Effects of β-alanine administration on selected parameters of oxidative stress and phosphoryltransfer network in cerebral cortex and cerebellum of rats

beta-Alanine is a beta-amino acid derivative of the degradation of pyrimidine uracil and precursor of the oxidative substrate acetyl-coenzyme A (acetyl-CoA). The accumulation of beta-alanine occurs in beta-alaninemia, an inborn error of metabolism. Patients with beta-alaninemia may develop neurological abnormalities whose mechanisms are far from being understood. In this study we evaluated the effects of beta-alanine administration on some parameters of oxidative stress and on creatine kinase, pyruvate kinase, and adenylate kinase in cerebral cortex and cerebellum of 21-day-old rats. The animals received three peritoneal injections of beta-alanine (0.3 mg /g of body weight) and the controls received the same volume (10 mu L/g of body weight) of saline solution (NaCl 0.85 %) at 3 h intervals. CSF levels of beta-alanine increased five times, achieving 80 mu M in the rats receiving the amino acid. The results of beta-alanine administration in the parameters of oxidative stress were similar in both tissues studied: reduction of superoxide dismutase activity, increased oxidation of 2',7'-dihydrodichlorofluorescein, total content of sulfhydryl and catalase activity. However, the results of the phosphoryltransfer network enzymes were similar in all enzymes, but different in the tissues studied: the beta-alanine administration was able to inhibit the enzyme pyruvate kinase, cytosolic creatine kinase, and adenylate kinase activities in cerebral cortex, and increase in cerebellum. In case this also occurs in the patients, these results suggest that oxidative stress and alteration of the phosphoryltransfer network may be involved in the pathophysiology of beta-alaninemia. Moreover, the ingestion of beta-alanine to improve muscular performance deserves more attention in respect to possible side-effects.