聚苯乙烯纳米塑料通过破坏脂质代谢和诱导DNA损伤来促进结肠炎相关的癌症

IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES
Shan Tian , Ruixue Li , Jiao Li , Jinhui Zou
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引用次数: 0

摘要

纳米塑料由于其在人体中的存在而引起了广泛的关注。最近的研究强调了NPs对消化道的有害影响。然而,没有研究报道NPs暴露与结肠炎相关癌症(CAC)之间的关联。采用偶氮氧甲烷/葡聚糖硫酸钠诱导的CAC模型,并选择聚苯乙烯纳米颗粒(PS-NPs)长期暴露。使用非靶向代谢组学和16S rRNA测序检测PS-NPs暴露后结肠代谢物和肠道微生物的变化。利用脂多糖(LPS)处理的癌细胞模型(Caco-2)暴露于PS-NPs,研究其潜在的分子机制。与正常对照组相比,PS-NPs组小鼠肿瘤淋巴结和活性氧(ROS)增加,pan-CK和Ki-67表达增加,DNA损伤更严重。16S rRNA测序显示,暴露于PS-NPs改变了Allobaculum和Lactobacillus的丰度,而代谢分析显示,最显著的代谢物主要富集在脂肪酸代谢中。LPS干预Caco-2细胞的实验表明,暴露于PS-NPs会导致Caco-2的脂质过氧化、氧化应激和DNA损伤。在AOM/DSS小鼠模型和细胞模型中,暴露于PS-NPs激活了磷脂酰肌醇3-激酶(PI3K)/AKT/哺乳动物雷帕霉素靶蛋白(mTOR)信号通路。在暴露于PS-NPs的Caco-2细胞中,参与脂肪酸代谢的关键蛋白下调。非诺贝特激活脂肪酸代谢途径,显著抑制了暴露于PS-NPs的癌细胞的代谢作用。PS-NPs暴露干扰脂质代谢,通过激活PI3K/AKT/mTOR诱导DNA损伤,促进CAC进展。抑制脂肪酸代谢是控制ps - np诱导的CAC的治疗靶点。本研究为从环境角度防治CAC提供了重要参考,提高了人们对塑料控制必要性的认识。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Polystyrene nanoplastics promote colitis-associated cancer by disrupting lipid metabolism and inducing DNA damage

Polystyrene nanoplastics promote colitis-associated cancer by disrupting lipid metabolism and inducing DNA damage

Polystyrene nanoplastics promote colitis-associated cancer by disrupting lipid metabolism and inducing DNA damage
Nanoplastics (NPs) have attracted widespread attention owing to their presence in the body. Recent studies highlighted the detrimental effects of NPs on the digestive tract. However, no studies have reported an association between NPs exposure and colitis-associated cancer (CAC). An azoxymethane/dextran sodium sulfate-induced CAC model was used, and polystyrene nanoparticles (PS-NPs) were selected for long-term exposure. Non-targeted metabolomics and 16S rRNA sequencing were used to detect changes in colonic metabolites and gut microbes following PS-NPs exposure. A lipopolysaccharide (LPS)-treated cancer cell model (Caco-2) exposed to PS-NPs was used to investigate the underlying molecular mechanism. Compared to the normal control group, mice in the PS-NPs group exhibited more tumor nodes and reactive oxygen species (ROS), higher expression of pan-CK and Ki-67, and more severe DNA damage. 16S rRNA sequencing revealed that exposure to PS-NPs altered the abundance of Allobaculum and Lactobacillus, whereas metabolic analysis showed that the most significant metabolites were enriched mostly in fatty acid metabolism. Experiments in LPS intervened Caco-2 cells showed that exposure to PS-NPs led to lipid peroxidation, oxidative stress, and DNA damage in Caco-2. Exposure to PS-NPs activated the phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway both in the AOM/DSS mouse model and cellular model. Key proteins involved in fatty acid metabolism were downregulated in Caco-2 cells exposed to PS-NPs. The metabolic effects of cancer cells exposed to PS-NPs were significantly inhibited by the activation of the fatty acid metabolism pathway by fenofibrate. PS-NPs exposure disturbed lipid metabolism and induced DNA damage via the activation of PI3K/AKT/mTOR to promote CAC progression. Inhibition of fatty acid metabolism is a therapeutic target for controlling PS-NP-induced CAC. Our study provides an important reference for the prevention and treatment of CAC from the perspective of the environment and enhances awareness of the necessity of plastic control.
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来源期刊
Environment International
Environment International 环境科学-环境科学
CiteScore
21.90
自引率
3.40%
发文量
734
审稿时长
2.8 months
期刊介绍: Environmental Health publishes manuscripts focusing on critical aspects of environmental and occupational medicine, including studies in toxicology and epidemiology, to illuminate the human health implications of exposure to environmental hazards. The journal adopts an open-access model and practices open peer review. It caters to scientists and practitioners across all environmental science domains, directly or indirectly impacting human health and well-being. With a commitment to enhancing the prevention of environmentally-related health risks, Environmental Health serves as a public health journal for the community and scientists engaged in matters of public health significance concerning the environment.
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