Coburn R F, Williams W J, White P, Kahn S B
J Clin Invest. 1967 Mar;46(3):346-56. doi: 10.1172/JCI105536.
Dogs anesthetized with pentobarbital were shown to produce carbon monoxide at an average rate of 0.21 +/- (SD) 0.05 ml per hour. After intravenous injection of erythrocytes damaged by incubation with N-ethylmaleimide, CO was produced in excess of base-line production for 3 to 4 hours with an average yield of 0.89 +/- (SE) 0.046 mumole of carbon monoxide to 1 mumole of heme degraded. After intravenous injection of N-ethylmaleimide (NEM)-treated erythrocytes containing hemoglobin labeled with (14)carbon, (14)CO was produced. Its specific activity was approximately one-eighth that of the injected heme. It was also produced after intravenous injection of solutions of hemoglobin-(14)C and of reconstituted methemoglobin containing hemin-(14)C, but not after injections of methemoglobin containing globin-(14)C. The average yields of (14)CO from metabolized heme in the experiments with damaged erythrocytes and hemoglobin solutions were 89 +/- (SE) 4.6 and 97 +/- (SE) 17.0%, respectively. These results demonstrate that the CO produced during hemoglobin degradation arises from the heme moiety. The yield of (14)CO after injection of hemoglobin-(14)C solutions decreased significantly to values of 35 and 42% in two experiments when exogenous CO was added to the body stores, resulting in blood carboxyhemoglobin levels of 11.3 and 13.2% saturation. This finding suggests that oxidative metabolism is required during catabolism of hemoglobin to CO and that carboxy-hemoglobin levels in this range are sufficient to cause inhibition. After intravenous injection of either hemin-(14)C or protoporphyrin-(14)C, (14)CO was also produced. After injection of protoporphyrin-(14)C labeled bilirubin was isolated from gall bladder bile, and labeled hemin was isolated from the liver. It is thus very likely that protoporphyrin is converted to heme before the formation of CO. There was a large difference between the maximal rates of catabolism of hemoglobin to CO observed after injection of damaged erythrocytes and hemoglobin solutions. The limiting parameters in these processes are not yet clear.
用戊巴比妥麻醉的狗每小时平均产生一氧化碳的速率为0.21±(标准差)0.05毫升。静脉注射经N - 乙基马来酰亚胺孵育损伤的红细胞后,一氧化碳的产生量在3至4小时内超过基线产生量,每降解1微摩尔血红素平均产生0.89±(标准误)0.046微摩尔一氧化碳。静脉注射含有用(14)C标记血红蛋白的N - 乙基马来酰亚胺(NEM)处理的红细胞后,产生了(14)CO。其比活性约为注射血红素的八分之一。静脉注射血红蛋白 - (14)C溶液和含有血红素 - (14)C的重组高铁血红蛋白溶液后也产生了(14)CO,但注射含有球蛋白 - (14)C的高铁血红蛋白后未产生。在红细胞损伤和血红蛋白溶液实验中,代谢血红素产生(14)CO的平均产率分别为89±(标准误)4.6%和97±(标准误)17.0%。这些结果表明,血红蛋白降解过程中产生的一氧化碳来自血红素部分。在两个实验中,当向体内储存中添加外源性一氧化碳,使血液中碳氧血红蛋白饱和度达到11.3%和13.2%时,注射血红蛋白 - (14)C溶液后(14)CO的产率显著下降至35%和42%。这一发现表明,血红蛋白分解为一氧化碳的过程中需要氧化代谢,并且这个范围内的碳氧血红蛋白水平足以导致抑制作用。静脉注射血红素 - (14)C或原卟啉 - (14)C后,也产生了(14)CO。注射原卟啉 - (14)C后,从胆囊胆汁中分离出标记胆红素,从肝脏中分离出标记血红素。因此,很可能在一氧化碳形成之前原卟啉就已转化为血红素。注射损伤红细胞和血红蛋白溶液后观察到的血红蛋白分解为一氧化碳的最大速率之间存在很大差异。这些过程中的限制参数尚不清楚。