Role of Combined Administration Of Copper - Nicotinic Acid Complex and Coenzyme Q10 Against Aluminium Chloride – Induced Oxidative Stress in Rat Brain Download PDF

Alzheimer's disease (AD) is the most common chronic neurodegenerative disorder associated with aging. This study aimed to explore the modulatory effects of Coenzyme Q10 (CoQ10) (10 mg mg/kg., b.w.) and [Cu (I) – (nicotinic acid) 2] 1 Cl – complex (Cu –N complex) (400 µg/kg., b.w.) on aluminium chloride (AlCl3) -100 mg/kg b.w.) induced rat model of AD. Our results revealed that oral administration of AlCl3 for 42 days significantly elevated the levels of brain myeloperoxidase(MPO) activity and IL-1β levels, while Catalase and Na+/ K+ ATPase activity were markedly decreased. Plasma ferric reducing ability of plasma (ferric reducing/antioxidant power (FRAP) and superoxide dismutase (SOD)levels were noticeably decreased but Aspartate Transaminase (AST) concentrations were significantly increased, confirming that abnormal inflammatory response is associated with AD. Treatment by CoQ10 and Cu–Ncomplex restored the above mentioned parameters to about normal levels comparable to those of AD, indicating that IL-1β and Na+ / K+ ATPase activity may be considered as new biomarkers for AD. Histopathological and comet assay examinations confirmed the neuroprotective effect of CoQ10and Cu – N complex. The present data advocate the possible beneficial effect of CoQ10 and Cu – N complex protecting the cells against hepatocellular damage and as therapeutic modality for Alzheimer's disease via its anti-inflammatory/antioxidant mechanism