The Effect of Sodium Metabisulphite on Locomotor Activity in the Experimental Model of Parkinson’s Disease: The Role of Cyclooxygenase

Abstract

Parkinson’s disease (PD) is characterized by a progressive and selective loss of dopaminergic neurons in substantia nigra (SN). PD is the second most common neurodegenerative disease after Alzheimer disease. Although the exact cause of disease is not known, oxidative stress, neuroinflammation, mitochondrial dysfunction and microglial activation are observed in PD. The aim of this study was to investigate the mechanism underlying possible toxic effects of sulphite on the experimental model of PD. Male Wistar rats were assigned into one of four groups Control (Control), Sulphite-treated (Sulphite), 6-hydroxydopamine (6-OHDA)-injected (6-OHDA) and sulphite-treated and 6-OHDA-injected (6-OHDA+Sulphite). Sodium metabisulphite was administered at a dose of 100 mg/kg/day for 45 days by gavage. Experimental PD was created stereotactically via the unilateral infusion of 6-OHDA into the medial forebrain bundle (MFB). 6-OHDA-injected rats exhibited reduced locomotor activity compared to control. A significant increase in catalepsy was found in the 6-OHDA-injected group as compared to the the control group. Plasma levels of S-sulfonate increased in Sulphite and 6-OHDA+Sulphite groups as compared to their respective controls. Cyclooxygenase (COX) enzyme activity, prostaglandin E2 (PGE2) and nuclear factor kappa B (NF-κB) levels increased in the 6-OHDA group as compared to control. The tyrosine hydroxylase (TH)-positive immunostainingdecreased significantly in the 6-OHDA-injected group where the sulphite and control groups had almost the same immunoreaction for the dopaminergic neurons. In conclusion, sulphite is not a potentially aggravating factor for the activity of COX and the levels of PGE2 or NF-κB in a 6-OHDA-induced experimental model of Parkinson’s disease.