Abstract

Despite mixed results with laboratory animals, recent studies indicate that elevated intake of fluoride in drinking water may, depending on circumstances, cause high blood pressure (hypertension) in humans. Although primary or essential hypertension has various causes and is known to be associated with higher levels of vasoconstrictors like endothelin 1 and thromboxane 2, increased oxidative stress, vascular inflammation, aortic stiffness, and magnesium deficiency, new evidence connecting this most common form of hypertension with increased intake of fluoride clearly deserves further investigation.

• Related Studies :

  • Cytoprotective effects of curcumin on sodium fluoride-induced intoxication in rat erythrocytes

    Curcumin is well known for its potent antioxidant activity. The result of numerous studies showed that antioxidants can protect against fluoride-induced toxicity. In the present study, protective effects of curcumin against sodium fluoride-induced toxicity in rat erythrocytes were evaluated. Curcumin (10 and 20 mg/kg) and vitamin C (10 mg/kg) were

  • Lipid peroxidation in fluorosis and the protective role of dietary factors

    The influence of chronic Fl intoxication on lipid peroxidation and the state of the antioxidant system was studied in rats on different diets. Chronic Fl intoxication inhibited antioxidant activity and caused an increase in the rate of peroxidation and the level of lipoperoxides in liver, brain and serum. Diets with

  • Toxic effects of fluoride and chlorpyrifos on antioxidant parameters in rats: protective effects of vitamins C and E

    In continuing our studies on the effects of fluoride (F) on the toxicity of pesticides, we investigated the interaction of 1 ppm and 10 ppm F in the drinking water of rats orally administered 1 and 10 mg chlorpyriphos/kg bw/day, alone and in combination for 28 days. Changes in antioxidant

  • Effects of fluoride and caffeine on the metabolism and motility of ejaculated bovine spermatozoa

    Treatment of washed, ejaculated bovine sperm with 30 mM sodium fluoride immobilized the cells in a characteristically rigid form. In cells metabolizing endogenous substrates, fluoride decreased respiration by about 60%, but did not inhibit the cells' ability to produce adenosine-5'-triphosphate (ATP) via oxidative phosphorylation and did not block access to

  • In vivo protective effects of gallic acid isolated from peltiphyllum peltatum against sodium fluoride-induced oxidative stress in rat erythrocytes

    Gallic acid has been identified as an antioxidant component of the edible and medicinal plant Peltiphyllum peltatum. The present study examined its potential protective role against sodium fluoride (NaF)-induced oxidative stress in rat erythrocytes. Oxidative stress was induced by NaF administration through drinking water (1030.675 mg m-3 for one week).

• Related FAN Content :

  • Nutrient Deficiencies Enhance Fluoride Toxicity

    It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,

  • Fluoride & Oxidative Stress

    A vast body of research demonstrates that fluoride exposure increases oxidative stress. Based on this research, it is believed that fluoride-induced oxidative stress is a key mechanism underlying the various toxic effects associated with fluoride exposure. It is also well established that fluoride's toxic effects can be ameliorated by exposure

  • Fluoride Exposure Increases Metabolic Requirement for Magnesium

    Fluoride's toxicity is significantly enhanced in the presence of nutritional deficiencies. Similarly, fluoride exposure increases the body's requirement for certain nutrients. An individual with a high intake of fluoride, for example, will need a proportional increase in calcium to avoid the mineralization defects (e.g., osteomalacia) that fluoride causes to bone

  • Skeletal Fluorosis & Individual Variability

    One of the common fallacies in the research on skeletal fluorosis is the notion that there is a uniform level of fluoride that is safe for everyone in the population. These "safety thresholds" have been expressed in terms of (a) bone fluoride content, (b) daily dose, (c) water fluoride level, (d) urinary fluoride level, and (e) blood fluoride level. The central fallacy with each of these alleged safety thresholds, however, is that they ignore the wide range of individual susceptibility in how people respond to toxic substances, including fluoride.

  • Fluoride Exposure Aggravates the Impact of Iodine Deficiency

    A consistent body of animal and human research shows that fluoride exposure worsens the impact of an iodine deficiency. Iodine is the basic building block of the T3 and T4 hormones and thus an adequate iodine intake is essential for the proper functioning of the thyroid gland. When iodine intake is inadequate during infancy and