Abstract
Clothianidin is a systemic neonicotinoid insecticide interfering with the central nervous system by acting as a nicotinic acetylcholine receptor agonist. Although previous studies on fish report low toxicity, its proven toxic potential for aquatic invertebrates and lack of data on its effect on juvenile fish have prompted us to investigate its adverse effects in environmentally relevant concentrations of 3, 15 and 30 μg/L for 7, 14 and 21 days on heart and spleen tissues of 10-month-old rainbow trout (Oncorhynchus mykiss). We detected a conspicuous increase in protein carbonyl and malondialdehyde (MDA) levels, which triggered antioxidant response of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), resulting in increased levels of glutathione (GSH). Clothianidin inhibited the activity of acetylcholinesterase (AChE) and lowered tissue protein levels. Heart tissue weight increased, while that of spleen decreased significantly. The effects were time- and concentration-dependent. What raises particular concern is the inhibition of AChE in the trout, even though clothianidin is claimed to be selective for insect receptors. Increased antioxidant activity in response to oxidative stress was clearly insufficient to keep MDA and protein carbonyl at normal levels, which evidences the pro-oxidant potency of the insecticide. All this calls for further investigation into potential adverse effects on biological pathways in different fish species.