Abstract
For decades, mouse and other rodents have been used for study of oxidative or related studies such as the effect of fluoride. It is known that rodents normally synthesize their own vitamin C (VC) due to the presence of a key enzyme in ascorbic acid synthesis, lgulonolactone-?-oxidase (Gulo), while humans do not have the capacity of VC synthesis due to the deletion of most part of the GULO gene. The spontaneous fracture (sfx) mouse recently emerged as a model for study of VC deficiency. We investigated the effect of fluoride on liver cells from wild type Balb/c and sfx mice. We found that reduction of SOD, GPx and CAT activities were reduced in both wild type and sfx mice; however, the amount of reduction in the sfx cells is more than that in Balb/c cells. In addition, while both cells increased MDA, the increase in the sfx cells is greater than that in Balb/c cells. Gene networks of Sod, Gpx and Cat in the liver of humans and mice are also different. Our study suggests that reaction to fluoride in Vitamin C deficient mice might be different from that of wild type mice.
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Tamarind seed coat extract restores fluoride-induced hematological and biochemical alterations in rats.
Fluoride (F-) is becoming an ineluctable environmental pollutant causing deleterious effects in humans. In the present study, we examined whether tamarind seed coat extract (TSCE) is beneficial against the F--induced systemic toxicity and hematological changes. Wistar rats were randomly grouped as follows: group I served as control; group II intoxicated
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Ameliorative effects of quercetin on sodium fluoride-induced oxidative stress in rat's kidney
OBJECTIVE: The in vivo nephroprotective effect of quercetin against sodium fluoride (NaF)-induced damage was studied. METHODS: Renal injury was induced by daily administration of NaF (600 ppm) through drinking water for 1 week. The levels of reduced glutathione (GSH), lipid peroxidation as well as superoxide dismutase and catalase activity of
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Mitigating effects of some antidotes on fluoride and arsenic induced free radical toxicity in mice ovary
The effects of oral administration of sodium fluoride (NaF) and/or arsenic trioxide (As(2)O(3)) (5 mg and 0.5 mg/kg body weight, respectively) for 30 days were investigated on free radical induced toxicity in the mouse ovary. The reversibility of the induced effects after withdrawal of NaF+As(2)O(3) treatment and by administration of
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Protective effects of vitamins C and E against endometrial damage and oxidative stress in fluoride intoxication
1. Fluoride (F) is an essential trace element that has protective effects against bone mineral loss. However, it becomes toxic at higher doses and induces some adverse effects on a number of physiological functions, including reproduction. The aims of this study were to examine F-induced oxidative stress that promotes production
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Antioxidant vitamin and mineral levels in sheep with fluorosis
The present study was carried out to determine the levels and changes of vitamins A, C, and E, fluoride, and calcium in 30 Morkaraman sheep with fluorosis, comparing them to unexposed healthy controls. The sheep exposed to fluoride showed significant differences in urinary fluoride and the blood levels of beta-carotene
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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,
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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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Fluoridated Water Causes Severe Dental Fluorosis in Children with Diabetes Insipidus
This section on Diabetes includes: • Fluoride & Impaired Glucose Tolerance • Fluoride & Insulin • Fluoride Sensitivity Among Diabetics • Fluoridated Water Causes Severe Dental Fluorosis in Children with Diabetes Insipidus • NRC (2006): Fluoride’s Effect on Glucose Metabolism Excessive exposure to fluoride causes a defect of the tooth enamel known as dental fluorosis. In
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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
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Dental Fluorosis & Enamel Hypoplasia in Children with Kidney Disease
Children with kidney disease are known to have high levels of fluoride in their blood and to be at risk for disfiguring tooth defects. Research suggests that high levels of fluoride in blood, which can cause the tooth defect known as dental fluorosis, can contribute to the defects that occur
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