ArticleScientific reports2026
Nrf2 activation by the monocarbonyl curcumin derivative GO-Y015 confers cellular protection against arsenite toxicity by reducing intracellular arsenic levels.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Curcumin, a bioactive phenolic compound derived from turmeric, attenuates heavy metal toxicity, including inorganic arsenite (As(III)), via activation of the Nrf2-Keap1 signaling pathway; however, its low solubility and stability limit its bioactivity. To address these limitations, we synthesized curcumin derivatives and investigated the cytoprotective effects of a monocarbonyl analog, GO-Y015. GO-Y015 exhibited cytotoxicity comparable to curcumin at concentrations below 8 µM but significantly reduced As(III)-induced cytotoxicity. Pretreatment with GO-Y015 markedly improved cell viability under cytotoxic As(III) exposure, whereas curcumin showed minimal protective effects. Mechanistically, GO-Y015 induced robust Nrf2 activation in a concentration- and time-dependent manner, resulting in increased expression of downstream targets, including HO-1, GCLC, and MRP2. Pharmacological inhibition of Nrf2 (ML385), GSH synthesis (BSO), or MRP transporters (MK571) abolished the cytoprotective effects, indicating dependence on the Nrf2-GSH-MRP axis. Furthermore, ICP-MS analysis demonstrated that GO-Y015 significantly reduced intracellular arsenic accumulation after 2 h exposure. These findings indicate that GO-Y015 enhances arsenic detoxification and reduces cytotoxicity by promoting GSH-dependent conjugation and MRP-mediated efflux.
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