A Multibiomarker Approach to Delineate the Toxicity of Methoxyfenozide on Oncorhynchus mykiss

Methoxyfenozide is a diacylhydrazine‐class insect growth regulator functioning as an ecdysone receptor agonist and inducing premature and lethal molt in susceptible larvae. This investigation was conducted to evaluate the impact of methoxyfenozide‐based commercial insecticide BYPASS on multiple end points in tissues of juvenile Oncorhynchus mykiss following 7, 14, and 21 days of exposure to sublethal concentrations of 0.042, 0.21, and 0.42 mg/L. There was not any significant change in CF and/or HSI. The treatment resulted in diminished AChE activity in brain and muscle together with a significant decline in Na+, K+‐ATPase in gill and kidney tissues. The increase in the activities of antioxidant enzymes was followed by elevated levels of TBARS and PC throughout the experiment in all tissues, proving the status of oxidative stress. It is supported by the observed increase in 8‐OHdG level following 21 days of exposure. Caspase‐3 activity rose in a tissue‐specific manner indicating the initiation of apoptosis via the mitochondrial pathway. Multi‐biomarker responses showed concentration‐dependent effects in calculated indexes as well as higher biomarker scores for antioxidant enzymes. Overall, the neurotoxic potential and pro‐oxidant activity of BYPASS, along with its potency to cause DNA damage, apoptosis, and to disrupt osmoregulation, were revealed. The outcomes manifest the first experimental sublethal effects caused by methoxyfenozide in tissues of O. mykiss, increasing our understanding of the risk insecticides represent and the need for strict regulatory scrutiny to mitigate the risk for non‐target organisms.