Powis G, Svingen B A, Appel P
Adv Exp Med Biol. 1981;136 Pt A:349-58. doi: 10.1007/978-1-4757-0674-1_22.
Isolated hepatocytes do not liberate appreciable amounts of superoxide into the external medium. Simple quinones stimulate the release of superoxide up to 15 nmol/min/10(6) hepatocytes. Superoxide release stimulated by a variety of simple quinones and more complex antitumor quinones was maximal at a quinone one-electron reduction potential of -70 mV. This was qualitatively similar to the pattern of superoxide formation seen with NADH-cytochrome b5 reductase and NADH: ubiquinone oxidoreductase. Superoxide production by NADPH-cytochrome P-450 reductase was maximal at a quinone single-electron reduction potential at -200 mV. Phenobarbital pretreatment had no effect on superoxide formation by hepatocytes suggesting that NADPH-cytochrome P-450 reductase activity is not rate limiting for quinone stimulated superoxide formation. Sulfonated stilbenes, specific inhibitors of anion exchange, had no effect on the release of superoxide by hepatocytes suggesting that superoxide is not transported through anion channels in the plasma membrane. Pretreatment of hepatocytes with 10(-5) M diethyldithiocarbamate produced over a two fold increase in the release of superoxide.
分离的肝细胞不会向细胞外培养基中释放大量超氧化物。简单醌类可刺激超氧化物释放，释放量可达15 nmol/分钟/10⁶个肝细胞。多种简单醌类和更复杂的抗肿瘤醌类所刺激的超氧化物释放，在醌类单电子还原电位为 -70 mV时达到最大值。这在定性上与用NADH - 细胞色素b5还原酶和NADH：泛醌氧化还原酶观察到的超氧化物形成模式相似。NADPH - 细胞色素P - 450还原酶产生超氧化物的量在醌类单电子还原电位为 -200 mV时达到最大值。苯巴比妥预处理对肝细胞超氧化物的形成没有影响，这表明NADPH - 细胞色素P - 450还原酶活性不是醌类刺激超氧化物形成的限速因素。阴离子交换特异性抑制剂磺化芪对肝细胞超氧化物的释放没有影响，这表明超氧化物不是通过质膜中的阴离子通道转运的。用10⁻⁵ M二乙基二硫代氨基甲酸盐预处理肝细胞，可使超氧化物的释放增加两倍以上。
