Abstract
INTRODUCTION: 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. METHODS: In this study, the mitochondria damage and oxidative stress of dinotefuran on Chironomus kiiensis 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. RESULTS: 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(50)) 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(2+)) in Chironomidae via dysregulating the gene expressions of atp2b, camk ii, and calm. Subsequently, the disruption of the Ca(2+) signaling pathway induced oxidative stress by raising reactive oxygen species (ROS), hydrogen peroxide (H(2)O(2)), and malonaldehyde (MDA) levels. Thus, the over-release of Ca(2+) and ROS disordered the normal functioning of mitochondrial-related pathways by dysregulating the expressions of mitochondria-related genes of atpef0a, sdha, and cyt b. CONCLUSION: Our findings showed that low environmental concentrations of dinotefuran caused paralysis of the midge via interfering the Ca(2+)-ROS-mitochondria pathway. These results provided data support for assessing the potential environmental risk of dinotefuran.