The effect of sulfite on apoptosis and relationship with electrophysiological parameters in brain

Humans are exposed to both endogenous and exogenous sulfites through separate sources. Whereas endogenous sulfites are formed through metabolism of some aminoacids, exogenous sulfites can stem from drugs, food consumption and inhalation of air pollution. It is a known fact that sulfite radicals, which are produced due to high amounts of sulfite injection or reduced oxidation capacity of the body, have negative effects on biomolecules. Therefore, in our study we investigated the effect of SO32- on the apoptosis and the relationship of this effect with electrophysiological parameters.In the present study, 40 wistar rats were divided randomly into four groups; control group (C), sulfite (Na2S2O5) administered group (S), PLA2 inhibitor (Quinacrine) administered group (Q) and Quinacrine+Sulfite administered (QS) group. Sulfite and Quinacrine were administered at the doses of 100 mg/kg/day via gavage and 10 mg/kg/day intraperitoneal injection respectively for thirty five-days. At the end of the period, somatosensory evoked potentials (SEPs) were recorded, blood samples and brain tissues were collected for biochemical analysis.The plasma-S-sulfonate levels, as an indicator of exposure to sulfur dioxide, were increased in the S and the QS groups. In our study, the formation of thiobarbituric acid reactive substances (TBARS) were used to determine the lipid peroxidation. A statistically significant increase in TBARS values was observed in other experimental groups compared with the control group. On the other hand, TBARS values were decreased in the S group compared with the QS group, but this decline was not significant.In the western blot and densitometric analysis of brain tissues, a significant increase in the level of sPLA2 of S, Q and QS groups was detected compared with the C group. Quinacrine treatment had no significant effect on the increased sPLA2 level of the sulfite administered group. Somatosensory evoked potential latencies did not change in the Q group compared with the C group, whereas a statistically significant prolongation of all wave forms was observed in the S group and the latencies of P1 and N1 components prolonged in the QS group. It was observed that N1, P2, N2 components of SEP latencies were shortened in the QS group compared with the latencies of S group, those of P1 and N1 components were statistically longer in the QS group than in the Q group.The level of caspase-3 enzyme was increased in the S group, however no change was observed in groups Q and QS compared with the C group. The data obtained from the tunnel analysis to determine the cells underwent apoptosis were consistent with our caspase-3 findings. While tunel positive cells were detected in the somatosensory area of the sulfite groups, they were not detected in the somatosensory area of C, Q and QS groups.As a result of our study, it is determined that the daily normal dietary intake of sulfide increased lipid peroxidation, induced apoptosis and prolonged SEP latencies. It is thought that sPLA2 enzyme could play a role in the detrimental effect of sulfite.Key words: sulfite, somatosensory evoked potentials (SEP), lipid peroxidation,secretory phospholipase A2 (sPLA2)