Abstract
In our experiment, the 1-month effects of caffeine (Caff) and fluoride (F) administered separately and together on nitric oxide and total antioxidant status in serum, brain, liver and kidney of rats were investigated. Also, the influence of caffeine on fluoride excretion with urine was studied. Thirty adult male Wistar rats were divided into five equal groups of six each: (I) controls drinking tap water; (II) controls drinking tap water and receiving intragastrically 0.5 ml of tap water; (III) animals receiving 25 mg F/L in drinking water; (IV) animals receiving 4.7 mg Caff/kg bw/day; (V) animals receiving 25 mg F/L in drinking water and 4.7 mg Caff/kg bw/day. The applied fluoride caused increase of nitric oxide level (NO), intensified lipid peroxidation (TBARS) and decreased total antioxidant status in serum (TAS), brain, kidney and liver. Caffeine administered intragastrically, as an antioxidant, was relatively efficient in alleviating these adverse effects of F. In rats treated only with fluoride the F excretion in urine significantly increased in an exposure-time dependent-manner and did not change both in rats treated with Caff and co-exposed to Caff and F.
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A possible mechanism for combined arsenic and fluoride induced cellular and DNA damage in mice
Arsenic and fluoride are major contaminants of drinking water. Mechanisms of toxicity following individual exposure to arsenic or fluoride are well known. However, it is not explicit how combined exposure to arsenic and fluoride leads to cellular and/or DNA damage. The present study was planned to assess (i) oxidative stress
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Effects of individual and combined exposure to sodium arsenite and sodium fluoride on tissue oxidative stress, arsenic and fluoride levels in male mice.
Arsenic and fluoride are potent toxicants, widely distributed through drinking water and food and often result in adverse health effects. The present study examined the effects of sodium meta-arsenite (100 mg/l in drinking water) and sodium fluoride (5 mg/kg, oral, once daily), administered either alone or in combination for 8
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Conceivable amelioration of NaF-induced toxicity in liver, kidney and brain of chicken by black tea extract: an in vitro study.
Sodium fluoride (NaF) toxicity on enzymatic and non-enzymatic oxidative stress markers of chicken liver, kidney and brain homogenate in in vitro condition where studied in present investigation. We studied alteration in the activity of superoxide dismutase (SOD), catalase (CAT), lipid peroxidation (LPO) and glutathione (GSH) content to study oxidative stress.
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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
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Evaluation of free radical-scavenging and anti-oxidant properties of black berry against fluoride toxicity in rats
Oxidative damage to cellular components such as lipids and cell membranes by free radicals and other reactive oxygen species is believed to be associated with the development of degenerative diseases. Fluoride intoxication is associated with oxidative stress and altered anti-oxidant defense mechanism. So the present study was extended to investigate
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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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Fluoridation of drinking water and chronic kidney disease: Absence of evidence is not evidence of absence
A fairly substantial body of research indicates that patients with chronic renal insufficiency are at an increased risk of chronic fluoride toxicity. Patients with reduced glomerular filtration rates have a decreased ability to excrete fluoride in the urine. These patients may develop skeletal fluorosis even at 1 ppm fluoride in the drinking water.
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Factors which increase the risk for skeletal fluorosis
The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.
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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 as a Cause of Kidney Disease in Humans
Because the kidney is exposed to higher concentrations of fluoride than all other soft tissues (with the exception of the pineal gland), there is concern that excess fluoride exposure may contribute to kidney disease - thus initiating a "vicious cycle" where the damaged kidneys increase the accumulation of fluoride, causing
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