Abstract
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 administrated intraperitoneally for 1 week followed by sodium fluoride (600 ppm) treatment for next week. Erythrocytes were isolated and superoxide dismutase and catalase activities as well as the levels of reduced glutathione, and lipid peroxidation were measured. The level of malondialdehyde in sodium fluoride treated rats (595.13 ± 20.23 nmol/g Hb) increased compared to the normal rats (315.44 ± 9.76 nmol/g Hb). Animals which were pretreated with curcumin at 20 mg/kg for 1 week prior to sodium fluoride intoxication showed significant reduction in the malondialdehyde level (320.22 ± 9.28 nmol/g Hb). Also, pretreated with curcumin (20 mg/kg) and vitamin C restored the superoxide dismutase and catalase activities and modified the level of reduced glutathione compared with control group (p > 0.01).
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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
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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 role of quercetin against sodium fluoride-induced oxidative stress in the rat brain
CONTEXT: Quercetin is a well known aglycone flavonoid that is widely found in different food sources. OBJECTIVE: In this study, the in vivo neuroprotective potential of quercetin against sodium fluoride-induced oxidative stress was evaluated. MATERIALS AND METHODS: Wistar rats were divided into five treatment groups and then subjected to daily
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Protective role of gallic acid on sodium fluoride induced oxidative stress in rat brain
Gallic acid is known as a potent antioxidant active compound of the edible and medicinal plant Peltiphyllum peltatum. The main objective of this study was to evaluate the neuroprotective effects of gallic acid against sodium fluoride induced oxidative stress in rat brain. Gallic acid (10 and 20 mg/kg) and vitamin C
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Endogenous and exogenous antioxidants status in seminal plasma of skeletal fluorotic patients
Fluoride contamination in water (>1.5ppm) is the global problem for health in general. Fluoride has been reported to be a causative factor for male infertility. However, limited scientific literature is available on this aspect. The objective of the present study was to examine the fluoride induced oxidative burden and its
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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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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.
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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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Kidney Patients Are at Increased Risk of Fluoride Poisoning
It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients
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