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<p>Aging is accompanied by cumulative oxidative stress that promotes tissue degeneration and reproductive decline. Here, we show that deficiency of superoxide dismutase 1 (SOD1) accelerates oxidative injury and reproductive aging through a ferroptosis-linked redox imbalance, and that ginseng root extract (GR) confers protection across species. Aged hairless <i>Sod1</i>⁻<sup>/</sup>⁻ mice exhibited markedly elevated skin and plasma oxidative stress markers—including 8-isoprostane, malondialdehyde (MDA), and pentosidine—together with dermal cyst formation and atrophic pathology. Complementary studies in <i>C</i>. <i>elegans</i> revealed that SOD1-deficient strains displayed increased reactive oxygen species, depleted glutathione, and elevated iron and lipid peroxidation—canonical features of ferroptosis-associated oxidative stress. These redox alterations coincided with shortened reproductive span and reduced progeny output, both rescued by ferroptosis inhibition or GR supplementation. In female <i>Sod1</i>⁻<sup>/</sup>⁻ mice, GR restored folliculogenesis, normalized estrous cyclicity, and improved ovarian morphology. Collectively, these findings identify SOD1 loss as a driver of ferroptosis-associated oxidative and reproductive aging and highlight GR as a promising redox-targeted intervention.</p>

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SOD1 deficiency drives ferroptosis-linked oxidative and reproductive aging, mitigated by ginseng root extract

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月12日

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  • Juewon Kim,
  • Shuichi Shibuya,
  • Yusuke Ozawa,
  • Yorino Sato,
  • Kazuhiro Kawamura,
  • Takahiko Shimizu

摘要

Aging is accompanied by cumulative oxidative stress that promotes tissue degeneration and reproductive decline. Here, we show that deficiency of superoxide dismutase 1 (SOD1) accelerates oxidative injury and reproductive aging through a ferroptosis-linked redox imbalance, and that ginseng root extract (GR) confers protection across species. Aged hairless Sod1⁻/⁻ mice exhibited markedly elevated skin and plasma oxidative stress markers—including 8-isoprostane, malondialdehyde (MDA), and pentosidine—together with dermal cyst formation and atrophic pathology. Complementary studies in C. elegans revealed that SOD1-deficient strains displayed increased reactive oxygen species, depleted glutathione, and elevated iron and lipid peroxidation—canonical features of ferroptosis-associated oxidative stress. These redox alterations coincided with shortened reproductive span and reduced progeny output, both rescued by ferroptosis inhibition or GR supplementation. In female Sod1⁻/⁻ mice, GR restored folliculogenesis, normalized estrous cyclicity, and improved ovarian morphology. Collectively, these findings identify SOD1 loss as a driver of ferroptosis-associated oxidative and reproductive aging and highlight GR as a promising redox-targeted intervention.