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

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.