Abstract
Highlights
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- Fluoride exposure alters acetylcholinesterase activity.
- Glutamate transport is modulated after fluoride exposure.
- Oxidative stress is regulated by prolonged fluoride exposure.
Fluoride is an essential chemical found in dental preparations, pesticides and drinking water. Excessive fluoride exposure is related to toxicological and neurological disruption. Zebrafish are used in translational approaches to understand neurotoxicity in both biomedical and environmental areas. However, there is no complete knowledge about the cumulative effects of fluoride on neurotransmission systems. Therefore, the aim of this study was to evaluate whether prolonged exposure to sodium fluoride (NaF) alters cholinergic and glutamatergic systems and oxidative stress homeostasis in the zebrafish brain. Adult zebrafish were used, divided into four experimental groups, one control group and three groups exposed to NaF at 30, 50 and 100?mg.L-1 for a period of 30 days. After NaF at 30 mg.L-1 exposure, there were significant decreases in acetylcholinesterase (29.8%) and glutamate uptake (39.3%). Furthermore, thiobarbituric acid-reactive species were decreased at NaF 50 mg.L-1 (32.7%), while the group treated with NaF at 30 mg.L-1 showed an increase in dichlorodihydrofluorescein oxidation (41.4%). NaF at 30 mg.L-1 decreased both superoxide dismutase (55.3%) and catalase activities (26.1%). The inhibitory effect observed on cholinergic and glutamatergic signalling mechanisms could contribute to the neurodegenerative events promoted by NaF in the zebrafish brain.
Graphical abstract
