Kurhaluk Natalia, Kamiński Piotr, Tkaczenko Halina
Institute of Biology, Pomeranian University in Słupsk, Arciszewski St. 22 B, 76-200 Słupsk, Poland.
Department of Medical Biology and Biochemistry, Division of Ecology and Environmental Protection, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, M. Skłodowska-Curie St. 9, 85-094 Bydgoszcz, Poland.
Cell Physiol Biochem. 2025 Aug 6;59(S2):2-52. doi: 10.33594/000000799.
The widespread presence of environmental pollutants, including toxic metals, microplastics, and antibiotics, has significantly altered gut microbiota composition and functionality, leading to dysbiosis and oxidative stress. These changes contribute to various adverse physiological effects, including systemic inflammation, mitochondrial dysfunction, and intestinal barrier dysfunction. This review provides a comprehensive analysis of the molecular mechanisms by which these environmental factors induce oxidative damage, emphasising the importance of redox imbalance, the overproduction of reactive oxygen species, and inflammatory signalling pathways. Key pathways involved include NF-κB, Nrf2/Keap1, PI3K/AKT, p38-MAPK, JAK/STAT and TLR4/MyD88. These pathways collectively contribute to the progression of chronic inflammatory conditions. Furthermore, this article synthesises findings from 354 studies published between 2016 and 2024, integrating human and animal research evidence. Existing literature suggests that gut dysbiosis exacerbates oxidative stress through impaired short-chain fatty acid production, downregulation of peroxisome proliferator-activated receptor gamma, and disruption of antioxidant enzyme activity. This review explores these mechanisms in more detail. Additionally, the review evaluates studies investigating microbiota-targeted therapeutic interventions to mitigate oxidative stress. These interventions include probiotics, prebiotics, polyphenols, and postbiotics, focusing on their reported modulation of Nrf2 and AMPK signalling pathways. The potential of faecal microbiota transplantation as an innovative approach to restoring a healthy gut ecosystem and counteracting pollutant-induced oxidative damage is also discussed. In light of the growing global exposure to environmental pollutants and their associated long-term health implications, it is imperative to gain a deeper understanding of their impact on gut microbiota and oxidative stress. This topic remains at the forefront of biomedical research due to its implications for public health, disease prevention, and developing novel therapeutic strategies.
包括有毒金属、微塑料和抗生素在内的环境污染物广泛存在，已显著改变肠道微生物群的组成和功能，导致生态失调和氧化应激。这些变化会引发各种不良生理效应，包括全身炎症、线粒体功能障碍和肠道屏障功能障碍。本综述全面分析了这些环境因素诱导氧化损伤的分子机制，强调了氧化还原失衡、活性氧过度产生和炎症信号通路的重要性。涉及的关键途径包括NF-κB、Nrf2/Keap1、PI3K/AKT、p38-MAPK、JAK/STAT和TLR4/MyD88。这些途径共同促成慢性炎症性疾病的进展。此外，本文综合了2016年至2024年间发表的354项研究结果，整合了人类和动物研究证据。现有文献表明，肠道生态失调通过短链脂肪酸生成受损、过氧化物酶体增殖物激活受体γ下调和抗氧化酶活性破坏加剧氧化应激。本综述更详细地探讨了这些机制。此外，该综述评估了针对微生物群的治疗干预措施以减轻氧化应激的研究。这些干预措施包括益生菌、益生元、多酚和后生元，重点关注它们对Nrf2和AMPK信号通路的调节作用。还讨论了粪便微生物群移植作为恢复健康肠道生态系统和对抗污染物诱导的氧化损伤的创新方法的潜力。鉴于全球范围内环境污染物暴露的增加及其对长期健康的影响，必须更深入地了解它们对肠道微生物群和氧化应激的影响。由于其对公共卫生、疾病预防和开发新治疗策略的影响，这个话题仍然是生物医学研究的前沿领域。
