The main purpose of this study was to evaluate changes in brain sulfur-containing amino acid (SCAA) metabolism to determine whether taurine intervened under continuous alcohol intake. We fed 80 male Sprague-Dawley rats 30% alcohol-containing water for 4 weeks. Eighty animals were divided into two groups (with or without 2 g/kg body weight taurine supplementation), and five were killed every week in each group for monitoring SCAA changes in the brain, liver, kidneys and heart. Results indicated that the plasma alcohol concentration increased from Weeks 1-4; however, animals with taurine supplementation showed a lower plasma concentration of ethanol in Week 2. As to SCAA concentrations, cysteine and taurine were both lower after a week of alcohol ingestion in the brain and plasma; the same declining trend was shown in the liver in Week 2. In contrast, plasma and hepatic concentrations of homocysteine were elevated in Week 2, and the plasma S-adenosylmethionine (SAM)/S-adenosylhomocysteine (SAH) ratio also decreased in Week 1. Furthermore, the key cofactor of transsulfuration, pyridoxal-5′-phosphate, significantly declined in the plasma after a week of the ethanol intervention, whereas an increase was observed in brain tissue. Under taurine supplementation, some recoveries were shown by delaying taurine depletion to Week 2, increasing the SAM/SAH ratio and elevating plasma and brain levels of vitamin B6 in Week 2. In conclusion, daily consumption of 30% alcohol interfered with SCAA metabolism, thus decreasing taurine's role in neurotransmission. The possible mechanism involved might be that ethanol interrupts the production of cysteine, which is the upstream SCAA of taurine, thus decreasing the homocysteine level. Additionally, taurine supplementation delayed this process.
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