2-AAPA inhibits glutathione reductase and thioredoxin reductase,IC50s=6.7 and 8.7 μM respectively, and impairs mitochondrial function.1 May be used to induce a cellular model of thiol oxidative stress.2 Enhances sensitivity of cancer cell lines to X-ray irradiation.3 Induces G2/M cell cycle arrest by inducing thiol oxidative stress resulting in α-tubulin S-glutathionylation-mediated microtubule depolymerization.4 Improves limb revascularization by glutathionylation and subsequent stabilization of HIF-1α5.
1) de Souza et al. (2017), Inhibition of reductase systems by 2-AAPA modulates peroxiredoxin oxidation and mitochondrial function in A172 glioblastoma cells Toxicol. In Vitro, 42 273
2) Xie et al. (2014), Evaluation of a dithiocarbamate derivative as a model of thiol oxidate stress in H9c2 rat cardiomyocytes; Free Radic. Biol. Med. 70 214
3) Zhao et al. (2009), Increase in thiol oxidative stress by glutathione reductase inhibition as a novel approach to enhance cancer sensitivity to X-ray irradiation; Free Radic. Biol. Med., 47 176
4) Li et al. (2017), 2-acetylamino-3-[4-(2-acetylamino-2-carboxyethylsulfanylcarbonylamino)phenylcarbamoylsulfanyl] propionic acid, a glutathione reductase inhibitior, induces G2/M cell cycles arrest through generation of thiol oxidative stress in human esophageal cancer cells; Oncotarget, 8 61846
5) Watanabe et al. (2016), Glutathione adducts induced by ischemia and deletion of glutatedoxin-1 stabilize HIF-1α and improve limb revascularization; Proc. Natl. Acad. Sci. USA, 113 6011