Christa L, Thuillier L, Perignon J L
Biochem Biophys Res Commun. 1983 Jun 15;113(2):425-32. doi: 10.1016/0006-291x(83)91743-6.
5'-Deoxy-5'-methylthioadenosine inhibits Concanavalin A induced rat T lymphocyte proliferation in a dose dependent manner (50 microM to 1000 microM). The extent of inhibition by MTA of lymphocyte proliferation was greatest when MTA was added to the cells at the same time as Concanavalin A. The determination of cyclic AMP level from 30 min to the 6th hour shows that 5'-Deoxy-5'-methylthioadenosine inhibition is correlated with an elevation of cyclic AMP at this mitogen recognition phase. 5'-Deoxy-5'-methylthioadenosine concentrations that inhibit rat T lymphocyte proliferation also inhibit phosphodiesterase activity. This biochemical mechanism could be specific to 5'-Deoxy-5'-methylthioadenosine inhibition since in an another model of inhibition of rat T lymphocyte proliferation (2'-Deoxyadenosine 10 microM, in adenosine deaminase deficiency conditions: 2'-Deoxycoformycin 10 microM), no significant modification of cyclic AMP level can be demonstrated.
5'-脱氧-5'-甲硫基腺苷以剂量依赖方式（50微摩尔至1000微摩尔）抑制伴刀豆球蛋白A诱导的大鼠T淋巴细胞增殖。当5'-脱氧-5'-甲硫基腺苷（MTA）与伴刀豆球蛋白A同时加入细胞时，MTA对淋巴细胞增殖的抑制程度最大。从30分钟至第6小时测定环磷酸腺苷水平表明，在这个促有丝分裂原识别阶段，5'-脱氧-5'-甲硫基腺苷的抑制作用与环磷酸腺苷的升高相关。抑制大鼠T淋巴细胞增殖的5'-脱氧-5'-甲硫基腺苷浓度也抑制磷酸二酯酶活性。这种生化机制可能是5'-脱氧-5'-甲硫基腺苷抑制所特有的，因为在另一种抑制大鼠T淋巴细胞增殖的模型中（在腺苷脱氨酶缺乏条件下，10微摩尔2'-脱氧腺苷：10微摩尔2'-脱氧助间型霉素），未显示环磷酸腺苷水平有明显改变。
