Abstract

The levels of neurotransmitters and receptors in brain tissue of aborted fetuses from areas of endemic fluorosis were tested. The results showed that in 10 fetuses from a high fluoride area ranging in age from 5 to 7 months, the levels of norepinephrine, 5-hydroxytryptamine, and a1-receptor were lower, and the level of epinephrine was higher as compared with levels seen in the control fetuses from a non-endemic fluorosis area; each of these differences was statistically significant (p<0.05). Other monoamine neurotransmitters and metabolic products, such as dopamine, 5-hydroxyindoleacetic acid and 3,4-dihydroxybenzoic acid, showed nonsignificant differences (p>0.05). The results suggest that the accumulation of fluoride in the brain tissue can disrupt the synthesis of certain neurotransmitters and receptors in nerve cells, leading to neural dysplasia or other damage.

Excerpt:

The mothers of the ten fetuses that formed the subject group for this study all had dental fluorosis, with a corresponding increase in urinary fluoride, indicating that these pregnant women were suffering from chronic fluoride poisoning. The excess fluoride of the mother was passed through the placental barrier into the fetus, and from there through the blood-brain barrier to accumulate in the fetal brain, leading to a significant rise in bone and brain fluoride levels. Our results are consistent with earlier reports. Previous experiments have shown that the brains of fetuses from endemic fluorosis areas as well as fluoride-poisoned rats manifest morphological changes. Following experimental testing of the monoamine neurotransmitters in fetuses from fluorosis endemic areas, the present study found lowered levels of norepinephrine and elevated levels of epinephrine. The presence of norepinephrine in the brain allows the organism to become alert, and guards against the intensification of reflex reactions and other behavior. Norepinephrine also plays a role in the regulation of complex response mechanisms, emotions, cerebrocardiovascular function, etc. When norepinephrine levels drop the ability to maintain an appropriate state of activation in the central nervous system is weakened. The elevated levels of epinephrine could be due to a blockage of the pathway that transforms epinephrine into norepinephrine or possibly due to suppression of the relevant metabolic enzymes, causing the brain levels of epinephrine to increase, and the levels of norepinephrine to decrease.

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