Abstract
The effects of ethanol and thiamin deficiency on the central nervous system was studied by applying a Lieber-DeCarli liquid diet. For a subacute experiment, Wistar male rats were divided into four groups: 1) fed on a control diet, 2) on an ethanol-containing diet, 3) on a thiamin deficient diet and 4) on a thiamin deficient and ethanol-containing diet. They were fed for 35 days. The former 3 groups were pair-fed with the forth one. For a chronic experiment, group 4 was supplemented with a minimal amount of thiamin and was fed for 75 days (group 5). Another group, fed on ethanol-containing diet, was fed ad lib for 135 days (group 6). Thiamin contents and transketolase activities (TKA) of the brain and liver, and blood alcohol levels were determined. Histopathological studies were performed on the vestibular nucleus, cerebellum and striatum with a light-and electron microscopies. Thiamin contents of liver and brain were not affected significantly by ethanol, group 3 being the lowest. Liver TKA was the lowest in group 4, although group 3 had the highest thiamin pyrophosphate effect. Histological studies disclosed a bilateral diapedesis and status spongiosus of the neuropile in the vestibular nucleus of group 3. Quite similar lesions were also seen in the cerebellum and striatum of group 4, 5 and 6. Degenerative changes in Purkinje cells and Bergmann glia were remarkable in group 4 and 5. Glial cell changes in the striatum were remarkable in group 6. From the above results, it was assumed that there was no obvious correlation between tissue thiamin levels and the susceptibility of certain parts of the neuraxis to the thiamin deprevation. The vestibular nucleus seemed to be an area highly sensitive to thiamin deficiency. Cerebellar lesions could be caused merely by a chronic ethanol administration, which is accelerated by thiamin deficiency. It is quite possible that the striatal lesions are the metabolic disorders resulting from ethanol or the metabolic products of ethanol oxidation.
