Lai J C, Barrow H N
Comp Biochem Physiol C Comp Pharmacol Toxicol. 1984;78(1):81-7. doi: 10.1016/0742-8413(84)90051-3.
Hg2+ (10-20 microM), at concentrations comparable to mercury levels reportedly occurring in mercury neurotoxicity (Minamata disease), effectively inhibited both cytosolic (IC50 for Hg2+ = 4.1 microM) and mitochondrial (IC50 for Hg2+ = 1.4 microM) rat brain hexokinases. Kidney (IC50 for Hg2+ approximately equal to 3 microM) and spleen hexokinases were less susceptible to inhibition by Hg2+. IC50 values for Hg2+ in inhibiting cytosolic and mitochondrial spleen hexokinases were 8.9 and 3.1 microM, respectively. In both brain and spleen, mitochondrial hexokinases were more susceptible to inhibition by Hg2+ than cytosolic forms, suggesting that the microenvironment of the mitochondrial membranes may exert some modulatory effects on the properties of hexokinases. These results also suggest that inhibition of glucose utilization may be an important mechanism of tissue damage in mercury poisoning.
据报道，汞神经毒性（水俣病）中汞的浓度与10-20微摩尔Hg2+相当，该浓度能有效抑制大鼠脑胞质（Hg2+的IC50 = 4.1微摩尔）和线粒体（Hg2+的IC50 = 1.4微摩尔）己糖激酶。肾脏（Hg2+的IC50约等于3微摩尔）和脾脏己糖激酶对Hg2+抑制作用的敏感性较低。Hg2+抑制胞质和线粒体脾脏己糖激酶的IC50值分别为8.9和3.1微摩尔。在脑和脾脏中，线粒体己糖激酶比胞质形式的己糖激酶对Hg2+抑制作用更敏感，这表明线粒体膜的微环境可能对己糖激酶的性质发挥一些调节作用。这些结果还表明，抑制葡萄糖利用可能是汞中毒时组织损伤的重要机制。
