Beije B, Arrhenius E
Chem Biol Interact. 1978 Jun;21(2-3):167-77. doi: 10.1016/0009-2797(78)90017-0.
Two rat strains, Wistar, strain R and Sprague--Dawley, were subjected to cystein deficiency and methyl mercury pretreatment, both separately and in combination, after which the hepatic microsomal N- and C-oxygenation of N,N-dimethylaniline (DMA) was studied. Cystein deficiency caused a reduction in C-oxygenation in strain R microsomes, and this reduction was nearly doubled by methyl mercury pretreatment of the depleted rats. Methyl mercury pretreatment per se of strain R rats on the standard diet gave no effect. By contrast microsomes from cystein deficient SpD rats showed no statistically significant decrease in C-oxygenation, and cystein deficiency did not further enhance the inhibitory effect obtained with methyl mercury pretreatment alone. N-oxygenation was not significantly affected by any treatment of the two strains.
选用两种大鼠品系,即Wistar品系R和Sprague-Dawley品系,分别单独以及联合进行半胱氨酸缺乏和甲基汞预处理,之后研究了N,N-二甲基苯胺(DMA)在肝脏微粒体中的N-氧化和C-氧化。半胱氨酸缺乏导致品系R微粒体中C-氧化减少,而对缺乏半胱氨酸的大鼠进行甲基汞预处理后,这种减少几乎增加了一倍。给标准饮食的品系R大鼠单独进行甲基汞预处理没有效果。相比之下,半胱氨酸缺乏的SpD大鼠的微粒体中C-氧化没有统计学上的显著降低,并且半胱氨酸缺乏并没有进一步增强单独甲基汞预处理所产生的抑制作用。两种品系的任何处理对N-氧化均无显著影响。