The effect of taurine depletion by beta-alanine treatment on the susceptibility to ethanol-induced hepatic dysfunction in rats

Alcohol was administered chronically to female Sprague-Dawley rats in a nut ritionally adequate totally liquid diet for 28 days. This resulted in signi ficant hepatic steatosis and lipid peroxidation. beta -Alanine, when co-adm inistered with alcohol, seemed to increase hepatic steatosis, as assessed h istologically, but decreased triglyceride levels as measured biochemically. In addition, beta -alanine and especially alcohol co-administered with p-a lanine, significantly increased homocysteine and cysteine excretion into ur ine throughout the 28-day period of ethanol administration. Serum homocyste ine levels were significantly higher in alcohol- and alcohol plus beta -ala nine-treated animals compared to pair-fed control animals. Alcohol did not affect the urinary excretion of taurine, except after 21 days, when levels were reduced. Levels of liver taurine were markedly depleted in animals rec eiving alcohol and particularly alcohol plus beta -alanine, compared to pai r-fed controls. Liver and serum taurine levels were also markedly depleted in animals receiving beta -alanine and alcohol plus beta -alanine, compared to non-beta -alanine-treated animals. There was evidence of slight cholest asis in animals treated with alcohol and more so with alcohol plus beta -al anine, as indicated by raised serum alkaline phosphatase and bile acids. Th ese in vivo findings demonstrate for the first time that animals treated wi th beta -alanine may be more susceptible to ethanol-induced hepatic dysfunc tion, possibly as a result of taurine depletion.