Mechanism and Changes Associated with Edible Camphor Induced Neurotoxicity

ABSTRACT Background and Purpose: Camphor is an additive in certain remedies for the treatment of coryza, bronchitis, musculoskeletal pains and wounds. This study investigated the possible seizure-induction mechanism of edible camphor (EC) and the biochemical changes in brain and blood after its administration. Methods: Seizure characteristics were evaluated in twenty-five male Wistar rats randomly distributed into five groups and given intraperitoneal injections of 0.5 mL coconut oil; 100 mg/kg pentylenetetrazol (PTZ); 1000 mg/kg EC; 5 mg/kg diazepam + 1000 mg/kg EC; and 250 mg/kg carbamazepine + 1000 mg/kg EC respectively. Oral acute toxicity was evaluated using 15 male rats assigned to 3 groups (n=5) and orally administered a single sub-convulsive dose (300 mg/kg) of EC and monitored for 3, 24, and 168 hours respectively. Fasting blood sugar, blood lipid parameters and brain weight were evaluated. In a 28-day toxicity evaluation, 300 mg/kg/day EC was administered to test and control groups of male rats (n=10) and brains were excised for evaluation of weight, oxidative, inflammatory and cell component changes.   Results: At 1000 mg/kg, EC had superior seizure-inducing potential, longer seizure latency but shorter duration than PTZ. Acute administration of EC increased blood sugar, decrease serum phospholipids and triglycerides. Daily treatment for 28 days increased brain weight, and lysosomal enzyme activities neuroinflammatory indicators (TNF?, IL-4, IL-8, IL-9 and IL-10) except IL-2. Treatment also resulted in the elevation of malondialdehyde (MDA) level but reduction in catalase (CAT) and reduced glutathione (GSH) levels decreased, decreased acetylcholinesterase activity. Photomicrographs of the cerebral cortex of treated animals showed degenerated axonal and dendritic projections as well as soma filled with neurofibrillary tangles. Conclusions: EC neurotoxicity may be due to inhibition of GABAergic neurotransmission resulting in oxidative, inflammatory and eventual neurodegenerative damages.