Gray I, Archer L J
J Bacteriol. 1967 Jan;93(1):36-9. doi: 10.1128/jb.93.1.36-39.1967.
Bacillus anthracis produces a toxin both in vitro and in vivo which, when injected intravenously into rats, brings about the death of the animals accompanied by gross pulmonary edema. Lung tissue removed prior to death showed, in vitro, a 30% reduction in overall oxidative metabolism (Q(o2)), whereas the nicotinamide adenine dinucleotide (NAD)-independent succinic dehydrogenase remained unaffected. The NAD concentration in the lungs of injected animals was reduced by 50%. Upon addition of NAD, the Q(o2) of lung tissue from injected animals rose to control values. At 45 min after toxin injection, the serum lactate concentration began to rise, showing about a 3.5-fold increase over controls after 75 min. No changes occurred in the pyruvate concentration. These changes may be explained by increased use of the pyruvate for glycolytic energy production with further loss of NAD. Additional experiments with liver, spleen, kidney, and brain tissues showed that the toxin-induced reduction of Q(o2) is an effect specific for lung tissue. Brain tissue showed a significant increase in oxidative metabolism upon the addition of the toxin, whereas the other tissues remained unaffected. It is suggested that a principal effect of the toxin is to inhibit, in lung tissue, the regeneration of NAD in the respiratory chain.
炭疽芽孢杆菌在体外和体内均能产生一种毒素，当将其静脉注射到大鼠体内时，会导致动物死亡并伴有严重的肺水肿。在动物死亡前取出的肺组织，在体外显示总体氧化代谢（Q(o2)）降低了30%，而不依赖烟酰胺腺嘌呤二核苷酸（NAD）的琥珀酸脱氢酶未受影响。注射动物肺部的NAD浓度降低了50%。添加NAD后，注射动物肺组织的Q(o2)升至对照值。毒素注射后45分钟，血清乳酸浓度开始升高，75分钟后比对照升高约3.5倍。丙酮酸浓度没有变化。这些变化可能是由于丙酮酸用于糖酵解能量产生的增加以及NAD的进一步损失所致。对肝脏、脾脏、肾脏和脑组织进行的额外实验表明，毒素诱导的Q(o2)降低是肺组织特有的效应。添加毒素后，脑组织的氧化代谢显著增加，而其他组织未受影响。有人认为，该毒素的主要作用是在肺组织中抑制呼吸链中NAD的再生。
