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<p>Silicon dioxide (SiO<sub>2</sub>) is widely used as an anti-caking agent in food and cosmetics. PANoptosis is a highly complex inflammatory programmed death pathway and plays a crucial role in disease and toxic injury. This study investigated the damage caused by 50&#xa0;nm, 300&#xa0;nm, and 1&#xa0;μm SiO<sub>2</sub> particles to the mice's colon and compared the toxicity differences among these particle sizes. The results showed that SiO<sub>2</sub> exposure induced ciliary damage and reduced intracellular serine content by inhibiting spermidine/spermine N1-acetyltransferase 1/2 (SAT1/2), thereby affecting mitochondrial one-carbon metabolism. Meanwhile, downregulation of mitochondrial overlapping with the m-complex activity 1 (OMA1)/optic atrophy 1 (OPA1) led to mitochondrial damage and mitochondrial reactive oxygen species (mtROS) release, eventually activating RIPK1-PANoptosome-mediated PANoptosis. Among them, 300&#xa0;nm had the strongest effect on mitochondrial damage, 50&#xa0;nm on apoptosis, and 1&#xa0;μm on amino acid metabolism, one-carbon metabolism, necroptosis, and pyroptosis. In conclusion, SiO<sub>2</sub> exposure induced RIPK-mediated PANoptosis via the serine/mitochondrial/mtROS pathway.</p> Graphical Abstract <p></p>

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Differential intestinal injury induced by nano- and micron-silicon dioxide: serine/mitochondrial/mtROS-mediated PANoptosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月23日

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  • Xu Shi,
  • Hao Wu,
  • Meichen Liu,
  • Xuejiao Yang,
  • Shiwen Xu,
  • Tong Xu

摘要

Silicon dioxide (SiO2) is widely used as an anti-caking agent in food and cosmetics. PANoptosis is a highly complex inflammatory programmed death pathway and plays a crucial role in disease and toxic injury. This study investigated the damage caused by 50 nm, 300 nm, and 1 μm SiO2 particles to the mice's colon and compared the toxicity differences among these particle sizes. The results showed that SiO2 exposure induced ciliary damage and reduced intracellular serine content by inhibiting spermidine/spermine N1-acetyltransferase 1/2 (SAT1/2), thereby affecting mitochondrial one-carbon metabolism. Meanwhile, downregulation of mitochondrial overlapping with the m-complex activity 1 (OMA1)/optic atrophy 1 (OPA1) led to mitochondrial damage and mitochondrial reactive oxygen species (mtROS) release, eventually activating RIPK1-PANoptosome-mediated PANoptosis. Among them, 300 nm had the strongest effect on mitochondrial damage, 50 nm on apoptosis, and 1 μm on amino acid metabolism, one-carbon metabolism, necroptosis, and pyroptosis. In conclusion, SiO2 exposure induced RIPK-mediated PANoptosis via the serine/mitochondrial/mtROS pathway.

Graphical Abstract