Imlay J, Fridovich I
Department of Biochemistry, Duke University Medical Center, Durham, North Carolina 27710.
Arch Biochem Biophys. 1992 Jul;296(1):337-46. doi: 10.1016/0003-9861(92)90581-g.
The ability of naphthoquinones to generate reactive oxygen species has been widely exploited in studies of oxidative stress. However, excess superoxide dismutase and catalase failed to protect Escherichia coli in rich medium against growth inhibition by plumbagin, indicating that its toxic effect was not due to the production of partially reduced oxygen species. Respiration failed immediately upon the addition of growth-inhibitory levels of plumbagin. Studies in vitro showed that plumbagin and other redox-active quinones intercept electrons from NADH dehydrogenase, the primary respiratory dehydrogenase in glucose-containing media. An excess of oxidative substrate, such as plumbagin, inactivates this enzyme, which appears to be redox-regulated. The resultant respiratory arrest is a cautionary example of metabolic dysfunction from redox-cycling drugs that cannot be attributed to superoxide or hydrogen peroxide.
萘醌类化合物产生活性氧的能力在氧化应激研究中得到了广泛应用。然而，在丰富培养基中，过量的超氧化物歧化酶和过氧化氢酶无法保护大肠杆菌免受白花丹素的生长抑制，这表明其毒性作用并非由于部分还原氧物种的产生。加入抑制生长水平的白花丹素后，呼吸立即停止。体外研究表明，白花丹素和其他具有氧化还原活性的醌类化合物会从含葡萄糖培养基中的主要呼吸脱氢酶NADH脱氢酶截取电子。过量的氧化底物，如白花丹素，会使这种似乎受氧化还原调节的酶失活。由此导致的呼吸停止是一个由氧化还原循环药物引起的代谢功能障碍的警示例子，这种功能障碍不能归因于超氧化物或过氧化氢。
