 1994/1/1/entrez SP - 273 EP - 9 JF - Alcohol and alcoholism (Oxford, Oxfordshire). Supplement JO - Alcohol Alcohol Suppl VL - 2 N2 - There is increasing evidence for the role of thiamine deficiency in ethanol neurotoxicity and in development of alcoholic organic brain disorders other than Wernicke-Korsakoff syndrome [WKS] and cerebellar degeneration. Investigations in humans and in animal models have implicated a reduction in the activities of thiamine-utilizing enzymes as the metabolic basis of tissue injury due to thiamine deficiency. We have investigated the interactions of the thiamine-utilizing enzyme transketolase [Tk], derived from human fibroblasts, lymphoblasts, and various brain regions, with its cofactor, thiamine pyrophosphate [TPP], in an attempt to elucidate the molecular basis of selective brain damage in alcoholism-associated thiamine deficiency. There were no significant differences in the isoelectric pattern of Tk among the nine brain regions (white matter and grey matter) examined. However, Tk activity/mg protein, increase in Tk activity with addition of excess TPP (TPP effect), and TPP-dependent rate of formation of active Tk holoenzyme (tau) varied 2.5-, 6-, and 4-fold, respectively, among these brain regions. These differences in tissue requirements for TPP may contribute to the selective vulnerability of certain brain regions to alcoholism-associated thiamine deficiency, and may influence the pattern of clinical impairment in the individual patient. SN - 1358-6173 UR - https://www.unboundmedicine.com/medline/citation/8974347/Thiamine_utilization_in_the_pathogenesis_of_alcohol_induced_brain_damage_ L2 - https://medlineplus.gov/alcoholusedisorderaud.html DB - PRIME DP - Unbound Medicine ER -