Narikawa S, Suzuki T, Yamamoto M, Nakamura M
Department of Laboratory Medicine, St Marianna University School of Medicine, Kanagawa, Japan.
J Antimicrob Chemother. 1991 Jul;28(1):47-53. doi: 10.1093/jac/28.1.47.
Enzymes acting on pyruvate as a parameter of the ATP regeneration system were studied as a cause of metronidazole resistance in Bacteroides fragilis NCTC 11295. The resistant strain had higher lactate dehydrogenase activity and produced more lactate than susceptible strains, suggesting that the enzyme is more active in lactic acid fermentation. Furthermore, the reaction catalysed by lactate dehydrogenase occurred up to 48 mg/L metronidazole, whereas the reaction catalysed by pyruvate: ferredoxin oxidoreductase reaction stopped at 2 mg/L. The mechanism of metronidazole resistance in B. fragilis NCTC 11295 may be due to the high activity of lactate dehydrogenase which compensates for the decreased activity of pyruvate: ferredoxin oxidoreductase in the presence of metronidazole.
作为ATP再生系统参数的作用于丙酮酸的酶被作为脆弱拟杆菌NCTC 11295中甲硝唑耐药性的一个原因进行了研究。耐药菌株比敏感菌株具有更高的乳酸脱氢酶活性且产生更多的乳酸，这表明该酶在乳酸发酵中更具活性。此外，乳酸脱氢酶催化的反应在甲硝唑浓度高达48mg/L时仍能发生，而丙酮酸：铁氧还蛋白氧化还原酶催化的反应在2mg/L时就停止了。脆弱拟杆菌NCTC 11295中甲硝唑耐药性的机制可能是由于乳酸脱氢酶的高活性，其在甲硝唑存在的情况下补偿了丙酮酸：铁氧还蛋白氧化还原酶活性的降低。
