Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033 (Japan).
Angew Chem Int Ed Engl. 2014 Jun 23;53(26):6772-5. doi: 10.1002/anie.201403221. Epub 2014 May 21.
We have developed an activatable photosensitizer capable of specifically inducing the death of β-galactosidase-expressing cells in response to photoirradiation. By using a selenium-substituted rhodol scaffold bearing β-galactoside as a targeting substituent, we designed and synthesized HMDESeR-βGal, which has a non-phototoxic spirocyclic structure owing to the presence of the galactoside moiety. However, β-galactosidase efficiently converted HMDESeR-βGal into phototoxic HMDESeR, which exists predominantly in the open xanthene form. This structural change resulted in drastic recovery of visible-wavelength absorption and the ability to generate singlet oxygen ((1)O2). When HMDESeR-βGal was applied to larval Drosophila melanogaster wing disks, which express β-galactosidase only in the posterior region, photoirradiation induced cell death in the β-galactosidase-expressing region with high specificity.
我们开发了一种可激活的光敏剂,能够在受到光照射时特异性地诱导β-半乳糖苷酶表达细胞的死亡。通过使用含有β-半乳糖苷作为靶向取代基的硒取代罗丹支架,我们设计并合成了 HMDESeR-βGal,由于半乳糖苷部分的存在,它具有非光毒性的螺环结构。然而,β-半乳糖苷酶能有效地将 HMDESeR-βGal 转化为光毒性的 HMDESeR,其主要以开链形式存在。这种结构变化导致可见光吸收的急剧恢复和生成单线态氧((1)O2)的能力。当 HMDESeR-βGal 被应用于仅在后区表达β-半乳糖苷酶的黑腹果蝇幼虫翅盘时,光照射能特异性地诱导β-半乳糖苷酶表达区的细胞死亡。