Conjugated linoleic acid protects brain mitochondrial function in acrolein induced male rats

Acrolein (AC) is a toxic substance that can have a neurotoxic effect. It can cause oxidative stress and mitochondrial dysfunction. Conjugated linoleic acid (CLA), a dietary supplement, has many biological functions. Limited information is available about the effect of CLA on AC-induced brain toxicity. Therefore, the present study aims to investigate the effect of CLA on mitochondrial oxidative stress, respiratory enzymes, krebs cycle enzymes and ATP levels in AC treated rat brain. Sprague Dawley male rats were given AC (5 mg/kg i.p.), CLA (200 mg/kg orally) and CLA with AC for six days per week for 30 days. Some oxidative stress parameters and mitochondrial enzymes such as manganese super oxide dismutase, glutathione peroxidase, NADP⁺-dependent isocitrate dehydrogenase (ICDH), alpha-ketoglutarate dehydrogenase (α-KGDH), malate dehydrogenase, reduced glutathione (GSH), lipid peroxidation (LP), protein carbonyl (PC), oxidative phosphorylation (OXPHOS) and tricarboxylic acid cycle (TCA) enzymes, and ATP levels were determined. AC significantly decreased the activities of GSH, antioxidant enzymes, OXPHOS enzymes (complex I and IV), TCA enzymes (ICDH and α-KGDH) and ATP levels. Significant increases were also observed in mitochondrial LP and PC levels in AC group. Co-treatment with AC + CLA improved oxidative stress and mitochondrial dysfunction caused by AC. As a result of our findings, it was observed that CLA was effective in improving oxidative stress and impaired mitochondrial functions in brain tissue by the effect of AC. Considering the association between neurodegenerative diseases and mitochondrial dysfunction, CLA can play a role in the prevention and therapy of neurodegenerative disorders.