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莠去津暴露通过 P450/ROS 途径诱导鲤鱼(Cyprinus carpioL.)鳃细胞发生坏死性凋亡并引发炎症反应。

Atrazine exposure induces necroptosis through the P450/ROS pathway and causes inflammation in the gill of common carp (Cyprinus carpioL.).

机构信息

College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China.

College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China.

出版信息

Fish Shellfish Immunol. 2022 Dec;131:809-816. doi: 10.1016/j.fsi.2022.10.022. Epub 2022 Oct 17.

DOI:10.1016/j.fsi.2022.10.022
PMID:36257555
Abstract

Atrazine (ATR) is used worldwide and has been confirmed be hazardous materials that harmful to the health of organisms. Since ATR was more persistent in the water, the specific damage caused by ATR to aquatic organisms should be concern. The role of P450/ROS has been proposed in many pathomechanisms. To explore whether P450/ROS mediated necroptosis and promote inflammatory response caused by ATR exposure, 120 common carp (Cyprinus carpio L.) were randomly divided into four groups which were exposed to 0 μg/L, 4 μg/L, 40 μg/L and 400 μg/L ATR respectively. The residual levels of ATR and its metabolites increased, signs of necrosis and inflammation were found in the gills of the ATR-treatment groups. The levels of ROS and cytochrome P450 content were increased, and P450 enzymes were activated. The expression levels of the core components of necroptosis (RIPK1, RIPK3 and MLKL) increased. Moreover, gene expression of inflammatory factors (TNF-α, NF-κB, iNOS, COX-2, IL-1β and PTGE) increased significantly in the ATR-spiked group. Our results suggested that ATR exposure triggered necroptosis through the P450/ROS pathway and causes inflammation of common carp gill. This study provides valuable clue about the mechanism by which ATR causes injury to common carp gill.

摘要

莠去津(ATR)在全球范围内被广泛使用,已被证实是对生物体健康有害的危险物质。由于 ATR 在水中更持久,因此应该关注 ATR 对水生生物造成的具体损害。P450/ROS 的作用已在许多病理机制中得到证实。为了探讨 P450/ROS 是否介导了 ATR 暴露引起的坏死和促炎反应,将 120 条鲤鱼(Cyprinus carpio L.)随机分为四组,分别暴露于 0μg/L、4μg/L、40μg/L 和 400μg/L 的 ATR。ATR 处理组的鳃中发现了 ATR 的残留水平及其代谢物增加、坏死和炎症的迹象。ROS 和细胞色素 P450 含量增加,P450 酶被激活。坏死的核心组成部分(RIPK1、RIPK3 和 MLKL)的表达水平增加。此外,ATR 处理组中炎症因子(TNF-α、NF-κB、iNOS、COX-2、IL-1β 和 PTGE)的基因表达显著增加。我们的结果表明,ATR 暴露通过 P450/ROS 途径引发坏死,并导致鲤鱼鳃的炎症。这项研究为 ATR 引起鲤鱼鳃损伤的机制提供了有价值的线索。

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