Petri W A, Poirier L A
Chem Biol Interact. 1977 Apr;17(1):1-7. doi: 10.1016/0009-2797(77)90066-7.
Acute doses of the hepatotoxic agents diethylnitrosamine (DEN) and alpha-naphthylisothiocyanate (ANIT) to young adult male rats led to the production of a folate deficiency as determined by an elevated urinary excretion of formiminoglutamic acid (FIGLU) 2 to 4 days following administration of the compounds. High dietary levels of methionine significantly reduced the elevated levels of FIGLU produced by the 2 chemicals. Dietary folate had no significant effect on the excretion of urinary FIGLU. Although the hepatic levels of S-adenosylmethionine (SAM) were significantly increased in rats fed the high dietary levels of methionine, an acute dose of DEN did not depress the hepatic levels of SAM. The results indicate that the methyl-reversible folate deficiency caused by hepatotoxic agents is not the direct consequence of altered hepatic levels of SAM.
给成年雄性幼鼠急性剂量的肝毒性药物二乙基亚硝胺(DEN)和α-萘基异硫氰酸盐(ANIT),会导致产生叶酸缺乏,这是通过在给予这些化合物后2至4天,尿中亚胺基谷氨酸(FIGLU)排泄量升高来确定的。高膳食水平的蛋氨酸显著降低了这两种化学物质所产生的FIGLU升高水平。膳食叶酸对尿中FIGLU的排泄没有显著影响。尽管在喂食高膳食水平蛋氨酸的大鼠中,肝脏S-腺苷甲硫氨酸(SAM)水平显著升高,但急性剂量的DEN并没有降低肝脏SAM水平。结果表明,肝毒性药物引起的甲基可逆性叶酸缺乏不是肝脏SAM水平改变的直接后果。