Salau_2020_J.Pharm.Pharmacol_72_1787

OBJECTIVES: This study was aimed at investigating neuroprotective effect of catechol on redox imbalance, cholinergic dysfunctions, nucleotide hydrolysing enzymes activities, and dysregulated metabolic pathways in iron-mediated oxidative brain injury. METHODS: Oxidative injury was induced in brain tissues by incubating with 0.1 mm FeSO(4) and treated with different concentrations of catechol. KEY FINDINGS: Catechol significantly elevated glutathione level, superoxide dismutase and catalase activities, while depleting malondialdehyde and nitric oxide levels. It also inhibited the activities of acetylcholinesterase, butyrylcholinesterase, and ATPase, with concomitant elevation of ENTPDase activity. GC-MS analysis revealed that treatment with catechol completely depleted oxidative-generated lipid metabolites. While LC-MS analysis revealed depletion of oxidative-generated metabolites in brain tissues treated with catechol, with concomitant restoration of oxidative-depleted metabolites. Catechol also led to reactivation of oxidative-inactivated taurine and hypotaurine, purine, glutathione, glycerophospholipid, nicotinate and nicotinamide, fructose and mannose, pyrimidine metabolisms and pentose phosphate pathways. Catechol was predicted in silico to be permeable across the blood-brain barrier with a predicted oral LD(50) value of 100 mg/kg and a toxicity class of 3. CONCLUSION: These results suggest the neuroprotective effects of catechol in iron-mediated oxidative brain injury.