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The Effect of Sodium Metabisulphite on Apoptosis in the Experimental Model of Parkinson’s Disease



The aim of this study was to investigate the mechanisms underlying possible
toxic effects of sulphite on neurodegeneration.



Male Wistar rats were assigned to each of the 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 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 S-sulfonate levels, caspase-3 activities, Bax and Bcl-2 levels, tyrosine hydroxylase (TH) and
cleaved caspase-3 double staining were investigated.



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
parameters.



Sulphite is not a potentially aggravating factor for the activity of caspase-3 in a 6-
OHDA-induced experimental model of Parkinson’s disease.
