Tissue-specific toxicity of clothianidin on rainbow trout (Oncorhynchus mykiss).

This study was performed to investigate the tissue-specific effects of clothianidin on Oncorhynchus mykiss by evaluating the biochemical and histological alterations following 21 days of treatment to environmentally relevant concentrations of 3, 15, and 30 µg/L. The emerged behavioral changes in feeding and swimming performance were considered as adaptive responses to avoid the chemical. The toxic effect of pesticide on nervous system and osmoregulation was evidenced with the inhibition of AChE and Na+K+-ATPase. The sustained lipid peroxidation, ranging from muscle (196%) > brain (154%) > gill (140%) > kidney (129%), might be suggested as a mechanism mediating the inhibition of membrane-bound enzymes. Histological evaluation showed clothianidin-induced lesions appearing as necrosis, atrophy, and edema in muscle, hyperplasia, and hypertrophy causing shortening and fusion of the secondary lamellae in gill, vacuolization, and hydropic degeneration in brain, degeneration of tubular epithelium, and existence of melanomacrophage centers in kidney. The pronounced degenerative changes observed in gill indicate the vulnerability of tissue possibly due to its role as first contact and entry point for the pesticide. Consequently, clothianidin exerted its toxic effects by altering normal behavior, causing neurotoxicity and disturbing osmoregulation. Moreover, the imposed stress was responded in a tissue-specific manner and histological lesions become more severe with increasing concentration. The findings clearly reveal the potential threat caused by environmentally relevant concentrations of clothianidin to early life stages of fish.