Nwawuba_2025_Environ.Toxicol.Pharmacol__104779

Nickel (II) chloride (NiCl) is an environmental toxicant that may cause neurotoxicity. This study investigated the effects of 30-day dietary exposure to NiCl (0.01, 0.1, and 1mg/g) in Nauphoeta cinerea, focusing on body weight, oxidative stress, behavior, and mitochondrial function. Exposure to 1mg/g reduced body weight and food intake. All concentrations impaired some exploratory behavioral parameters (e.g., distance travelled and average speed). Oxidative stress markers, including TBARS and ROS, increased, along with GST and SOD activity. Neurotransmitter metabolism was affected, with elevated acetylcholinesterase and reduced monoamine oxidase activity. Mitochondrial respiration showed impaired oxidative phosphorylation, altered proton leakage, and decreased complex II activity, indicating mitochondrial dysfunction. These findings demonstrate that NiCl (1mg/g) disrupts mitochondrial neuroenergetics and redox balance. Notably, behavioral impairments occurred even at the lowest concentrations, suggesting that subtle changes in activity may serve as early indicators of NiCl-induced neurotoxicity.