Effects of sublethal exposure to new pesticides lufenuron and flonicamid on common carp, Cyprinus carpio, hydromineral balance to further saltwater exposure

The effects of 21 days exposure to lufenuron and flonicamid were investigated on common carp responses to saltwater exposure. Fish were assigned in three groups: control (21 days in freshwater), lufenuron (exposed for 21 days) and flonicamid (exposed for 21 days). After 21 days, all fish were subjected to 15 g/l saltwater for further 4 days. Plasma glucose, cortisol, sodium, potassium, chloride, calcium and phosphorus levels were monitored 0, 24, 72 and 120 h after saltwater exposure. Type of pesticides and time of salt water exposure had interaction on plasma glucose and cortisol levels. These two stress indicators were increased significantly in all groups after saltwater exposure. The cortisol elevation continued until 72 h after salinity challenge and then decreased significantly after 120 h salinity exposure in all treatments. Plasma glucose level showed fluctuation during saltwater exposure. It was increased after 24 h saltwater exposure, then decreased after 72 h and again it was increased after 120 h salinity challenge. Increased plasma sodium showed significant elevation along with elongation of saltwater exposure. Pesticide exposure significantly affected plasma chloride levels as the flonicamid group had significantly lower chloride compared to the control and lufenuron groups. Plasma chloride showed significant elevation along with elongation of saltwater exposure. Pesticide and time of salinity challenge had interaction on plasma calcium levels as 24 h after salinity challenge calcium level of pesticide groups increased significantly. Along with elongation of saltwater exposure, calcium level of pesticides treatments decreased but it higher than the pre salinity challenge. Plasma phosphorus level increased 24 h after saltwater exposure and decreased along with elongation of saltwater exposure. In conclusion, lufenuron and flonicamid induce stress and alter gill function and blood ionic homeostasis during saltwater exposure.