Self-healing Demonstration in Imidacloprid Toxicity with Multibiomarkers and Biologic Pathways

Imidacloprid (IMI) pesticide has significant environmental and ecotoxicological pollution effects. Also, its high potential to enter the aquatic environment reveals the importance of early evaluation of the toxic effects of this compound. This study aimed to evaluate organ responses that can be associated with outcomes at higher levels of biological organization in fish. In this respect, the toxicity mechanism and recovery response process of IMI in rainbow trout (Oncorhyncus mykiss)’ s different tissues (blood, brain, gill and liver) were analyzed with important biomarkers [(hematological indices (RBC, WBC, Hg, Hct, MCV, MCH, MCHC), antioxidant enzyme activities (SOD, CAT, GPx, GSH), MDA, DNA damage (8-OHdG), apoptosis (caspase 3), AChE, TNF α, interleukin 6, Nrf-2, NF-kB activities, histopathological and immunofluorescence analyses (NeuN, BDNF, JNK and Nop10]. Exposure to different concentrations of IMI caused a decrease in RBC, WBC, Hg and Hct levels in O. mykiss. The effect of the same application on brain, gill and liver tissues was determined as inhibitions in antioxidant enzyme activities (SOD, CAT and GPx) and GSH level, inductions on MDA level, DNA damage, caspase-3, TNF α, IL- 6, Nrf-2 and NF-kB activities. As a result of three tissues’ histopathological examination; the degeneration, necrosis and hyperemia in the brain and liver, adhesion, desquamation and inflammation in the lamellar epitheliums has been determined in company with stress-induced responses inducing DNA damage. In the reflection of this situation on histomap results, increases were recorded in BDNF and NeuN levels. In the recovery response, tissue damage profile and detoxification process were differentiated according to dose and marker, and it manifested itself with moderate and mild symptoms. These findings revealed that IMI-mediated oxidative stress was effective in the Nrf-2/GSH/NF-kB pathways, showing strong hemato/hepato, and neurotoxic effects. It has become clear that the severity of the effects caused by IMI exposure is felt more in the brain and liver tissues, and that such contaminants should be taken into account in the risk assessment. During the post-exposure recovery period (after 15 days), AChE activity increased by 21% at high-dose administration. The recovery period was effective in regulating the oxidant/antioxidant balance of the organism by exhibiting serious induction/inhibition in each tissue and biomarker performance.