Pentachlorophenol (PCP) was used widely as preservative and biocide and has been banned due to with various harmful effects, such as carcinogenicity and teratogenicity. However, the effects of PCP on colitis induced by dextrose sodium sulfate (DSS) remain largely unknown. Serum metabolomics and gut microbiota were investigated to elucidate the underlying mechanisms. Exposure to 20 μg/L PCP aggravated DSS‐induced body weight loss, colon shortening, severe histological injuries, and upregulation of TNFα, iNOS, IL‐1β, and IL‐6. Serum metabolomics showed that both DSS and PCP could significantly disrupted tryptophan metabolism in normal mice. Interestingly, PCP exposure intensified the disturbance in purine metabolism but not tryptophan metabolism caused by DSS. Quantitative analysis of tryptophan and metabolites further confirmed that PCP exposure significantly increased the serum contents of serotonin, adenine, guanine, guanosine, inosine monophosphate (IMP), inosine, and hypoxanthine in DSS‐treated mice. The overall gut microbial community was significantly modified by PCP and DSS treatment alone. Rikenellaceae_RC9_Gut_group, Colidextribacter, and Desulfovibrio were more abundant in colitis mice following PCP exposure. Further integrative analysis of differential bacteria and purine metabolites highlighted a significant correlation between Desulfovibrio and several purine metabolites, including guanine, guanosine, hypoxanthine, IMP, and inosine. Adenosine ribonucleotides de novo biosynthesis, inosine‐5′‐phosphate biosynthesis I, and urate biosynthesis/inosine 5′‐phosphate degradation pathways were depleted in colitis mice upon PCP treatment. Taken together, PCP exposure delayed the recovery of colitis induced by DSS in association with altered gut microbiota and serum metabolites, which were enriched in tryptophan and purine metabolism.

中文翻译：

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五氯苯酚暴露会延迟结肠炎的恢复，与肠道菌群和嘌呤代谢改变有关


五氯苯酚 （PCP） 被广泛用作防腐剂和杀菌剂，由于具有致癌性和致畸性等各种有害影响而被禁用。然而，PCP 对葡萄糖硫酸钠 （DSS） 诱导的结肠炎的影响在很大程度上仍然未知。研究血清代谢组学和肠道菌群以阐明潜在机制。暴露于 20 μg/L PCP 会加剧 DSS 诱导的体重减轻、结肠缩短、严重的组织学损伤以及 TNFα、iNOS、IL-1β 和 IL-6 的上调。血清代谢组学显示，DSS 和 PCP 均可显著破坏正常小鼠的色氨酸代谢。有趣的是，PCP 暴露加剧了 DSS 引起的嘌呤代谢紊乱，但没有加剧色氨酸代谢的紊乱。色氨酸和代谢物的定量分析进一步证实，PCP 暴露显着增加了 DSS 处理小鼠血清中血清血清中血清中的血清血清含量，腺嘌呤、腺嘌呤、鸟嘌呤、鸟苷、肌苷一磷酸 （IMP）、肌苷和次黄嘌呤。单独的 PCP 和 DSS 处理显着改变了整个肠道微生物群落。Rikenellaceae_RC9_Gut_group、Colidextribacter 和 Desulfovibrio 在 PCP 暴露后的结肠炎小鼠中含量更高。对差异细菌和嘌呤代谢物的进一步综合分析强调了 Desulfovibrio 与几种嘌呤代谢物之间的显着相关性，包括鸟嘌呤、鸟苷、次黄嘌呤、IMP 和肌苷。在 PCP 处理后，结肠炎小鼠的腺苷核糖核苷酸从头生物合成、肌苷-5′-磷酸生物合成 I 和尿酸盐生物合成/肌苷 5'-磷酸降解途径被耗尽。 综上所述，PCP 暴露延迟了 DSS 诱导的结肠炎的恢复，这与肠道微生物群和血清代谢物的改变有关，这些代谢物富含色氨酸和嘌呤代谢。