Fluorosis is a serious public health problem in many parts of the world where drinking water contains more than 1 ppm of fluoride. The main manifestations of skeletal fluorosis are crippling bone deformities, spinal compressions, and restricted movements of joints. Although fluorosis is irreversible, it could be prevented by appropriate and timely intervention through understanding the process at biochemical and molecular levels. As in the case of many chronic degenerative diseases, increased production of reactive oxygen species (ROS) and lipid peroxidation has been considered to play an important role, even in the pathogenesis of chronic fluoride toxicity. However, there is inconclusive proof for an altered oxidative stress and antioxidant balance in fluorosis, and the existing data are not only conflicting but also contradictory. In the present communication we have evaluated the antioxidant defense system (both enzymatic and nonenzymatic) and lipid peroxidation in both humans from an endemic fluorosis area (5 ppm fluoride in the drinking water) and in rabbits receiving water with 150 ppm of fluoride for six months. There was no significant difference in lipid peroxidation, glutathione, and vitamin C in the blood of human fluorotic patients and fluoride-intoxicated rabbits as compared to respective controls. Neither were there any changes in the activities of catalase, superoxide dismutase, glutathione peroxidase, or glutathione S-transferase in the blood due to fluoride intoxication (of rabbits) or fluorosis in humans. The results together do not subscribe to oxidative stress theory in fluorosis. Thus, in the absence of clear proof of oxidative damage and to counter toxic effects of fluoride through supplementation of antioxidants, extensive investigations are needed to conclusively prove the role of oxidative stress in skeletal fluorosis.
Objective: To evaluate the effect of tamarind (Tamarindus indicus) ingestion on excretion of fluoride in school children. Design: Randomized, diet-control study. Subject: Twenty healthy boys were included and 18 of them completed the study. Interventions: Each subject consumed 10 g tamarind daily with lunch for 18 days at the social welfare boys' hostel. The nutrient composition of the daily diet was constant throughout the experimental period. Results: Tamarind intake led to significant increase (P < 0.001) in the excretion of fluoride in 24 h urine (4.8 AE 0.22 mg=day) as compared to excretion on control diet (3.5 AE 0.22 mg=day). However, excretion of magnesium and zinc decreased significantly (7.11 AE 1.48 mg of Mg and 252.88 AE 12.84 mg of Zn per day on tamarind diet as compared to 23.39 AE 3.68 mg of Mg and 331.78 AE 35.31 mg Zn per day on control diet). Excretion of calcium and phosphorous were not significantly different while creatinine excretion decreased with tamarind intake (225.66 AE 81 mg creatinine=day with tamarind and 294.5 AE 78.76 mg creatinine=day without tamarind). Conclusion: Tamarind intake is likely to help in delaying progression of fluorosis by enhancing urinary excretion of fluoride.
After almost 40 years of water fluoridation in the United States, its effect in the food chain is now being appreciated. Current surveys indicate significant increases in the F content of infant formulas, toddler cereals, fruit juices, and popular beverages, largely because fluoridated water is used in their processing. According to the best estimates, the daily total F intake of children from foods, beverages including water, and other sources such as unintentional ingestion of dentifrices containing F is on the rise, although it is generally within the currently accepted range for this age group. It is encouraging to note that appropriate steps are now being taken by some manufacturers of infant formulas to monitor F levels and keep them within an acceptable range. Because of the increasing contribution of dietary F to total F intake, dietary F should be included in any estimate of daily total F intake in children before F supplements are prescribed, whether the children live in communities with fluoridated or nonfluoridated water. To achieve this goal, it is essential to develop a generally accepted, sensitive method for the analysis of F in foods and beverages. This should help develop the bioavailability profiles for individual foods and beverages essential for accurate assessment of dietary F intake. Fluoridated salt, used in some European countries, appears to be the only food ingredient currently in use as an alternative to water fluoridation. Attempts to utilize staple foods and beverages as vehicles for systemic F delivery have generally failed because of the decreased bioavailability of F in such products, and because it is difficult to make them available to the general population and especially to the lower socioeconomic segments of the population.
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