Skinner M A, Ho H J, Chan V L
Arch Biochem Biophys. 1986 May 1;246(2):725-32. doi: 10.1016/0003-9861(86)90329-2.
An adenosine-sensitive (Ados) mutant of baby hamster kidney (BHK) cells, ara-S10d, when treated with a toxic concentration of adenosine (Ado), displayed a substantial elevation of S-adenosylhomocysteine (SAH), S-adenosylmethionine (SAM), and methylthioadenosine (MTA). Wild-type BHK cells treated with the same concentration of Ado (not toxic to these parental cells) produced an elevation of SAH 1.5 times higher than that of ara-S10d cells without a concurrent elevation of SAM or MTA. Inhibition of methylation of DNA and tRNA is greater in ara-S10d cells treated with Ado than that of similarly treated wild-type cells. This inhibition was correlated with the enhanced Ado toxicity, suggesting inhibition of methylation as a possible causal factor for the great increase in Ado sensitivity. Inhibition of methylation may be due to the elevated level of MTA and not solely to the elevation of SAH, a well-known potent inhibitor of numerous methyltransferases.
仓鼠肾（BHK）细胞的一种对腺苷敏感（Ados）的突变体ara-S10d，在用有毒浓度的腺苷（Ado）处理时，其S-腺苷同型半胱氨酸（SAH）、S-腺苷甲硫氨酸（SAM）和甲基硫代腺苷（MTA）显著升高。用相同浓度的Ado（对这些亲代细胞无毒）处理的野生型BHK细胞，其SAH升高幅度比ara-S10d细胞高1.5倍，而SAM或MTA没有同时升高。用Ado处理的ara-S10d细胞中DNA和tRNA甲基化的抑制作用比同样处理的野生型细胞更大。这种抑制作用与Ado毒性增强相关，表明甲基化抑制可能是Ado敏感性大幅增加的一个可能原因。甲基化抑制可能是由于MTA水平升高，而不仅仅是由于SAH水平升高，SAH是众多甲基转移酶的一种众所周知的强效抑制剂。
