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<p>Bisphenol A (BPA) is an environmental pollutant with toxic effects associated with disruption of redox balance and activation of inflammatory cascades. This study investigated the protective efficacy of carbocisteine (S-carboxymethylcysteine (SCMC)), a cysteine derivative with established antioxidant and cytoprotective properties, against BPA-induced kidney damage. Adult male rats were orally exposed to BPA and/or SCMC for 28 consecutive days. BPA elevated serum creatinine, BUN, uric acid, and Kim-1, in parallel with histological alterations and excessive collagen deposition in renal tissue. BPA exposure markedly enhanced lipid peroxidation, upregulated NF-κB p65 and pro-inflammatory cytokines, and suppressed GSH, SOD, catalase, and IL-10. Additionally, BPA provoked endoplasmic reticulum (ER) stress and apoptotic signaling, as evidenced by upregulated CHOP, GRP78, GRP75, and cleaved caspase-3. Co-administration of SCMC ameliorated BPA-induced renal dysfunction, preserved tissue architecture, attenuated oxidative damage, and mitigated inflammatory responses. SCMC further alleviated ER stress and apoptosis by downregulating CHOP, GRP78, GRP75, and cleaved caspase-3. SCMC suppressed Keap1 while enhancing Nrf2 and HO-1. In conclusion, these findings demonstrate that SCMC confers protection against BPA-induced nephrotoxicity by restoring antioxidant capacity, activating Nrf2/HO-1 signaling, and inhibiting inflammatory response, ER stress, and apoptosis. SCMC may therefore represent a promising therapeutic candidate for preventing kidney injury associated with BPA and related environmental toxicants.</p>

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Carbocisteine mitigates bisphenol A-mediated renal injury by modulating oxidative stress, Keap1/Nrf2/HO-1 pathway, endoplasmic reticulum stress, and inflammation

  • 期刊论文

  • 发表日期：

    2026年6月20日

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  • Reem S. Alruhaimi,
  • Reem N. Alotaibi,
  • Sulaiman M. Alnasser,
  • Wafa S. Al-Thubiani,
  • Nouf Aldawood,
  • Emad H. M. Hassanein,
  • Ayman M. Mahmoud

摘要

Bisphenol A (BPA) is an environmental pollutant with toxic effects associated with disruption of redox balance and activation of inflammatory cascades. This study investigated the protective efficacy of carbocisteine (S-carboxymethylcysteine (SCMC)), a cysteine derivative with established antioxidant and cytoprotective properties, against BPA-induced kidney damage. Adult male rats were orally exposed to BPA and/or SCMC for 28 consecutive days. BPA elevated serum creatinine, BUN, uric acid, and Kim-1, in parallel with histological alterations and excessive collagen deposition in renal tissue. BPA exposure markedly enhanced lipid peroxidation, upregulated NF-κB p65 and pro-inflammatory cytokines, and suppressed GSH, SOD, catalase, and IL-10. Additionally, BPA provoked endoplasmic reticulum (ER) stress and apoptotic signaling, as evidenced by upregulated CHOP, GRP78, GRP75, and cleaved caspase-3. Co-administration of SCMC ameliorated BPA-induced renal dysfunction, preserved tissue architecture, attenuated oxidative damage, and mitigated inflammatory responses. SCMC further alleviated ER stress and apoptosis by downregulating CHOP, GRP78, GRP75, and cleaved caspase-3. SCMC suppressed Keap1 while enhancing Nrf2 and HO-1. In conclusion, these findings demonstrate that SCMC confers protection against BPA-induced nephrotoxicity by restoring antioxidant capacity, activating Nrf2/HO-1 signaling, and inhibiting inflammatory response, ER stress, and apoptosis. SCMC may therefore represent a promising therapeutic candidate for preventing kidney injury associated with BPA and related environmental toxicants.