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Adverse effects of fenpropathrin on the intestine of common carp (Cyprinus carpio L.) and the mechanism involved.
Xiu, Wenyao; Ding, Weikai; Mou, Shaoyu; Li, Yuanyuan; Sultan, Yousef; Ma, Junguo; Li, Xiaoyu.
Afiliação
  • Xiu W; College of Life Science, Henan Normal University, Xinxiang, Henan 453007, China.
  • Ding W; Henan International Joint Laboratory of Aquatic Toxicology and Health Protection, Henan Normal University, Xinxiang, Henan 453007, China.
  • Mou S; College of Life Science, Henan Normal University, Xinxiang, Henan 453007, China.
  • Li Y; Henan International Joint Laboratory of Aquatic Toxicology and Health Protection, Henan Normal University, Xinxiang, Henan 453007, China. Electronic address: 2017052@htu.edu.cn.
  • Sultan Y; Department of Food Toxicology and Contaminants, National Research Centre, Dokki, Cairo 12622, Egypt.
  • Ma J; College of Life Science, Henan Normal University, Xinxiang, Henan 453007, China. Electronic address: majunguo@htu.edu.cn.
  • Li X; Henan International Joint Laboratory of Aquatic Toxicology and Health Protection, Henan Normal University, Xinxiang, Henan 453007, China.
Pestic Biochem Physiol ; 199: 105799, 2024 Feb.
Article em En | MEDLINE | ID: mdl-38458669
ABSTRACT
Fenpropathrin (FEN), a pyrethroid pesticide, is frequently detected in natural water bodies, unavoidable pose adverse effects to aquatic organisms. However, the harmful effects and potential mechanisms of FEN on aquatic species are poorly understood. In this study, common carp were treatment with FEN at 0.45 and 1.35 µg/L for 14 d, and the toxic effects and underlying mechanisms of FEN on the intestine of carp were revealed. RNA-seq results showed that FEN exposure cause a wide range of transcriptional alterations in the intestine and the differentially expressed genes were mainly enrichment in the pathways related to immune and metabolism. Specifically, FEN exposure induced pathological damage and altered submicroscopic structure of the intestine, elevated the levels of Bacteroides fragilis enterotoxin, altered the contents of claudin-1, occludin, and zonula occluden-1 (ZO-1), and causing injury to the intestinal barrier. In addition, inflammation-related index TNF-α in the serum and IL-6 in the intestinal tissues were generally increased after FEN exposure. Moreover, FEN exposure promoted an increase in reactive oxygen species (ROS), altered the levels of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH), upregulated the contents of malondialdehyde (MDA) in the intestines. The apoptosis-related parameter cytochrome c, caspase-9, and caspase-3 were significantly altered, indicating that inflammation reaction, oxidative stress, and apoptosis may be involved in the toxic mechanism of FEN on carp. Moreover, FEN treatment also altered the intestinal flora community significantly, which may affect the intestinal normal physiological function and thus affect the growth of fish. Overall, the present study help to clarify the intestinal reaction mechanisms after FEN treatment, and provide a basis for the risk assessment of FEN.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Piretrinas / Carpas Limite: Animals Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Piretrinas / Carpas Limite: Animals Idioma: En Ano de publicação: 2024 Tipo de documento: Article