Tsuchiya T, Yamaha T
J Toxicol Sci. 1983 Aug;8(3):213-22. doi: 10.2131/jts.8.213.
The urine of the mice fed on a 15% sorbic acid diet was treated with or without beta-glucuronidase and was fractionated by XAD-2 column chromatography. The non-polar urine fraction was slightly mutagenic towards TA 98 when metabolically activated, but not towards TA 100. From the comparison of thin-layer chromatograms between the intestinal and urinary samples, it was suggested that a part of the mutagens produced in the intestine was excreted in the urine. As for the lipid peroxidation, the levels of lipid peroxide in the liver of the mice fed on a 15% sorbic acid diet were lower than those in the control over the feeding period of 15 months. Moreover, there was a correlation between the concentration of sorbic acid (X) in the diet and the lipid peroxide level (Y) in mice fed on potassium sorbate diets, obeying the linear equation, Y=-8.39X+ 341 (p less than 0.01). However, the lipid peroxide levels of 15% sorbic acid group did not fit with the above equation, and was higher than those of 20.1% potassium sorbate group, which was equivalent to 15% sorbic acid group in respect of sorbic acid concentration. Accordingly, the difference of lipid peroxide levels between the two groups (15% sorbic acid and 20.1% potassium sorbate group) might reflect productive difference of the mutagens.
给喂食15%山梨酸饮食的小鼠尿液，分别在添加或不添加β-葡萄糖醛酸酶的情况下进行处理，然后通过XAD - 2柱色谱法进行分离。非极性尿液组分在代谢活化时对TA 98有轻微致突变性，但对TA 100没有。通过比较肠道和尿液样本的薄层色谱图，表明肠道中产生的部分诱变剂会随尿液排出。至于脂质过氧化，在15个月的喂养期内，喂食15%山梨酸饮食的小鼠肝脏中的脂质过氧化物水平低于对照组。此外，在喂食山梨酸钾饮食的小鼠中，饮食中山梨酸浓度（X）与脂质过氧化物水平（Y）之间存在相关性，符合线性方程Y = -8.39X + 341（p小于0.01）。然而，15%山梨酸组的脂质过氧化物水平不符合上述方程，且高于20.1%山梨酸钾组，后者在山梨酸浓度方面与15%山梨酸组相当。因此，两组（15%山梨酸组和20.1%山梨酸钾组）之间脂质过氧化物水平的差异可能反映了诱变剂产生的差异。
