Yoshizawa T, Swanson S P, Mirocha C J
Appl Environ Microbiol. 1980 Nov;40(5):901-6. doi: 10.1128/aem.40.5.901-906.1980.
T-2 toxin was rapidly converted in the 9,000 X g supernatant fraction of rat liver homogenate into HT-2 toxin, T-2 tetraol, and two unknown metabolites designated as TMR-1 and TMR-2. TMR-1 was characterized as 4-deacetylneosolaniol (15-acetoxy-3 alpha, 4 beta, 8 alpha-trihydroxy-12,13-epoxytrichothec-9-ene) by spectroscopic analyses. Since the same metabolites were also obtained from HT-2 toxin used as substrate, it was concluded that T-2 toxin was hydrolyzed preferentially at the C-4 position to give HT-2 toxin, which was then metabolized to T-2 tetraol via 4-deacetylneosolaniol. In addition to HT-2 toxin, 4-deacetylneosolaniol and T-2 tetraol, a trace amount of neosolaniol was transformed from T-2 toxin by rat intestinal strips. In vitro metabolic pathways for T-2 toxin in rats are proposed.
T-2毒素在大鼠肝脏匀浆9000×g的上清液组分中迅速转化为HT-2毒素、T-2四醇以及两种未知代谢产物,分别命名为TMR-1和TMR-2。通过光谱分析,TMR-1被鉴定为4-脱乙酰新茄病醇(15-乙酰氧基-3α,4β,8α-三羟基-12,13-环氧单端孢霉烯-9-烯)。由于以HT-2毒素作为底物时也能得到相同的代谢产物,因此得出结论:T-2毒素优先在C-4位水解生成HT-2毒素,然后HT-2毒素通过4-脱乙酰新茄病醇代谢为T-2四醇。除了HT-2毒素、4-脱乙酰新茄病醇和T-2四醇外,大鼠肠段可将微量的新茄病醇从T-2毒素转化而来。本文提出了大鼠体内T-2毒素的体外代谢途径。