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<p>Hexavalent chromium [Cr(VI)] is a well-established environmental nephrotoxicant that induces renal injury. Lycopene (LYC), one of the most potent naturally occurring antioxidants found in plants, has demonstrated protective effects against various forms of oxidative damage; however, its therapeutic role and underlying mechanisms in Cr(VI)-induced nephrotoxicity remain unclear. In this study, eighty female SPF-grade ICR mice were randomly assigned to four groups: control (Con), LYC, Cr(VI), and LYC + Cr(VI), and treated for 28 days. The results demonstrated that LYC significantly alleviated Cr(VI)-induced renal dysfunction and structural damage. Cr(VI) exposure markedly increased malondialdehyde (MDA) and hydrogen peroxide (H₂O₂) levels while suppressing antioxidant enzyme activities, including catalase (CAT), glutathione peroxidase (GSH-Px), and total superoxide dismutase (T-SOD). In contrast, LYC supplementation effectively restored antioxidant capacity and activated the Nuclear factor-erythroid 2-related factor 2(Nrf2) signaling pathway. Moreover, LYC mitigated Cr(VI)-induced mitochondrial dysfunction by suppressing excessive activation of mitochondrial fission-related proteins (Fis1, Drp1, and MFF) and PINK1/Parkin-mediated mitophagy. Notably, LYC co-treatment enhanced the expression of key mitochondrial biogenesis regulators, including Sirt1 and PGC-1α, in renal tissue. Collectively, these findings indicate that LYC protects against Cr(VI)-induced kidney injury, at least in part, by regulating mitochondrial biogenesis, mitochondrial dynamics, mitophagy, and the Nrf2 antioxidant signaling pathway.</p>

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Lycopene Attenuates Hexavalent Chromium–Induced Kidney Injury By Modulating PINK1/Parkin-Mediated Mitophagy

  • 期刊论文

  • 发表日期：

    2026年5月6日

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  • Quan-mei Zhang,
  • Xia Zhang,
  • Lun-Bin Xia,
  • Kai Ge,
  • De-Yong She,
  • Shao-Shuai Bi

摘要

Hexavalent chromium [Cr(VI)] is a well-established environmental nephrotoxicant that induces renal injury. Lycopene (LYC), one of the most potent naturally occurring antioxidants found in plants, has demonstrated protective effects against various forms of oxidative damage; however, its therapeutic role and underlying mechanisms in Cr(VI)-induced nephrotoxicity remain unclear. In this study, eighty female SPF-grade ICR mice were randomly assigned to four groups: control (Con), LYC, Cr(VI), and LYC + Cr(VI), and treated for 28 days. The results demonstrated that LYC significantly alleviated Cr(VI)-induced renal dysfunction and structural damage. Cr(VI) exposure markedly increased malondialdehyde (MDA) and hydrogen peroxide (H₂O₂) levels while suppressing antioxidant enzyme activities, including catalase (CAT), glutathione peroxidase (GSH-Px), and total superoxide dismutase (T-SOD). In contrast, LYC supplementation effectively restored antioxidant capacity and activated the Nuclear factor-erythroid 2-related factor 2(Nrf2) signaling pathway. Moreover, LYC mitigated Cr(VI)-induced mitochondrial dysfunction by suppressing excessive activation of mitochondrial fission-related proteins (Fis1, Drp1, and MFF) and PINK1/Parkin-mediated mitophagy. Notably, LYC co-treatment enhanced the expression of key mitochondrial biogenesis regulators, including Sirt1 and PGC-1α, in renal tissue. Collectively, these findings indicate that LYC protects against Cr(VI)-induced kidney injury, at least in part, by regulating mitochondrial biogenesis, mitochondrial dynamics, mitophagy, and the Nrf2 antioxidant signaling pathway.