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Chronic Exposure to Sodium Fluoride Triggers Oxidative Biochemistry Misbalance in Mice: Effects on Peripheral Blood
Giza Hellen Nonato Miranda1, Bruno Alexandre Quadros Gomes2, Leonardo Oliveira Bittencourt1
1Laboratory of Functional and Structural Biology, Institute of Biological Sciences, Federal University of Pará, Belém, PA, Brazil.
Abstract:
The excessive fluoride (F) exposure is associated with damage to cellular processes of different tissue types, due to changes in enzymatic metabolism and breakdown of redox balance. However, few studies evaluate doses of F compatible with human consumption. Thus, this study evaluated the effects of chronic exposure to sodium fluoride (NaF) on peripheral blood of mice from the evaluation of biochemical parameters. The animals were divided into three groups (n = 10) and received three concentrations of NaF in the drinking water for 60 days: 0 mg/L F, 10 mg/L F, and 50 mg/L F. The blood was then collected for trolox equivalent antioxidant capacity (TEAC), thiobarbituric acid reactive substances (TBARS), concentrations of nitric oxide (NO), superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH). The results showed that doses of 10 mg/L F and 50 mg/L F were able to increase TBARS concentration and decrease NO levels and CAT activity in the blood, but there was no statistical difference for SOD levels. The 50 mg/L F group showed an increase in TEAC levels and a decrease in the GSH content when compared to the control group. In this way, oxidative changes in blood from chronic exposure to F, especially at the highest dose, indicate that F may be a toxic agent and, therefore, the long-term exposure to excessive doses should be avoided.
Insights
Excessive fluoride (F) exposure damages cellular processes. Chronic exposure to sodium fluoride (NaF) in mice increased oxidative stress markers and decreased antioxidant capacity in peripheral blood.
Area of Science:
- Biochemistry
- Toxicology
- Environmental Health
Background:
- Excessive fluoride (F) exposure can disrupt cellular processes by altering enzymatic metabolism and redox balance.
- Limited research exists on fluoride doses relevant to human consumption and their impact on biological systems.
- Understanding fluoride's effects on blood biochemistry is crucial for assessing its toxicity.
Purpose of the Study:
- To investigate the biochemical effects of chronic sodium fluoride (NaF) exposure on peripheral blood in mice.
- To evaluate oxidative stress biomarkers and antioxidant capacity following controlled NaF intake.
- To determine safe or harmful dosage ranges of fluoride relevant to human exposure.
Main Methods:
- Mice were divided into three groups and exposed to 0, 10, or 50 mg/L NaF in drinking water for 60 days.
- Peripheral blood was collected for analysis of trolox equivalent antioxidant capacity (TEAC), thiobarbituric acid reactive substances (TBARS), nitric oxide (NO), superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH).
- Biochemical parameters were measured to assess oxidative stress and antioxidant status.
Main Results:
- NaF exposure (10 and 50 mg/L) increased TBARS (lipid peroxidation marker) and decreased nitric oxide (NO) levels and catalase (CAT) activity.
- Superoxide dismutase (SOD) levels showed no significant statistical difference between groups.
- The 50 mg/L NaF group exhibited increased TEAC (antioxidant capacity) and decreased reduced glutathione (GSH) content.
Conclusions:
- Chronic fluoride exposure induces oxidative changes in peripheral blood, particularly at higher doses.
- Fluoride acts as a toxic agent, highlighting the need to avoid long-term excessive intake.
- These findings underscore the importance of monitoring fluoride levels in drinking water and public health.
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