Smith S H, Shipman C, Drach J C
Cancer Res. 1978 Jul;38(7):1916-21.
Deoxyadenosine but not adenosine reversed the antiviral activity of 9-beta-D-arabinofuranosyladenine (ara-A) and 9-beta-D-arabinofuranosylhypoxanthine (ara-H) when used in the presence of coformycin, an inhibitor of adenosine deaminase. In suspension cultures of KB cells, 10 muM ara-A inhibited the replication of herpes simplex virus type 1 by 80%. Concomitant addition of 50 muM deoxyadenosine reduced the antiviral activity of 10 muM ara-A to only 40% inhibition. Adenosine failed to antagonize the antiviral activity. In monolayer cultures of KB cells, the 50% inhibitory concentration of ara-A was increased from 1.5 to 2.9 muM by 2 muM deoxyadenosine and to 8.5 muM by 10 muM deoxyadenosine. Analysis of the dose-response data by a double reciprocal plot method indicated that the antagonism was competitive. The antiviral activity of ara-H also was antagonized by deoxyadenosine. The 50% inhibitory concentration of ara-H was increased from 42 muM to 70, 91, or 121 muM by the concurrent addition of 5, 10, or 20 muM deoxyadenosine. Competitive antagonism could not be demonstrated. In the absence of the adenosine deaminase inhibitor, neither ara-A nor ara-H was antagonized by deoxyadenosine. Since such inhibitors were not available unitl recently, previous investigators were unable to observe the antagonistic capacity of deoxyadenosine.
在腺苷脱氨酶抑制剂助间霉素存在的情况下，脱氧腺苷而非腺苷可逆转9-β-D-阿拉伯呋喃糖基腺嘌呤（ara-A）和9-β-D-阿拉伯呋喃糖基次黄嘌呤（ara-H）的抗病毒活性。在KB细胞悬浮培养物中，10 μM ara-A可抑制单纯疱疹病毒1型的复制达80%。同时加入50 μM脱氧腺苷可将10 μM ara-A的抗病毒活性降低至仅40%的抑制率。腺苷未能拮抗抗病毒活性。在KB细胞单层培养物中，2 μM脱氧腺苷可使ara-A的50%抑制浓度从1.5 μM增加至2.9 μM，10 μM脱氧腺苷则使其增加至8.5 μM。采用双倒数作图法分析剂量反应数据表明，这种拮抗作用具有竞争性。脱氧腺苷也拮抗ara-H的抗病毒活性。同时加入5、10或20 μM脱氧腺苷可使ara-H的50%抑制浓度从42 μM分别增加至70、91或121 μM。未证明存在竞争性拮抗作用。在不存在腺苷脱氨酶抑制剂的情况下，脱氧腺苷既不拮抗ara-A也不拮抗ara-H。由于直到最近才有此类抑制剂，以前的研究人员无法观察到脱氧腺苷的拮抗能力。
