Excess fluoride intake has been linked with various pathological conditions. The objective of the present study was to understand the role of fluoride in neurotoxic, neuroinflammatory, and neurodegenerative changes in the brain tissue of Wistar rats. Wistar rats were fed with water containing 20–100 ppm (ppm) sodium fluoride (NaF). An array of neurotransmitters (acetylcholine, dopamine, epinephrine, norepinephrine, serotonin, histamine, and glutamate) expression levels were estimated with respect to different fluoride concentrations. Additionally, its effect on the expression levels of specific neuroinflammatory markers (iNOS, COX-2, TNF-α, PKC, VEGF, and HSP-70) in brain tissues of Wister rats was assessed. An increase in NaF concentration resulted in increased fluoride deposition in the brain which in turn caused increase levels of epinephrine, histamine, serotonin, and glutamate and decreased levels of norepinephrine, acetylcholine, and dopamine in a dose-dependent manner. Tissue fluoride levels of the hippocampus, neocortex, cerebellum, spinal cord, and sciatic nerve increased significantly in fluoride fed rats. Transmission electron microscopy in the experimental animals revealed axon deterioration, myelin sheath degeneration, and dark cells with scanty cytoplasm in the spinal cord and sciatic nerve. Additionally, vacuolated swollen mitochondria were observed in the neocortex, hippocampus, and cerebellum. Results suggest excess fluoride intake modulates a set of biological marker and promote neuroinflammatory and neurodegenerative condition in Wister rats. Therefore, we conclude that the accumulation of NaF alters the neurological function which leads to neurodegenerative disorders.

过量的氟化物摄入与各种病理状况有关。本研究的目的是了解氟化物在 Wistar 大鼠脑组织的神经毒性、神经炎症和神经退行性变化中的作用。用含有 20–100 ppm (ppm) 氟化钠 (NaF) 的水喂养 Wistar 大鼠。一系列神经递质（乙酰胆碱、多巴胺、肾上腺素、去甲肾上腺素、5-羟色胺、组胺和谷氨酸）的表达水平被估计为不同氟化物浓度。此外，还评估了其对 Wister 大鼠脑组织中特定神经炎症标志物（iNOS、COX-2、TNF-α、PKC、VEGF 和 HSP-70）表达水平的影响。NaF 浓度的增加导致大脑中氟化物沉积增加，从而导致肾上腺素水平增加，组胺、血清素和谷氨酸盐，并以剂量​​依赖性方式降低去甲肾上腺素、乙酰胆碱和多巴胺的水平。在喂食氟化物的大鼠中，海马、新皮质、小脑、脊髓和坐骨神经的组织氟化物水平显着增加。实验动物的透射电镜显示轴突退化、髓鞘变性以及脊髓和坐骨神经中细胞质稀少的暗细胞。此外，在新皮质、海马和小脑中观察到空泡化的肿胀线粒体。结果表明过量的氟化物摄入会调节一组生物标志物并促进 Wister 大鼠的神经炎症和神经退行性疾病。因此，我们得出结论，NaF 的积累改变了导致神经退行性疾病的神经功能。