Srinivas L, Rao P B
Int J Vitam Nutr Res. 1976;46(1):3-10.
Urinary arylsulphatases (E.C.3.1.6.1) A and B were increased in male rats fasted for 24 hours. Excretion of non dialysable protein nitrogen decreased whereas creatinine excretion increased. On refeeding diet arylsulphatase A activity was restored to normal whereas arylsulphatase B was not normalised. A single oral supplementation of vitamin A acetate (20 000 IU) to rats fasted for 24 hours resulted in a significant reduction of both arylsulphatase A and B eventhough no further reduction of protein nitrogen excretion was evident. In vitamin A deficient male rats significant reduction in urinary excretion of both arylsulphatases A and B occured. In a smaller number of female rats depression of only arylsulphatase A was observed. This effect of vitamin A deficiency leading to reduced urinary arylsulphatase activity was evident even at the "weight plateau" stage when no reduction in food intake or growth had occurred. These results suggest a possible direct or indirect role for vitamin A on urinary excretion pattern of arylsulphatases presumably released from lysosomes of tissues.
禁食24小时的雄性大鼠尿中芳基硫酸酯酶(E.C.3.1.6.1)A和B的含量增加。非透析性蛋白氮的排泄减少,而肌酐排泄增加。重新喂食后,芳基硫酸酯酶A的活性恢复正常,而芳基硫酸酯酶B未恢复正常。对禁食24小时的大鼠单次口服补充维生素A醋酸酯(20000国际单位),即使蛋白氮排泄没有进一步减少,芳基硫酸酯酶A和B的含量也显著降低。在维生素A缺乏的雄性大鼠中,尿中芳基硫酸酯酶A和B的排泄量显著减少。在数量较少的雌性大鼠中,仅观察到芳基硫酸酯酶A降低。即使在“体重平稳期”,即食物摄入量和生长均未减少的阶段,维生素A缺乏导致尿中芳基硫酸酯酶活性降低的这种效应也很明显。这些结果表明,维生素A可能对组织溶酶体释放的芳基硫酸酯酶的尿排泄模式具有直接或间接作用。