McConnell W R, Kari P, Hill D L
Cancer Chemother Pharmacol. 1979;2(3):221-3. doi: 10.1007/BF00258299.
N-methyl-N-nitrosourea (MNU), N-(2-chloroethyl)-N'-(trans-4-methylcyclohexyl)-N-nitrosourea (methylCCNU), and N,N'-bis(2-chloroethyl)-N-nitrosourea (BCNU) were examined for their effect on glutathione (GSH) levels of various tissues of normal and L1210-leukemic mice. BCNU produced significant decreases in the GSH levels of livers of both groups, but caused no change in the GSH content of the L1210 tumor or in the lungs. The GSH content of the kidneys of L1210 tumor-bearing mice, however, was significantly decreased by BCNU at early time points. A small increase in the liver content of oxidized glutathione could not account for the decrease content of GSH. Methyl CCNU and MNU were without effect on any of the tissues examined. These data are consistent with our previous observation that BCNU is a substrate for GSH S-transferase, and suggest that a GSH-dependent process is an important pathway for the metabolism of BCNU.
研究了N-甲基-N-亚硝基脲（MNU）、N-（2-氯乙基）-N'-（反式-4-甲基环己基）-N-亚硝基脲（甲基环己亚硝脲）和N，N'-双（2-氯乙基）-N-亚硝基脲（卡莫司汀）对正常小鼠和L1210白血病小鼠各种组织中谷胱甘肽（GSH）水平的影响。卡莫司汀使两组小鼠肝脏中的GSH水平显著降低，但对L1210肿瘤或肺中的GSH含量没有影响。然而，在早期时间点，卡莫司汀使携带L1210肿瘤小鼠肾脏中的GSH含量显著降低。肝脏中氧化型谷胱甘肽含量的小幅增加并不能解释GSH含量的降低。甲基环己亚硝脲和MNU对所检测的任何组织均无影响。这些数据与我们之前的观察结果一致，即卡莫司汀是谷胱甘肽S-转移酶的底物，并表明依赖GSH的过程是卡莫司汀代谢的重要途径。
