Background: The aim of this study was to investigate the mechanisms underlying possible
toxic effects of sulphite on neurodegeneration.
Methods: Male Wistar rats were assigned to each of the four groups: Control (Control), Sulphitetreated
(Sulphite), 6-hydroxydopamine (6-OHDA)-injected (6-OHDA), and sulphite-treated and 6-
OHDA-injected (6-OHDA+Sulphite). Sodium metabisulphite was administered orally by gavage at a
dose of 100 mg/kg/day for 45 days. Experimental PD was created stereotactically via the unilateral infusion
of 6-OHDA into the medial forebrain bundle (MFB). Rotarod performances, plasma Ssulfonate
levels, caspase-3 activities, Bax and Bcl-2 levels, tyrosine hydroxylase (TH) and cleaved
caspase-3 double staining were investigated.
Results: The rotarod test showed that the 6-OHDA-injected animals exhibited shorter time on the rod
mile compared to the control group; however, there was no difference between 6-OHDA and 6-
OHDA+Sulphite groups. Plasma levels of S-sulfonate in Sulphite and 6-OHDA+ Sulphite groups increased
in contrast to their corresponding control groups. Caspase-3 enzyme activity increased in the
6-OHDA group whereas it did not in control. However, sulphite treatment did not affect these activity
levels. Anti-apoptotic protein Bcl-2 concentration decreased, but the concentration of pro-apoptotic
protein Bax increased in the 6-OHDA group compared to the control group. The expression of
caspase-3 increased, while the number of tyrosine hydroxylase (TH)-positive neurons decreased in 6-
OHDA group as compared to the control groups. However, sulphite treatment had no effect on these
Conclusion: Sulphite is not a potentially aggravating factor for the activity of caspase-3 in a 6-
OHDA-induced experimental model of Parkinson’s disease.