Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Science 9 June 1972:
Vol. 176. no. 4039, pp. 1133 - 1135
DOI: 10.1126/science.176.4039.1133

Articles

Ethanol Oxidation: Effect on the Redox State of Brain in Mouse

A. K. Rawat 1 and K. Kuriyama 2

1 division of Biochemistry and uropharmacology, Department of pychiatry, Downstate Medical Center, state University of New York, woklyn 11203
2 Department of Pharmacology, oto Prefectural University of medicine, Kawarmachi-Hirokoji, mikyo-Ku, Kyoto, Japan

Administration of a single large dose of ethanol to mice results in increases, for concentrations in the brain, of ratios of lactate to pyruvate, of aglycerophosphate to dihydroxyacetone phosphate, of malate to oxaloacetate, and of glutamate to the product of agr-ketoglutarate and ammonium ion. These changes are noticed as early as 5 minutes after the single dose is given. Ethanol administration for 30 days also produces these changes in metabolite concentrations in the brain. However, in contrast to the single alcohol dose, long-term alcohol administration results in a marked decrease in the concentration of adenosine triphosphate in brain and increases in those of adenosine diphosphate and adenosine monophosphate. Pyrazole, an inhibitor of alcohol dehydrogenase, prevents the effects of ethanol on the concentration of brain metabolites. These results may provide new insight into the biochemical and pharmacological effects of alcohol on brain metabolism and the importance of alcohol dehydrogenase activity in the brain.





To Advertise     Find Products


Science. ISSN 0036-8075 (print), 1095-9203 (online)