The final, formatted version of the article will be published soon.
ORIGINAL RESEARCH article
Front. Public Health
Sec. Environmental Health and Exposome
Volume 12 - 2024 |
doi: 10.3389/fpubh.2024.1468384
This article is part of the Research Topic Toxicity Mechanisms of Environmental Pollutants and Health Risk Assessment View all 12 articles
Paralysis caused by dinotefuran at environmental concentration via interfering Ca 2+ -ROS-mitochondria pathway in Chironomus kiiensis
Provisionally accepted- Jiaying University, Meizhou, China
Dinotefuran as the third-generation of neonicotinoid insecticides, is extensively used in agriculture worldwide, posing a potential toxic threat to non-target animals and humans. However, it is unclear that the chronic toxicity mechanism related to mitochondria damage of dinotefuran to non-target animals at environmental concentration. The objective of this study was to evaluate the chronic toxic effects and reveal the association between mitochondrial damage and behavioral inhibition. Our present study showed that chronic exposure to environmental concentrations of dinotefuran resulted in behavioral inhibition in the larvae of Chironomidae. For burrowing inhibition of 10-d, the lowest-observed-effect concentration (LOEC) and 50% inhibitory concentration (IC50) were 0.01 (0.01~0.04) and 0.60 (0.44~0.82) μg/L, respectively. Dinotefuran promoted the release of intracellular calcium ion (Ca 2+ ) in Chironomidae via dysregulating the gene expressions of atp2b, camk ii, and calm. ubsequently, the disruption of Ca 2+ signaling pathway induced oxidative stress by upraising reactive oxygen species (ROS), hydrogen peroxide (H2O2), and malonaldehyde (MDA) levels. Thus, the over-release of Ca 2+ and ROS disordered the normal functioning of mitochondrial-related pathway by dysregulating the expressions of mitochondria-related genes of atpef0a, sdha, and cyt b. Our findings showed that low environmental concentrations of dinotefuran caused paralysis of the midge via interfering Ca 2+ -ROS-mitochondria pathway. These results provided data support for assessing dinotefuran's potential environmental risk.
Keywords: Neonicotinoid insecticides, Long-term exposure, Mitochondria, Chironomidae, Environmental Dose
Received: 22 Jul 2024; Accepted: 09 Sep 2024.
Copyright: © 2024 Wei, Gu, Zhang and Wu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Weiwen Gu, Jiaying University, Meizhou, China
Fengru Zhang, Jiaying University, Meizhou, China
Shuangxin Wu, Jiaying University, Meizhou, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.