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Transcriptome Analysis Provides Insights into Hepatic Responses to Trichloroisocyanuric Acid Exposure in Goldfish (Carassius auratus)

文献类型： 外文期刊

作者： Zhou, Shun 1 ; Dong, Jing 1 ; Liu, Yongtao 1 ; Yang, Qiuhong 1 ; Xu, Ning 1 ; Yang, Yibin 1 ; Ai, Xiaohui 1 ;

作者机构： 1.Chinese Acad Fishery Sci, Yangtze River Fisheries Res Inst, Wuhan 430223, Peoples R China

2.Hubei Prov Engn & Technol Res Ctr Aquat Prod Qual, Wuhan 430223, Peoples R China

关键词： histopathology; metabolism; oxidative stress; transcriptome; trichloroisocyanuric acid

期刊名称：ANIMALS （ 影响因子：2.752； 五年影响因子：2.942 ）

ISSN： 2076-2615

年卷期： 2021 年 11 卷 10 期

页码：

收录情况： SCI

摘要： Simple Summary

Trichloroisocyanuric acid (TCCA) has been widely used in public health and aquaculture for the prevention and treatment of diseases. As a strong oxidative disinfectant, TCCA may cause adverse influences on aquatic organisms and further poses a threat to the aquatic ecosystems. Nonetheless, the toxicological influences of TCCA on aquatic animals are still scarce and the mechanisms of the toxicity at the molecular levels in goldfish (Carassius auratus) have not been illustrated. The current study investigated the influences of sublethal concentration of TCCA on transcriptomic responses, the molecular indices of oxidative stress, and histopathological alterations in the hepatic and gill tissues of goldfish. The results indicated that TCCA exposure induced the disturbance of energy metabolism and the detoxification process. Furthermore, TCCA exposure also induced oxidative stress in the liver and caused pathological damage in gills. These findings could be useful to help understand the toxicological influences of TCCA on goldfish.

In this study, goldfish (Carassius auratus) were exposed to 0 (control group) and 0.81 mg/L TCCA for four consecutive days. The liver transcriptome, the molecular indices of oxidative stress, and gills histopathology were investigated. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that energy metabolism-related pathways such as glycolysis/gluconeogenesis were significantly enriched, suggesting their perturbation in the liver of goldfish. Additionally, TCCA exposure also caused pathological damage in gills, which compromised physiological function and decreased oxygen intake capacity of gills, thus leading to the enhancement of anaerobic metabolism. This finding was confirmed by the significant upregulation of lactate dehydrogenase in the liver of goldfish. Moreover, many phase I and phase II metabolic enzymes might be activated to alleviate TCCA-induced toxicity in goldfish, and glutathione S-transferases (GSTs) and cytochrome P450s (CYPs) play a crucial role in the metabolism of TCCA in the liver of goldfish. Furthermore, the antioxidant enzyme analysis showed that TCCA exposure induced oxidative damage in the liver and partially impaired the antioxidant defense system of goldfish, evidenced by decreased superoxide dismutase (SOD) and catalase (CAT), and increased malondialdehyde (MDA) level. In summary, this study will improve our understanding of the molecular mechanisms of the TCCA-induced toxicity in goldfish.

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