Mechanistic Insights into Furfuraldehyde-Induced Toxicity and the Protective Role of L-Carnitine in Male Rats Following 90-Day Exposure

Fadhil, Samer Riyadh; Hassan, Salima Lafta

doi:10.29079/qjvms.2026.170786.1182

	Mechanistic Insights into Furfuraldehyde-Induced Toxicity and the Protective Role of L-Carnitine in Male Rats Following 90-Day Exposure
Al-Qadisiyah Journal of Veterinary Medicine Sciences
Volume 25, Issue 1, May 2026, Pages 113-120 PDF (857.85 K)
Document Type: Research Paper
DOI: 10.29079/qjvms.2026.170786.1182
Authors
Samer Riyadh Fadhil^* ; Salima Lafta Hassan
Department of Pathology and Poultry Diseases, College of Veterinary Medicine, University of Baghdad, Baghdad, Iraq
Abstract
Furfuraldehyde is an industrial aldehyde that is associated with significant oxidative stress and mitochondrial dysfunction. This study explores furfuraldehyde-related hepatorenal toxicity and the mitigating effects of L-carnitine in male rats after subchronic exposure. Fifty male Wistar rats were assigned into five groups (n = 10): control; low-dose furfuraldehyde (20 mg/kg); high-dose furfuraldehyde (40 mg/kg); and both doses with L-carnitine (200 mg/kg) in co-administration. Dosing was done orally for 90 days. Evaluated parameters included: oxidative stress and mitochondrial function (ATP, mitochondrial membrane potential, cytochrome c release), apoptosis (BAX (Bcl-2-associated X protein), Bcl-2 (B-cell lymphoma 2), caspase-3) gene expression, and histopathology of the kidney and liver. Furfuraldehyde caused a significant increase in reactive oxygen species and Malondialdehyde, and a significant decrease in catalase and ATP production (p < 0.001). It caused mitochondrial depolarization, cytochrome c release, BAX and caspase-3 up regulation, Bcl-2 down regulation, and apoptosis in the kidney and liver. Furfuraldehyde caused necrosis, inflammation, and mitochondrial ultra-structural damage as assessed by histopathology and transmission electron microscopy. L-carnitine co-administration reversed these effects and restored balance in redox, mitochondrial integrity, and architecture of the tissue (ATP restored to 70–75%). Furfuraldehyde exposure caused the kidney and liver to undergo mitochondria-mediated apoptosis and oxidative injury. L-carnitine appears to protect the cells by maintaining the function of the mitochondria and reducing apoptosis, demonstrating its potential in treating aldehyde-related organ toxicity.
Keywords
Furfuraldehyde; L-Carnitine; Oxidative stress; Mitochondrial dysfunction; toxicity

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