Effect of Maternal Exposure of Fluoride on Biometals and Oxidative Stress Parameters in Developing CNS of Rat

Abstract

Excessive intake of essential elements agitates elemental homeostasis resulting in their heterogeneous distribution. Distraction of these elements in central nervous system (CNS) have been demonstrated in many neurological disorders, which are vital in generating free radicals, causing oxidative stress, and contributing to neuronal maladies. The developing CNS is highly vulnerable to environmental agents, including fluoride. Fluorosis is one such disorder ensued from excessive consumption of fluoride containing water and/or foods that poses a greater threat to the life. Present study offers perturbations caused by fluoride toxicity on the level of biometal and antioxidant homeostasis and their interactions. Pregnant Wistar rats were exposed to 100- and 200-ppm fluoride (F(-)) in drinking water and controls with tap water. The pups born to them were used for the study. On 21st postnatal day, the concentration of fluoride, biometals, and oxidative stress markers were determined in discrete regions of CNS. The levels of fluoride, copper, and iron increased whereas manganese and zinc were decreased considerably. Among antioxidant enzymes, catalase, superoxide dismutase, and glutathione peroxidase were decreased and lipid peroxidation was increased with regional alterations. The correlation coefficient values among oxidative stress markers and biometals were either positive or negative and showed less significance during correlation. The results confirm that the fluoride provoked oxidative stress and biometal deformations are synergistic that successively governs the neuronal damage and developing CNS no longer prevents exacerbations of fluoride.

Pre and Post Natal Exposure of Fluoride Induced Oxidative Macromolecular Alterations in Developing Central Nervous System of Rat and Amelioration by Antioxidants

“…Zinc acts as an important antioxidant in BBB membrane stability and offering protection to membrane protein thiol groups [43], also involved in brain phospholipid metabolism [44]. The supplementation of zinc in the present study augmented its depleted levels in brain which was observed in our previous study during pre and post-natal fluoride exposure [25]. F interacts with zinc binding sites on an important DNA associated protein called protamine.…”

“…Physiologically the brain uses over 20% of the body oxygen and generates very large levels of ROS as it has poor endogenous antioxidant defense system and relies on the dietary intake of antioxidants. The ingestion of excessive F in this study significantly decreased animal (mother) growth symptomised by depressed appetite leading to the poor growth rate in pups [25]. This is because F may result in primary malnutrition by displacing other nutrients (minerals/elements) in the diet.…”

“…The accumulated F acts as a crucial factor in altering the cellular processes via other vital elemental alterations such as Fe, Cu, Zn, Se, Mn, etc. that in turn alter cellular redox homeostasis [25]. The pups treated with antioxidants have shown considerable reduction in F levels, this may be attributed to the antioxidants in restoring the perturbed redox status and antioxidant homeostasis of cell.…”

Efficacy of lycopene against fluoride toxicity in rats

“…In this study, fluoride treatment increased LP and NO production, whereas the estimated antioxidant parameters were diminished in red blood cells and in examined heart and brain tissues. These results suggested that the balance between the oxidative system and anti-oxidant system in the rats was out of order during fluoride exposure (Narayanaswamy & Piler, 2010). The present findings are in harmony with recent observations by Inkielewicz-Stepniak and Czarnowski (2010), indicating that the excessive fluoride exposure can induce LP, specifically polyunsaturated fatty acids.…”

“…Epidemiological investigations indicated that long-term high-level fluoride intake can lead to severe damage in the metabolism of many systems and organs in animals and humans (Hassan & Yousef, 2009). Recent studies suggest that increased generation of ROS and enhanced LP have been shown to play an important role in fluorosis (Narayanaswamy & Piler, 2010).…”