AUTHOR=Wei Fenghua , Gu Weiwen , Zhang Fengru , Wu Shuangxin 

TITLE=Paralysis caused by dinotefuran at environmental concentration via interfering the Ca2+–ROS–mitochondria pathway in Chironomus kiiensis

JOURNAL=Frontiers in Public Health

VOLUME=Volume 12 - 2024

YEAR=2024

URL=https://www.frontiersin.org/journals/public-health/articles/10.3389/fpubh.2024.1468384

DOI=10.3389/fpubh.2024.1468384

ISSN=2296-2565

ABSTRACT=<sec><title>Introduction</title><p>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, the chronic toxicity mechanism related to mitochondria damage of dinotefuran to non-target animals at environmental concentration is unclear.</p></sec><sec><title>Methods</title><p>In this study, the mitochondria damage and oxidative stress of dinotefuran on <italic>Chironomus kiiensis</italic> were investigated at environmental concentrations by long-term exposure. At the same time, relevant gene expressions of these toxicity indexes were measured as sensitive ecotoxicity biomarkers to reflect the toxic effects of dinotefuran on Chironomidae.</p></sec><sec><title>Results</title><p>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 days, the lowest observed-effect concentration (LOEC) and 50% inhibitory concentration (IC<sub>50</sub>) were 0.01 (0.01–0.04) and 0.60 (0.44–0.82) μg/L, respectively. Dinotefuran promoted the release of intracellular calcium ions (Ca<sup>2+</sup>) in Chironomidae via dysregulating the gene expressions of <italic>atp2b</italic>, <italic>camk ii</italic>, and <italic>calm</italic>. Subsequently, the disruption of the Ca<sup>2+</sup> signaling pathway induced oxidative stress by raising reactive oxygen species (ROS), hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), and malonaldehyde (MDA) levels. Thus, the over-release of Ca<sup>2+</sup> and ROS disordered the normal functioning of mitochondrial-related pathways by dysregulating the expressions of mitochondria-related genes of <italic>atpef0a</italic>, <italic>sdha</italic>, and <italic>cyt b</italic>.</p></sec><sec><title>Conclusion</title><p>Our findings showed that low environmental concentrations of dinotefuran caused paralysis of the midge via interfering the Ca<sup>2+</sup>–ROS–mitochondria pathway. These results provided data support for assessing the potential environmental risk of dinotefuran.</p></sec>