Sustained exposure to triclocarban and triclosan at environmental relevant concentration disrupts gut-liver axis in the black-spotted frog

IF 4.1 2区 环境科学与生态学 Q1 MARINE & FRESHWATER BIOLOGY
Bingyi Wang , Wenhui Sun , Xindi Ye , Tyler D. Hoskins , Yu Han , Xia Yuan , Qi Chen , Zhiquan Liu , Hangjun Zhang
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引用次数: 0

Abstract

Triclocarban (TCC) and triclosan (TCS) are broad-spectrum biocides that are extensively utilized frequently contaminate water bodies and have high environmental persistence. However, the safety of TCC and TCS for wild organisms remains largely unknown. Here, we evaluated the potential health risks for black-spotted frogs (Pelophylax nigromaculatus) when exposed to TCC and TCS at concentrations of 1, 10, and 100 μg/L for 21 consecutive days. TCC and TCS significantly disrupted the gut microbiome, specifically phylum Proteobacteria, which resulted in elevated serum levels of lipopolysaccharide (LPS), a bacterial endotoxin. After entering the bloodstream, LPS subsequently passes through the liver, where inflammatory cytokines are stimulated, including interleukin-1 β, interleukin-6, and tumor necrosis factor-alpha. Genes related to the inflammatory processes are also activated. This inflammatory response led to an increase in the activity of superoxide anion radicals and oxidative stress markers in the liver, mainly superoxide dismutase, catalase, glutathione peroxidase, and malondialdehyde. In addition to oxidative stress, damage to the liver has also been reported as elevated concentrations of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Collectively, these findings suggest that TCC and TCS exert hepatotoxic effects on frogs by disrupting the gut-liver axis, thereby inducing hepatic inflammation and oxidative stress. This study highlights the potential health risks posed by TCC and TCS exposure in wild organisms.
持续暴露于环境相关浓度的三氯卡班和三氯生会破坏黑斑蛙的肠肝轴
三氯卡班(TCC)和三氯生(TCS)是广泛使用的广谱杀菌剂,经常污染水体,具有较高的环境持久性。然而,TCC和TCS对野生生物的安全性在很大程度上仍然未知。本研究对黑斑蛙(Pelophylax nigromaculatus)连续21天暴露于浓度分别为1、10和100 μg/L的TCC和TCS环境下的潜在健康风险进行了评估。TCC和TCS显著破坏肠道微生物群,特别是变形菌门,导致血清脂多糖(LPS)水平升高,这是一种细菌内毒素。进入血液后,脂多糖随后通过肝脏,在那里炎症细胞因子被刺激,包括白细胞介素-1 β,白细胞介素-6和肿瘤坏死因子- α。与炎症过程相关的基因也被激活。这种炎症反应导致肝脏中超氧化物阴离子自由基和氧化应激标志物的活性增加,主要是超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和丙二醛。除了氧化应激外,肝脏损伤也被报道为谷丙转氨酶(ALT)和天冬氨酸转氨酶(AST)浓度升高。总的来说,这些发现表明TCC和TCS通过破坏肠-肝轴对青蛙产生肝毒性作用,从而诱导肝脏炎症和氧化应激。本研究强调了TCC和TCS在野生生物中的暴露所带来的潜在健康风险。
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来源期刊
Aquatic Toxicology
Aquatic Toxicology 环境科学-毒理学
CiteScore
7.10
自引率
4.40%
发文量
250
审稿时长
56 days
期刊介绍: Aquatic Toxicology publishes significant contributions that increase the understanding of the impact of harmful substances (including natural and synthetic chemicals) on aquatic organisms and ecosystems. Aquatic Toxicology considers both laboratory and field studies with a focus on marine/ freshwater environments. We strive to attract high quality original scientific papers, critical reviews and expert opinion papers in the following areas: Effects of harmful substances on molecular, cellular, sub-organismal, organismal, population, community, and ecosystem level; Toxic Mechanisms; Genetic disturbances, transgenerational effects, behavioral and adaptive responses; Impacts of harmful substances on structure, function of and services provided by aquatic ecosystems; Mixture toxicity assessment; Statistical approaches to predict exposure to and hazards of contaminants The journal also considers manuscripts in other areas, such as the development of innovative concepts, approaches, and methodologies, which promote the wider application of toxicological datasets to the protection of aquatic environments and inform ecological risk assessments and decision making by relevant authorities.
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