Hsieh K P, Yu S, Wei Y H, Chen C F, Wei R D
Toxicon. 1986;24(2):153-60. doi: 10.1016/0041-0101(86)90117-0.
The effects of PR toxin, a mycotoxin from Penicillium roqueforti, on the mitochondrial HCO3- -ATPase activity of the brain, heart and kidney from male Sprague-Dawley rats were determined by measuring colorimetrically the inorganic phosphate liberated by the ATPase in the presence or absence of bicarbonate ion. The IC50 (the concentration at which 50% of the enzyme activity is inhibited) of PR toxin on the mitochondrial HCO3- -ATPase from brain, heart and kidney were 12.7, 9.2 and 14.8 microM, respectively. The Michaelis-Menten constants (Km) of the enzyme from brain (1.1 mM), heart (1.5 mM) and kidney (2.3 mM) were not changed by PR toxin. Neither neutral nor anionic detergent increased the inhibitory potency of the toxin. It was concluded that of the three tissues tested, HCO3- -ATPase of the heart mitochondria was most sensitive to PR toxin, and that the toxin inhibited the HCO3- -ATPase in a non-competitive and irreversible manner.
通过比色法测量在有无碳酸氢根离子存在的情况下，ATP酶释放的无机磷酸盐，来确定来自罗克福青霉的霉菌毒素PR毒素对雄性斯普拉格-道利大鼠脑、心脏和肾脏线粒体HCO3--ATP酶活性的影响。PR毒素对脑、心脏和肾脏线粒体HCO3--ATP酶的IC50（抑制50%酶活性的浓度）分别为12.7、9.2和14.8微摩尔。来自脑（1.1毫摩尔）、心脏（1.5毫摩尔）和肾脏（2.3毫摩尔）的该酶的米氏常数（Km）不受PR毒素影响。中性和阴离子去污剂均未提高毒素的抑制效力。得出的结论是，在所测试的三种组织中，心脏线粒体的HCO3--ATP酶对PR毒素最敏感，并且该毒素以非竞争性和不可逆的方式抑制HCO3--ATP酶。
