Aims: Fluoride known environmental pollutant and also neurotoxicant and functions through oxidative stress and excitotoxicity mechanisms in brain. Balanced levels of neurotransmitters (NTs) are essential for healthy condition while their imbalanced status leads to illnesses and associated abnormalities. The present study focused on maternal as well as post-natal exposure of fluoride and its effects on NTs and protective effects of Abelmoschus moschatus seed extract through regulation of NTs system.
Materials and Methods: The pregnant Wistar rats were randomly categorized into six groups of five animals each. Group I is of control rats which received normal tap water. Group II is sodium fluoride (NaF) exposed group with 20 ppm (or 20 mg/kg body wt.) in their drinking water. Group III and Group IV rats were treated with A. moschatus aqueous (AMAE) and ethanolic (AMEE) extract (at the rate of 300 mg/kg body wt./day/rat), respectively, along with NaF water (20 ppm). Group V and Group VI rats were treated with AMAE and AMEE (300 mg/kg body wt./day/rat) respectively. On 1st, 7th, 14th, 21st, and 30th day (postpartum days), the pups were sacrificed to assess NTs levels of brain of all experimental groups.
Results: The epinephrine and glutamate levels were increased, while nor-epinephrine, dopamine, serotonin, and acetylcholine levels were decreased significantly (P < 0.001) in NaF-fed rats with respect to control group and were restored on the treatment of AMAE and AMEE toward control. In addition, monoamine oxidase (MAO-A and MAO-B) activity also increased in NaF intoxicated rats than the control, and its activity was reverted to normal in NaF-received rats along with AMAE and AMEE.
Discussion: These findings suggested that NaF exposure during developmental stages alter the NTs levels where as their levels are regulated on the treatment of A. moschatus toward NaF. AMEE showed better efficacy over AMAE.
Conclusion: It can be concluded that the seed extract of Abelmoschus has therapeutically significant efficacy in protection from NaF toxicity.