Case G L
J Nutr. 1976 Dec;106(12):1721-36. doi: 10.1093/jn/106.12.1721.
Experiments conducted with rats in vivo comparing the metabolism of methionine and S-methyl-L-cysteine and in vitro comparing methionine, S-methyl-L-cysteine and S-adenosyl-L-methionine indicate that a substantial portion of the oxidative metabolism of the methionine methyl group occurs by pathways that are independent of S-adenosylmethionine formation. Inclusion of 1.2% or 2.4% of S-methyl-L-cysteine in a diet containing 3% of L-methionine depressed the conversion of the methionine methyl and carboxyl carbons to CO2 by 39% and 28%, and 52% and 33%, respectively, for the two levels of S-methyl-L-cysteine. Inclusion of 1.65% of methionine in a diet containing 2.4% of S-methyl-L-cysteine did not affect the conversion of the methyl group of S-methylcysteine to CO2, but 3% of methionine depressed the conversion of the S-methylcysteine methyl group to CO2 to 87% of control values. Greater inhibitions were seen when these substrates were compared in a liver homogenate. In a rat liver homogenate system optimized for the conversion of the methyl group of methionine to CO2, the rate of conversion of the methyl group of S-adenosyl-L-methionine to CO2 was less than 1% of that of methionine even when the concentration of S-adenosylmethionine was saturating. Addition of saturating levels of unlabeled S-adenosymethionine to the homogenate system did not effect the rate of conversion of the methionine methyl carbon to CO2. Although S-adenosylmethionine-dependent metabolism of methionine, leading to incorporation of the methyl carbon into sarcosine and serine, could be demonstrated in liver homogenates, essentially all of the CO2 produced from the methionine methyl group was derived by a pathway or pathways independent of S-adenosylmethionine formation. Formaldehyde and formate have been tentatively identified as intermediates in catabolism of the methionine methyl group by this (these) pathway(s).
在体内用大鼠进行的比较蛋氨酸和S-甲基-L-半胱氨酸代谢的实验,以及在体外比较蛋氨酸、S-甲基-L-半胱氨酸和S-腺苷-L-蛋氨酸的实验表明,蛋氨酸甲基的大部分氧化代谢是通过独立于S-腺苷甲硫氨酸形成的途径进行的。在含有3%L-蛋氨酸的日粮中添加1.2%或2.4%的S-甲基-L-半胱氨酸,两种水平的S-甲基-L-半胱氨酸分别使蛋氨酸甲基和羧基碳向CO2的转化降低了39%和28%,以及52%和33%。在含有2.4%S-甲基-L-半胱氨酸的日粮中添加1.65%的蛋氨酸,对S-甲基半胱氨酸甲基向CO2的转化没有影响,但3%的蛋氨酸使S-甲基半胱氨酸甲基向CO2的转化降低至对照值的87%。当在肝匀浆中比较这些底物时,观察到更大的抑制作用。在一个针对蛋氨酸甲基向CO2转化进行优化的大鼠肝匀浆系统中,即使S-腺苷甲硫氨酸浓度达到饱和,S-腺苷-L-蛋氨酸甲基向CO2的转化速率也不到蛋氨酸的1%。向匀浆系统中添加饱和水平的未标记S-腺苷甲硫氨酸,对蛋氨酸甲基碳向CO2的转化速率没有影响。虽然在肝匀浆中可以证明蛋氨酸的S-腺苷甲硫氨酸依赖性代谢导致甲基碳掺入肌氨酸和丝氨酸中,但基本上所有由蛋氨酸甲基产生的CO2都是通过独立于S-腺苷甲硫氨酸形成的一条或多条途径衍生而来的。甲醛和甲酸已被初步确定为通过该途径(这些途径)代谢蛋氨酸甲基的中间产物。