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<p>Hyperuricemia is a common metabolic disease. Epidemiological studies have suggested an association between hyperuricemia and tris(2-chloroethyl) phosphate (TCEP), yet the mechanism underlying their interaction and relevant empirical research remain lacking. This study used Kunming mice as subjects and conducted an 8-group controlled experiment (including a control group, TCEP exposure group, hyperuricemia group, and different intervention groups) over 40&#xa0;days. Detection was performed from three aspects: oxidative stress and inflammation, uric acid metabolism and organ damage, and molecular mechanisms. The study aimed to verify the toxicological association between TCEP and hyperuricemia, as well as to clarify the uric acid-lowering effect and mechanism of caffeic acid. The experimental results showed that TCEP exposure further increased the uric acid level in hyperuricemic mice; further detection revealed that the plasma xanthine oxidase (XOD) activity in mice of the TCEP exposure group was significantly higher than that in the non-exposure group. Meanwhile, TCEP exposure induced a significant inflammatory response in mice without increasing the malondialdehyde (MDA) level, and was accompanied by signs of renal damage, specifically manifested as renal tubular dilation and glomerular atrophy. After intervention with caffeic acid, the uric acid level and abnormally increased organ coefficients of mice were significantly reduced; further analysis via qPCR and Western blotting experiments indicated that caffeic acid might reduce uric acid concentration by downregulating the protein expression of GLUT9 and upregulating the protein expression of OAT1.</p>

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Tris(2-chloroethyl) phosphate (TCEP) modulates hyperuricemia by regulating the expression of renal urate transporters OAT1, URAT1, and GLUT9

  • 期刊论文

  • 发表日期：

    2026年3月25日

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  • Yongxiao Huang,
  • Hairui Lu,
  • Fangyao Li,
  • Caina Jiang,
  • Xianli Ma

摘要

Hyperuricemia is a common metabolic disease. Epidemiological studies have suggested an association between hyperuricemia and tris(2-chloroethyl) phosphate (TCEP), yet the mechanism underlying their interaction and relevant empirical research remain lacking. This study used Kunming mice as subjects and conducted an 8-group controlled experiment (including a control group, TCEP exposure group, hyperuricemia group, and different intervention groups) over 40 days. Detection was performed from three aspects: oxidative stress and inflammation, uric acid metabolism and organ damage, and molecular mechanisms. The study aimed to verify the toxicological association between TCEP and hyperuricemia, as well as to clarify the uric acid-lowering effect and mechanism of caffeic acid. The experimental results showed that TCEP exposure further increased the uric acid level in hyperuricemic mice; further detection revealed that the plasma xanthine oxidase (XOD) activity in mice of the TCEP exposure group was significantly higher than that in the non-exposure group. Meanwhile, TCEP exposure induced a significant inflammatory response in mice without increasing the malondialdehyde (MDA) level, and was accompanied by signs of renal damage, specifically manifested as renal tubular dilation and glomerular atrophy. After intervention with caffeic acid, the uric acid level and abnormally increased organ coefficients of mice were significantly reduced; further analysis via qPCR and Western blotting experiments indicated that caffeic acid might reduce uric acid concentration by downregulating the protein expression of GLUT9 and upregulating the protein expression of OAT1.