Lycopene attenuates imidacloprid-induced cardio-renal toxicity with concomitant modulation of KIM-1, SLC22A2, TNNT2, and Caspase-3 expression in male Wistar albino rats.

Authors

Marwa M Eid, Yasser S El-Sayed, Mohamed F El-Dakroury, Ahmed Abdeen, Mustafa Shukry, Doaa Abdelrahman, Ehab Y Abdelhiee

Published in

Tissue & cell. Volume 104. Issue Pt 3. Pages 104081. Oct 20, 2026. Epub Oct 20, 2026.

Abstract

Imidacloprid (IMI), a widely used neonicotinoid insecticide, induces systemic organ toxicity at sub-lethal doses; however, the relative susceptibility of cardiac and renal tissues and organ-differential protection by lycopene (LYC) have not been experimentally investigated. This study characterized subacute IMI-induced cardio-renal toxicity and evaluated LYC co-administration. Thirty-two adult male Wistar albino rats were allocated to four groups (n = 8): Control, LYC (10 mg/kg/day), IMI (90 mg/kg/day), and LYC + IMI, and received treatments orally for 28 days. Tissue MDA, GSH, GSSG, TNF-α, and IL-6 were measured in cardiac and renal homogenates; mRNA expression of TNNT2, ANP, KIM-1, SLC22A2, and Caspase-3 was profiled by qRT-PCR; and serum biomarkers and histopathology were assessed. IMI produced significant injury in both organs (p < 0.05). Renal tissue showed greater deviation from controls in most parameters (8 of 11), suggesting greater renal susceptibility: higher MDA (3.38- vs. 2.00-fold), TNF-α (4.92- vs. 3.66-fold), Caspase-3 (3.99- vs. 2.14-fold), KIM-1 (2.88-fold), creatinine (3.02-fold), and lesion scores (renal Median 3.0 vs. cardiac Median 2.0) with tubular degeneration, necrosis, desquamation, and thickening glomerular basement membrane. Cardiac tissue showed selective vulnerability with IL-6 (7.99-fold), GSH/GSSG collapse (to 0.29 × control), TNNT2 downregulation, ANP upregulation, and 5.11-fold CK-MB increase, along with myofibrillar disorganization, focal necrosis, and inflammatory infiltration. LYC provided potential renal protection, with recoveries of 71% for MDA, 65% for TNF-α, 63% for Caspase-3, and 84% creatinine, together with amelioration of renal lesions (62% recovery), whereas cardiac protection was statistically significant for most parameters but less complete, particularly for inflammatory and gene expression endpoints, with partial preservation of myocardial architecture. In conclusion, IMI causes multi-pathway cardio-renal toxicity mainly affecting the kidney; LYC co-administration offers significant renal and some cardiac protection by reducing oxidative, inflammatory, apoptotic, and organ injury markers. These results support further investigation of LYC as a nephro- and cardioprotective supplement against neonicotinoid toxicity.

PMID:
42913189
Bibliographic data and abstract were imported from PubMed on 24 Oct 2026.

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