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Sulfite, commonly used as a preservative in foods, beverages, and pharmaceuticals, is a very reactive and potentially toxic molecule which is detoxified by sulfite oxidase (SOX). Changes induced by aging may be exacerbated by exogenous chemicals like sulfite. The aim of this study was to investigate the effects of ingested sulfite on visual evoked potentials (VEPs) and brain antioxidant statuses by measuring superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities. Brain lipid oxidation status was also determined via thiobarbituric acid reactive substances (TBARS) in normal- and SOX-deficient aged rats. Rats do not mimic the sulfite responses seen in humans because of their relatively high SOX activity level. Therefore this study used SOX-deficient rats since they are more appropriate models for studying sulfite toxicity. Forty male Wistar rats aged 24 months were randomly assigned to four groups: control (C), sulfite (S), SOX-deficient (D) and SOX-deficient + sulfite (DS). SOX deficiency was established by feeding rats with low molybdenum (Mo) diet and adding 200 ppm tungsten (W) to their drinking water. Sulfite in the form of sodium metabisulfite (25 mg kg(-1) day(-1)) was given by gavage. Treatment continued for 6 weeks. At the end of the experimental period, flash VEPs were recorded. Hepatic SOX activity was measured to confirm SOX deficiency. SOX-deficient rats had an approximately 10-fold decrease in hepatic SOX activity compared with the normal rats. The activity of SOX in deficient rats was thus in the range of humans. There was no significant difference between control and treated groups in either latence or amplitude of VEP components. Brain SOD, CAT, and GPx activities and brain TBARS levels were similar in all experimental groups compared with the control group. Our results indicate that exogenous administration of sulfite does not affect VEP components and the antioxidant/oxidant status of aged rat brains.

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In our study, the protective effects of vitamin E and Se (selenium) against cigarette smoke hazards on second-hand smoker (passive smoker) male mice (Balb/c) were investigated. Serum MDA levels in the smoke-exposed mice were found higher than serum MDA levels of control mice and Se- and vitamin E-treated mice. But, the MDA levels of smoke-exposed plus Se- and vitamin E-treated mice were found lower than MDA levels of smoke-exposed mice at the end of the three and five months. According to these results, application of vitamin E and Se, when given to smoke-exposed mice together, had an additive protective effect against cigarette smoke hazards (p < 0.05). Vitamin E also had protective effect on formation of 8-OHdG in smoke-exposed mice. The serum 8-OHdG amounts of smoke-exposed plus vitamin E-treated mice were found low, but the serum 8-OHdG amounts of smoke-exposed mice were found high. Also 8-OHdG levels in the serum of the smoke-exposed mice were increased which occurs as a result of DNA oxidation (p < 0.05). At the end of the three and five months, COMT (catechol-o-methyl transferase) activity of smoke-exposed mice livers were increased but, vitamin E and/or Se showed a significant protective effect on changing of COMT activity only at the end of the 5 months. Our results showed that MDA levels and 8-OHdG amounts were increased in the serum of smoke-exposed mice. On the other hand, vitamin E and Se had an additive protective effect against increasing MDA level. Also vitamin E had a protective effect against formation of 8-OHdG amounts and COMT activity alterations.