Zhang Z, Wang X, Zhou J, Gao S, Jin X
Laboratory of Molecular Toxicology, School of Public Health, Nanjing Medical University, Nanjing 210029, China.
Wei Sheng Yan Jiu. 1999 Jul;28(4):194-5.
The activity of Ca(2+)-ATPase and phosphorylase A(P-A) of liver in rats was determined to study the effect of acrylonitrile (ACN) on calcium homeostasis and to clarify the toxicological mechanism of ACN. Adult male Sprague-Dawley rats were administered ACN daily per os for 42 days, at the dosage of 0, 10, 30 and 50 mg.kg-1. The activities of Ca(2+)-ATPase and phosphorylase A was determined at 14, 28, 42 days after ACN administration. The results indicated that ACN could significantly inhibit the activity of Ca(2+)-ATPase and increase the activity of P-A (P < 0.01), especially in the high dose group and exposed for 42 days, and there was significantly dose- and time-respond relationship (P < 0.01). ACN contamination could result in the disharmony of calcium homeostasis of liver in rats.
测定大鼠肝脏中Ca(2+)-ATP酶和磷酸化酶A（P-A）的活性，以研究丙烯腈（ACN）对钙稳态的影响，并阐明ACN的毒理学机制。将成年雄性Sprague-Dawley大鼠每日经口给予ACN，持续42天，剂量分别为0、10、30和50 mg·kg-1。在给予ACN后的第14、28、42天测定Ca(2+)-ATP酶和磷酸化酶A的活性。结果表明，ACN可显著抑制Ca(2+)-ATP酶的活性并增加P-A的活性（P < 0.01），尤其是在高剂量组且暴露42天时，并且存在显著的剂量-时间反应关系（P < 0.01）。ACN污染可导致大鼠肝脏钙稳态失调。
