Owais W M, Kleinhofs A
Department of Biological Sciences, Yarmouk University, Irbid, Jordan.
Mutat Res. 1988 Feb;197(2):313-23. doi: 10.1016/0027-5107(88)90101-7.
Inorganic azide (N3-) mutagenicity is mediated through a metabolically synthesized organic azide, L-azidoalanine (N3-CH2-CH(-NH2)-COOH). L-Azidoalanine appears to be formed by the action of O-acetylserine (thiol)-Lyase (EC 4.2.99.8) using O-acetylserine and azide as substrates. In both plants and bacteria tested, azide substitutes for the natural substrate sulfide (S2-) in this reaction. Azide (L-azidoalanine) mutagenesis is highly attenuated by a deficiency in the excision of UV-like DNA damage (uvr-). Thus a premutation lesion recognizable by the bacterial excision-repair enzymes must be formed. Mutagenesis appears to proceed from this by 'direct mispairing' pathway. Azide (L-azidoalanine) mutagenicity is highly specific and involves a stereoselective process, but the molecular nature of the specificity has not been determined.
无机叠氮化物（N3-）的致突变性是通过代谢合成的有机叠氮化物L-叠氮丙氨酸（N3-CH2-CH(-NH2)-COOH）介导的。L-叠氮丙氨酸似乎是由O-乙酰丝氨酸（硫醇）裂合酶（EC 4.2.99.8）以O-乙酰丝氨酸和叠氮化物为底物作用形成的。在测试的植物和细菌中，叠氮化物在该反应中替代天然底物硫化物（S2-）。叠氮化物（L-叠氮丙氨酸）诱变作用因UV样DNA损伤切除缺陷（uvr-）而高度减弱。因此，必须形成一种可被细菌切除修复酶识别的前突变损伤。诱变作用似乎由此通过“直接错配”途径进行。叠氮化物（L-叠氮丙氨酸）的致突变性具有高度特异性，涉及立体选择性过程，但特异性的分子本质尚未确定。
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