Fluoride Action Network

Abstract

Background: Low Fluoride use has been advocated as a therapeutic agent for delaying tooth decay however, high fluoride exposure has been associated with behavioral changes, low IQ, and altered brain functions and development. Although Fluoride generally does not generate free radicals but is still implicated in free radical associated damage to biomembranes and cellular biomolecules in various tissues and organs

Methods: The present study was conducted to investigate the alterations in brain and intestinal oxidative stress after chronic fluoride ingestion for varying durations (20, 40 and 90 days) in rats. 30 animals were randomized into 2 groups (control and fluoride treated) of 15 animals each. Test group animals were given sodium fluoride (25mg/kg body weight) dissolved in double distilled water orally for the study period. Animals had access to water and standard pellet diet ad libitum throughout the treatment period. Overnight fasted animals from each group were euthanized on 20, 40 and 90th day. Various antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione-s-transferase (GST) were measured in post mitochondrial supernatant (PMS).

Results: All antioxidant enzymes decreased in both tissues for the three studied durations. Decrease in SOD activity was highest for 40 days treatment in brain (67.17%) and intestine (66.44%). Catalase activity showed a regular decrease in intestine (10.28, 14.85, and 24.17%) and in brain (36.24, 65.81, and 75.10%) after 20, 40 and 90 days respectively. Although GR activity was decreased in both tissues except in intestine (increased 25.41% after 40 days), but they didn’t reveal duration specific trend. Alterations in GST levels were similar to GR with maximum decrease for 20 days in intestine (77.92 %) and for 40 days in brain (42.49 %).

Conclusions: From our results we conclude that fluoride exposure results in alterations in the antioxidant defense enzymes in an age related manner and speculate that in long term exposures it may be related to age related neurodegenerative diseases especially when it interacts with aluminum. We also suggest more age related studied with combined exposures to fluoride and aluminum should be carried out with a special focus on Alzheimer’s disease.