Akdeniz University, Faculty of Medicine, Department of Biophysics, Turkey.
Neurotoxicol Teratol. 2011 Mar-Apr;33(2):244-54. doi: 10.1016/j.ntt.2010.09.002. Epub 2010 Sep 25.
The aim of this study was to clarify the dose-dependent effect of sulfite (SO₃²⁻) ingestion on brain and retina by means of electrophysiological and biochemical parameters. Fifty two male Wistar rats, aged 3 months, were randomized into four experimental groups of 13 rats as follows; control (C), sulfite treated groups (S(1); 10 mg/kg/day, S₂; 100mg/kg/day, S₃; 260 mg/kg/day). Control rats were administered distilled water, while the other three groups were given sodium metabisulfite (Na₂S₂O₅) of amounts mentioned above, via gavage for a period of 35 days. All components of visual evoked potential (VEP) were prolonged in S₂ and S₃ groups compared with S₁ and C groups. Plasma-S-sulfonate levels, which are an indicator of sulfur dioxide (SO₂) exposure, were increased in Na₂S₂O₅ treated groups in a dose-dependent manner. Furthermore, the significant increments in thiobarbituric acid reactive substances (TBARS) and 4-hydroxy-2-nonenal (4-HNE) levels occurred with increasing intake of Na₂S₂O₅. Though not significant, glutathione (GSH) and oxidized glutathione (GSSG) levels were observed to decrease with increasing doses of Na₂S₂O₅. In conclusion, Na₂S₂O₅ treatment in rats caused a dose-dependent increase in lipid peroxidation and all VEP latencies. The data indicate that lipid peroxidation could play an important role in sulfite toxicity.
本研究旨在通过电生理和生化参数阐明亚硫酸盐（SO₃²⁻）摄入对脑和视网膜的剂量依赖性影响。将 52 只 3 月龄雄性 Wistar 大鼠随机分为 4 个实验组，每组 13 只；对照组（C）、亚硫酸盐处理组（S₁；10mg/kg/天，S₂；100mg/kg/天，S₃；260mg/kg/天）。对照组大鼠给予蒸馏水，而其他三组大鼠通过灌胃给予上述剂量的偏亚硫酸钠（Na₂S₂O₅），持续 35 天。与 S₁和 C 组相比，S₂和 S₃组的视觉诱发电位（VEP）的所有成分均延长。血浆-S-亚磺酸盐水平（SO₂暴露的指标）在 Na₂S₂O₅处理组中呈剂量依赖性增加。此外，随着 Na₂S₂O₅摄入量的增加，硫代巴比妥酸反应物质（TBARS）和 4-羟基-2-壬烯醛（4-HNE）水平显著增加。虽然不显著，但观察到谷胱甘肽（GSH）和氧化型谷胱甘肽（GSSG）水平随 Na₂S₂O₅剂量的增加而降低。总之，Na₂S₂O₅ 处理大鼠导致脂质过氧化和所有 VEP 潜伏期呈剂量依赖性增加。数据表明，脂质过氧化可能在亚硫酸盐毒性中起重要作用。
