Imidacloprid induces hepatorenal toxicity in male albino rats via oxidative, immune inflammatory, and proliferative effects: a 90-day study

Abstract Imidacloprid (IM), a systemic neonicotinoid pesticide, is widely used globally due to its high effectiveness against a broad range of insects at minimal application rates. The current study aimed to examine how this insecticide can induce oxidative stress, disrupt the inflammatory process, and influence cellular proliferation in hepatorenal tissues, even at low doses. Thirty adult male albino rats were divided into five groups ( n = 6). The first group served as the control, while the other four groups received IM at 0.3, 3, 30, and 60 ppm, respectively, over 90 days through drinking water. Results revealed significant histopathological changes in the liver and kidneys of rats exposed at all doses. A notable increase in hepatorenal markers, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), urea, and creatinine levels, and a slight decrease in total serum protein (TP) were observed. There was a significant rise in malondialdehyde (MDA) levels, along with increased production of pro-inflammatory cytokines, including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and NOD-like receptor protein-3 (NLRP3). This was accompanied by strong immunopositivity of proliferating cell nuclear antigen (PCNA) and Ki-67 protein expression, while adipocyte-specific adhesion molecule (ASAM) levels showed insignificant changes. The study concludes that IM can induce hepatorenal damage accompanied by lipid peroxidation, elevated inflammatory mediators, and altered proliferative indicators. The effects were generally more apparent at higher dosages.