Abstract
The present study was aimed to evaluate curcumin as a potential natural antioxidant to mitigate the genotoxic effects of arsenic (As) and fluoride (F) in human peripheral blood lymphocytes. The study was divided into nine groups consisting of negative control, positive control treated with ethyl methane sulphonate (EMS; 1.93 mM) and curcumin control with only curcumin (1.7 microM) in blood culture. As (1.4 microM) and F (34 microM) were added alone as well as in combination, to the cultures, with and without curcumin. Cultures were analysed for chromosomal aberrations (both structural and numerical) and primary DNA damage via comet assay as the genotoxic parameters after an exposure duration of 24h. Results revealed that curcumin efficiently ameliorates the toxic effect of As and F by reducing the frequency of structural aberrations (>60%), hypoploidy (>50%) and primary DNA damage. In conclusion, curcumin mitigates the genotoxic effects of the two well known water contaminants (As and F) effectively and efficiently at the given concentration in vitro.
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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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[Modifying effect of nutrition on the mutagenic activity of phosphorus and fluorine compounds].
The test animals were fed with low-grade food during 2-5 months under conditions of acute and chronic action of hydrogen phosphide and hydrogen fluoride induced by inhalation, that resulted in the pronounced impairment of the chromosomal apparatus of the bone marrow cells in the rats. A principal possibility has been
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[A clinical study on the syndrome of arsenism and fluorosis].
A clinical study was made on 65 cases with the syndrome of arsenism and fluorosis (SAD) from March 1982 to August 1989. All the cases with this syndrome had drunk a well water containing arsenic 0.6 mg/L and fluorine 3.45 mg/L for a long period. The patients all had the
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Amelioration by melatonin of chromosomal anomalies induced by arsenic and/or fluoride in human blood lymphocyte cultures
Standard cytochemical methods were used to investigate the ameliorative effect of melatonin (0.2 mM) on chromosomal aberrations in human lymphocyte cultures induced by arsenic (As2O3, 1.4 ?M) and/or fluoride (NaF, 34 ?M). As2O3 and/or NaF generated a significant increase in the incidence of chromosomal aberrations as compared to control levels.
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Significance of Inflammation and Apoptosis in Hepatocellular Death in Rat, Co-treated with Arsenic and Fluoride.
Health effects elicited by combined environmental exposures to xenobiotics, in many instances, still remain unresolved. One of these examples is the combined toxicity of arsenic and fluoride. The present study was undertaken to delineate the role of inflammation and apoptosis in hepatocellular death caused by co-exposure to arsenic and fluoride
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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 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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Unheeded Warnings: Government Health Authorities Ignore Fluoride Risk for Kidney Patients
Despite the well known fact that individuals with kidney disease are at much higher risk of fluoride toxicity than the general population, there has yet to be any attempt in the United States, or any other country that practices mass-scale water fluoridation to determine the prevalence of fluoride-related effects (e.g.,
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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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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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