Thornalley P J, Strath M, Wilson R J
Department of Chemistry and Biological Chemistry, University of Essex, Colchester, U.K.
Biochem Pharmacol. 1994 Jan 20;47(2):418-20. doi: 10.1016/0006-2952(94)90035-3.
S-p-Bromobenzylglutathione diethyl ester induced toxicity in the malarial parasite Plasmodium falciparum in infected human red blood cells in culture. The median inhibitory concentration, IC50, was 4.77 +/- 0.12 microM (N = 10) for incorporation of [3H]hypoxanthine in nucleotide synthesis and 5.20 +/- 0.1 microM (N = 10) for incorporation of [14C]isoleucine into protein. The prospective mechanism of action is inhibition of glyoxalase I by the de-esterified metabolite, S-p-bromobenzylglutathione, and accumulation of the cytotoxic substrate methylglyoxal.
S-对溴苄基谷胱甘肽二乙酯在体外培养的受疟原虫恶性疟原虫感染的人类红细胞中诱导毒性。[3H]次黄嘌呤掺入核苷酸合成的半数抑制浓度(IC50)为4.77±0.12微摩尔(N = 10),[14C]异亮氨酸掺入蛋白质的IC50为5.20±0.1微摩尔(N = 10)。预期的作用机制是去酯化代谢产物S-对溴苄基谷胱甘肽对乙二醛酶I的抑制作用以及细胞毒性底物甲基乙二醛的积累。