Abstract
Excess fluoride intake could induce apoptosis in the cells. As an essential micronutrient and cytoprotectant, zinc is involved in many types of apoptosis. Here, we studied the effects of zinc and ZIP1 on fluoride-induced apoptosis in mouse MC3T3-E1 cells and examined the underlying molecular mechanisms. Our study found that fluoride not only inhibited cell proliferation and increased the intracellular reactive oxygen species (ROS) but also induced cell apoptosis. Whereas pretreatment with zinc significantly attenuated fluoride-induced ROS production and partly protected cells against fluoride-induced apoptosis through MAPK/ERK signaling pathway. Our study also found that fluoride upregulated the expression of ZIP1 in a time-dependent manner. Moreover, overexpression of ZIP1 also inhibited fluoride-induced apoptosis by activation of PI3K/Akt pathway. This cytoprotective effect of zinc and ZIP1 may be new factors that affect the physiological activity of fluoride and need study further.
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Association Between Antioxidant Nutrients, Oxidative Stress-Related Gene Polymorphism and Skeletal Fluorosis in Guizhou, China.
Background: Oxidative stress plays an important role in the pathogenesis of endemic fluorosis. We analyzed associations between oxidative stress-related gene polymorphisms (PON1 rs662, CAT rs769217, rs2300182, and SOD2 rs11968525) and skeletal fluorosis, and examined potential gene–environment interactions with dietary vitamin C, vitamin E, zinc, and selenium intake. Methods: A cross-sectional study
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Zinc protection from fluoride-induced testicular injury in the bank vole (Clethrionomys glareolus)
Previous work has shown that a high fluoride intake in rodents leads to histopathological changes in the germinal epithelium of testes that is associated with zinc deficiency. The purpose of this study was to determine whether supplemental dietary Zn would protect against testicular toxicity induced by fluoride in a small
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Influence of supplementary vitamins and minerals on lipid peroxidation and redox state in heart, kidney and liver of rats exposed to fluoride.
The effect of fluoride (F) and supplementary vitamins and minerals on lipid peroxidation (LPO) and redox state (RS) in heart , kidney and liver of 40 (4 groups of 10) male Wistar rats were studied. One group of rats was left untreated as control, group 1 was received 5 mg/l
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Neuroprotective effect of ascorbic acid and ginkgo biloba against fluoride caused neurotoxicity
Excessive consumption of fluoride through drinking water or other sources lead to skeletal and dental fluorosis. According to the world health organization 23 nations are facing the problem of fluorosis. In the recent past researchers describe the non-skeletal fluorosis where soft tissues and major organs are the victims of fluoride
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Changes in basic metabolic elements associated with the degeneration and ossification of ligamenta flava
OBJECTIVE: To determine the association between levels of basic metabolic elements and degeneration and ossification of the ligamentum flavum (LF). SUBJECTS: Fourteen consecutive patients with degenerative lumbar stenosis, 11 with ossification of the thoracic ligamenta flava, and 11 control subjects. METHODS: The basic elements of calcium (Ca), phosphorus (P), magnesium (Mg), zinc
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Fluoride Is Not an Essential Nutrient
In the 1950s, dentists believed that fluoride was a “nutrient.” A nutrient is a vitamin or mineral that is necessary for good health. Dentists believed that fluoride ingestion during childhood was necessary for strong, healthy teeth. A “fluoride deficiency” was thus believed to cause cavities, just like a deficiency of calcium can
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Fluoride & Rickets
One of fluoride's most well-defined effects on bone tissue is it's ability to increase the osteoid (unmineralized bone) content of bone. When bones have too much osteoid, they become soft and prone to fracture -- a condition known as osteomalacia. When osteomalacia develops during childhood, it is called "rickets." The potential for fluoride
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Fluoride Exposure Increases Metabolic Requirement for Calcium & Vitamin D
It is well known that individuals with nutrient deficiencies are more susceptible to fluoride toxicity, including fluoride's bone effects. As discussed in the following studies, fluoride increases the skeleton's need for calcium (and vitamin D) by increasing the amount of unmineralized tissue (osteoid) in the bone. When insufficient calcium and
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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
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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
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