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Objective <p>Exposure to fluoride above the recommended dose has been shown to have toxicological consequences on several body systems. There is a paucity of information on neurotoxic effect of exposure of varying doses of sodium fluoride (NaF) on specific brain regions. Hence, we investigated the toxicological consequences of 30- and 60-day exposure to varying doses of NaF on neurobehavioral outcomes and region-specific brain alterations in adult Wistar rats, with biochemical analyses conducted in the hippocampus and striatum, and immunohistochemical assessment of astrocytic activation in the striatum and myelin integrity in the corpus callosum.</p> Methods <p>Eighty-four Wistar rats of 100–120&#xa0;g were randomly divided into six groups. Rats in experimental groups (groups B–F) were administered NaF in deionized water at concentrations of 25, 50, 100, 150, and 300&#xa0;ppm, respectively, via oral administration for 30 and 60&#xa0;days. The control group (group A) received only deionized water for the same duration. Neurobehavioral assessments were carried out, and brain samples (striatum and hippocampus) were collected for biochemical assays and immunohistochemistry.</p> Results <p>Sodium fluoride caused a significant influence on locomotor activities and anxiety. Moreover, NaF caused a significant increase in malondialdehyde and decreased GSH level, superoxide dismutase and glutathione peroxidase activities. The activity of acetylcholinesrase (AchE) was also significantly reduced by all the administered doses of NaF. There was increased GFAP immunoreactivity in the NaF treated rats, and reduced myelin basic protein immunoreactivity in the corpus callosum.</p> Conclusions <p>NaF exposure compromises brain health by disrupting antioxidant defenses, altering neurochemical balance, promoting astrocytic activation, and inducing demyelination, ultimately resulting in neurobehavioral impairments.</p>

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30- and 60-days exposure of sodium fluoride induces neurobehavioral deficits and alters neurochemical parameters in adult Wistar rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月25日

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  • Ademola Adetokunbo Oyagbemi,
  • Ifeoluwa Awogbindin,
  • Ebenezer Oyedele Ajiboye,
  • Yusuf Ekundayo Mustapha,
  • Fatimah Salami-Ayodeji,
  • Omowumi Moromoke Femi-Akinlosotu,
  • Adedunsola Adewunmi Obasa,
  • Oluwabusayo Racheal Folarin,
  • Temitayo Olabisi Ajibade,
  • Olumayowa Olawumi Igado,
  • Adeola Temitope Salami,
  • Oluwaseun Olanrewaju Esan,
  • Taiwo Olaide Oyagbemi,
  • Adewunmi Victoria Adeogun,
  • Ishmael Festus Jaja,
  • Olufunke Eunice Ola-Davies,
  • Temidayo Olutayo Omobowale,
  • Adebowale Bernard Saba,
  • James Olukayode Olopade,
  • Sanah Malomile Nkadimeng,
  • Lyndy Joy McGaw,
  • Prudence Ngalula Kayoka-Kabongo,
  • Oluwafemi Omoniyi Oguntibeju,
  • Momoh Audu Yakubu

摘要

Objective

Exposure to fluoride above the recommended dose has been shown to have toxicological consequences on several body systems. There is a paucity of information on neurotoxic effect of exposure of varying doses of sodium fluoride (NaF) on specific brain regions. Hence, we investigated the toxicological consequences of 30- and 60-day exposure to varying doses of NaF on neurobehavioral outcomes and region-specific brain alterations in adult Wistar rats, with biochemical analyses conducted in the hippocampus and striatum, and immunohistochemical assessment of astrocytic activation in the striatum and myelin integrity in the corpus callosum.

Methods

Eighty-four Wistar rats of 100–120 g were randomly divided into six groups. Rats in experimental groups (groups B–F) were administered NaF in deionized water at concentrations of 25, 50, 100, 150, and 300 ppm, respectively, via oral administration for 30 and 60 days. The control group (group A) received only deionized water for the same duration. Neurobehavioral assessments were carried out, and brain samples (striatum and hippocampus) were collected for biochemical assays and immunohistochemistry.

Results

Sodium fluoride caused a significant influence on locomotor activities and anxiety. Moreover, NaF caused a significant increase in malondialdehyde and decreased GSH level, superoxide dismutase and glutathione peroxidase activities. The activity of acetylcholinesrase (AchE) was also significantly reduced by all the administered doses of NaF. There was increased GFAP immunoreactivity in the NaF treated rats, and reduced myelin basic protein immunoreactivity in the corpus callosum.

Conclusions

NaF exposure compromises brain health by disrupting antioxidant defenses, altering neurochemical balance, promoting astrocytic activation, and inducing demyelination, ultimately resulting in neurobehavioral impairments.