Malondialdehyde is a typical product of biomolecule oxidation, and it is also a major product of lipid peroxidation reactions. Tissue deterioration and aging have long been associated with the accumulation of such a compound which induces protein and DNA damage. Taurine (2-aminoethanesulfonic acid) is also involved in a number of crucial physiological processes, and GABA (γ-aminobutyric acid) is a important inhibitory neurotransmitter in nervous system, both of them are two important non-protein amino acids. The purpose of this study is to determine if taurine or GABA can trap MDA directly and thereby prevent advanced lipoxidation end products (ALEs) formation. Direct reaction between MDA and taurine or GABA was researched by using different analytical methods, such as high performance liquid chromatography (HPLC), liquid chromatography/mass spectrometry (LC/MS). The results indicated that taurine or GABA reacted readily with MDA at supraphysiological conditions to form different products. Two nonfluorescent enamines with an absorption peak at 274～278 nm were obtained, and two lipofuscin-like fluorescent (Ex. 392～395 nm/Em. 456～364 nm) 1,4-dihydropyridine products were derived from reaction of equimolar of taurine＋MDA or GABA＋MDA using HPLC separation within 48 h. The reaction of taurine or GABA with MDA suggested a novel scavenging reactive carbonyl function of taurine or GABA in pathophysiological situations related to carbonyl stress related diseases.

Key words: taurine, GABA (γ-aminobutyric acid), malondialdehyde (MDA), carbonyl toxification, mechanism