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在环境中暴露于 UV-B 下,光敏剂 CDRI-97/78 诱导细胞凋亡死亡的 II 型途径的作用。

Role of type-II pathway in apoptotic cell death induction by photosensitized CDRI-97/78 under ambient exposure of UV-B.

机构信息

Photobiology Division, CSIR-Indian Institute of Toxicology Research, Post Box No. 80, M.G. Marg, Lucknow, 226001, India.

出版信息

Toxicol Lett. 2013 Oct 24;222(2):122-31. doi: 10.1016/j.toxlet.2013.06.210. Epub 2013 Jun 14.

Abstract

Novel trioxane 97/78, developed by Central Drug Research Institute (CDRI), Lucknow has shown promising antimalarial activity. Clinical experience of anti-malarial drugs registered the occurrence of phototoxicity in patients exposed with sunlight subsequent to medication. Photodegradation study has identified one photo-product up to 4h under UV-B/Sunlight by LC-MS/MS. UV-B irradiated 97/78 compound produced ¹O₂ via type-II dependent reaction mechanism, corroborated by its specific quencher. 2'-dGuO degradation and % tail development in photochemical as well as comet test, advocated the genotoxic potential of 97/78. The photocytotoxicity assays (MTT and NRU) on HaCaT cell line revealed the considerable decline in cell viability by 97/78. Cell cycle and Annexin V/PI double stain along with AO/EB demonstrated the G2/M phase arrest and apoptosis. Significant caspase-3 activity was measured in photoexcited 97/78 by colorimetric assay. Fluorescence stain with AO/JC-1 confirmed the lysosomal disruption and mitochondrial membrane destabilization by UV-B irradiated 97/78. Gene expression by RT-PCR showed significant upregulation of p21 and pro-apoptotic Bax, but no change observed in Bcl-2. In conclusion, the study highlights ROS mediated DNA damage, lysosomal and mitochondrial destabilization via upregulation of Bax and activation of caspase-3 which further leads to apoptosis.

摘要

新型三氧杂环庚烷 97/78,由印度中央药物研究所(CDRI)开发,具有良好的抗疟活性。抗疟药物的临床经验表明,患者在服药后暴露在阳光下会发生光毒性。光降解研究通过 LC-MS/MS 在 4 小时内鉴定出一种光产物。UV-B 辐照 97/78 化合物通过 II 型依赖反应机制产生 ¹O₂,这与它的特定淬灭剂相符。2'-脱氧鸟苷(2'-dGuO)的降解和光化学和彗星试验中的 %尾巴发展,表明了 97/78 的遗传毒性潜力。在 HaCaT 细胞系上进行的光细胞毒性测定(MTT 和 NRU)显示,97/78 显著降低了细胞活力。细胞周期和 Annexin V/PI 双重染色以及 AO/EB 显示 G2/M 期阻滞和凋亡。通过比色法测量了光激发的 97/78 中的显著 caspase-3 活性。用 AO/JC-1 荧光染色证实了 UV-B 辐照的 97/78 导致溶酶体破裂和线粒体膜不稳定。通过 RT-PCR 进行的基因表达显示,p21 和促凋亡 Bax 的表达显著上调,但 Bcl-2 没有变化。总之,该研究强调了 ROS 介导的 DNA 损伤、溶酶体和线粒体的不稳定,这是通过 Bax 的上调和 caspase-3 的激活导致细胞凋亡的。

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