Telolahy P, Morel G, Cluet J L, Yang H M, Thieffry N, de Ceaurriz J
Laboratory of Chemical Toxicology of the Environment, Faculty of Pharmacy, Chatenay-Malabry, France.
Toxicology. 1995 Nov 30;103(2):105-12. doi: 10.1016/0300-483x(95)03111-r.
Forty C57 BL/6J mice, injected subcutaneously with 0.5 mg/kg arsenic as sodium arsenite, were examined for 24-h urinary excretion of total arsenic metabolites, creatinine and S-adenosylmethionine (SAM) and for 24-h faecal excretion of arsenic and levels of arsenic in the blood, liver, kidneys, lung, skin, spleen and bone at 24-h post-dose. Total urinary arsenic metabolites were calculated by summing up the inorganic (Asi), monomethylated (MMA) and dimethylated (DMA) derivatives directly measured by selective arsine generation-atomic absorption spectrometry (AG-AAS) or were measured by AG-AAS following complete mineralization. Both sets of results showed interindividual differences varying by as much as 7-fold and correlated with the 24-h urinary excretion of both SAM (r = 0.84 and r = 0.86, respectively) and creatinine (r = 0.82 and r = 0.87, respectively). There was interindividual variability of about a 30-fold range in 24-h faecal excretion of arsenic which correlated inversely with 24-h urinary excretion of arsenic metabolites (r = -0.69) and 24-h urinary excretion of both creatinine (r = -0.70) and SAM (r = -0.67). Body tissue levels of arsenic were low and not related to 24-h urinary excretion of arsenic metabolites, SAM and creatinine. Taken together, the results indicate that differences in the profile of urinary arsenic excretion and in the retention of arsenic in a particular organ do not contribute to interindividual variability in 24-h urinary excretion of arsenic metabolites by C57 BL/6J mice, but that variability in faecal excretion does, at least in part. It is speculated that there is most likely a predominant contribution from a diffuse tissue retention of arsenic or from a third route of arsenic elimination, i.e. respiratory, to this phenomenon in view of the small faecal contribution.
40只C57 BL/6J小鼠皮下注射0.5mg/kg亚砷酸钠形式的砷，在给药后24小时检测其总砷代谢产物、肌酐和S-腺苷甲硫氨酸（SAM）的24小时尿排泄量，以及砷的24小时粪便排泄量和血液、肝脏、肾脏、肺、皮肤、脾脏和骨骼中的砷含量。总尿砷代谢产物通过选择性砷化氢生成-原子吸收光谱法（AG-AAS）直接测量的无机（Asi）、单甲基化（MMA）和二甲基化（DMA）衍生物的总和来计算，或者在完全矿化后通过AG-AAS测量。两组结果均显示个体间差异高达7倍，且与SAM（分别为r = 0.84和r = 0.86）和肌酐（分别为r = 0.82和r = 0.87）的24小时尿排泄量相关。砷的24小时粪便排泄量个体间差异约为30倍，与砷代谢产物的24小时尿排泄量（r = -0.69）、肌酐的24小时尿排泄量（r = -0.70）和SAM的24小时尿排泄量（r = -0.67）呈负相关。身体组织中的砷含量较低，与砷代谢产物、SAM和肌酐的24小时尿排泄量无关。综合来看，结果表明尿砷排泄谱和特定器官中砷保留的差异对C57 BL/6J小鼠砷代谢产物24小时尿排泄量的个体间差异没有贡献，但粪便排泄的差异至少部分起到了作用。鉴于粪便贡献较小，推测这种现象很可能主要是由于砷在组织中的弥散性保留或砷的第三条消除途径（即呼吸途径）所致。
