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<p>In this study, we aimed to assess the effect of sodium fluoride (NaF)-induced toxicity on oxidative stress markers and apoptosis in the brain and serum of mice, and the potential protective effect of quercetin. Forty male Swiss albino mice were divided into Control, NaF (12 mg/kg/day), Q&#xa0;(40 mg/kg/day), and NaF + Q groups and oral gavaged for 30&#xa0;days. The 8‑OHdG content in the brain tissue was higher in the NaF group than in the control group (<i>p</i> &lt; 0.05). The TOS levels of the serum were significantly higher in every treatment group (<i>p</i> &lt; 0.001), and the serum Aβ-42 levels were significantly higher in the NaF,&#xa0;Q, and NaF + Q groups (<i>p</i> &lt; 0.001) than those in the control group. The serum TAS levels were significantly declined in the NaF group and NaF + Q group (<i>p</i> &lt; 0.01). There was no significant difference among the groups in the brain Aβ-40 and Aβ-42 concentrations. Our results indicate that NaF results in oxidative stress, DNA damage in the brain being one of its triggering effects. Application of quercetin was also observed to attenuate some of these deleterious effects. These findings suggest that quercetin may exert its neuroprotective effect by modulating oxidative stress rather than directly affecting amyloid beta accumulation in brain tissue. Based on such data, quercetin could be a&#xa0;promising candidate for being a&#xa0;protective agent against fluoride-mediated oxidative stress.</p>

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Effect of quercetin on oxidative stress markers, 8-OHdG, and amyloid-beta levels in the serum and brain tissues of mice treated with sodium fluoride

  • 期刊论文

  • 发表日期：

    2026年5月26日

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  • Oktan Erboğa,
  • Sena Çenesiz

摘要

In this study, we aimed to assess the effect of sodium fluoride (NaF)-induced toxicity on oxidative stress markers and apoptosis in the brain and serum of mice, and the potential protective effect of quercetin. Forty male Swiss albino mice were divided into Control, NaF (12 mg/kg/day), Q (40 mg/kg/day), and NaF + Q groups and oral gavaged for 30 days. The 8‑OHdG content in the brain tissue was higher in the NaF group than in the control group (p < 0.05). The TOS levels of the serum were significantly higher in every treatment group (p < 0.001), and the serum Aβ-42 levels were significantly higher in the NaF, Q, and NaF + Q groups (p < 0.001) than those in the control group. The serum TAS levels were significantly declined in the NaF group and NaF + Q group (p < 0.01). There was no significant difference among the groups in the brain Aβ-40 and Aβ-42 concentrations. Our results indicate that NaF results in oxidative stress, DNA damage in the brain being one of its triggering effects. Application of quercetin was also observed to attenuate some of these deleterious effects. These findings suggest that quercetin may exert its neuroprotective effect by modulating oxidative stress rather than directly affecting amyloid beta accumulation in brain tissue. Based on such data, quercetin could be a promising candidate for being a protective agent against fluoride-mediated oxidative stress.