Role of Gut Microbiota in Modulating Oxidative Stress Induced by Environmental Factors.

IF 2 Q3 CELL BIOLOGY
Natalia Kurhaluk, Piotr Kamiński, Halina Tkaczenko
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引用次数: 0

Abstract

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.

肠道菌群在环境因素诱导的氧化应激中的作用。
环境污染物的广泛存在,包括有毒金属、微塑料和抗生素,已经显著改变了肠道微生物群的组成和功能,导致生态失调和氧化应激。这些变化可导致各种不良生理反应,包括全身性炎症、线粒体功能障碍和肠屏障功能障碍。这篇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、活性氧过剩和炎症信号通路的重要性。参与的关键信号通路包括NF-κB、Nrf2/Keap1、PI3K/AKT、p38-MAPK、JAK/STAT和TLR4/MyD88。这些途径共同促进慢性炎症的进展。此外,本文综合了2016年至2024年间发表的354项研究的结果,整合了人类和动物研究的证据。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而加剧氧化应激。本文将更详细地探讨这些机制。此外,该综述评估了针对微生物群的治疗干预以减轻氧化应激的研究。这些干预措施包括益生菌、益生元、多酚和后益生菌,重点关注它们对Nrf2和AMPK信号通路的调节。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引起的氧化损伤的创新方法的潜力也进行了讨论。鉴于全球暴露于环境污染物及其相关的长期健康影响的增加,有必要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、疾病预防和发展新的治疗策略的影响,该主题仍然是生物医学研究的前沿。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
5.80
自引率
0.00%
发文量
86
审稿时长
1 months
期刊介绍: Cellular Physiology and Biochemistry is a multidisciplinary scientific forum dedicated to advancing the frontiers of basic cellular research. It addresses scientists from both the physiological and biochemical disciplines as well as related fields such as genetics, molecular biology, pathophysiology, pathobiochemistry and cellular toxicology & pharmacology. Original papers and reviews on the mechanisms of intracellular transmission, cellular metabolism, cell growth, differentiation and death, ion channels and carriers, and the maintenance, regulation and disturbances of cell volume are presented. Appearing monthly under peer review, Cellular Physiology and Biochemistry takes an active role in the concerted international effort to unravel the mechanisms of cellular function.
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