Abstract
The present study was designed to investigate the anti-genotoxic effect of Ocimum sanctum on fluoride induced genotoxicity and its impact on oxidative stress. Exposure to fluoride can mainly occur through drinking water when the levels far exceed the permissible limit. Fluorosis is a serious problem the world over resulting in damage to DNA. Micronuclei assessment from bone marrow and peripheral blood was used in the present study to assess the damage to DNA. Sodium fluoride in a single dose (30 mg/kg, i.p.) was used to induce micronuclei in albino mice. Treatment with the aqueous extract of Ocimum sanctum was initiated in the single dose study (100, 400 & 800 mg/kg) and as a time course for 1 day, 3 days and 7 days (100 mg/kg). 24 h after injecting sodium fluoride, the animals were sacrificed and micronuclei were determined from smears prepared from bone marrow and peripheral blood. The antioxidant impact of the extract was determined using ferric ion reducing capacity of plasma and thiobarbituric acid reactive substances as a measure of lipid peroxidation. All doses were capable of preventing the formation of micronuclei but 100 mg/kg of the aqueous extract was most efficacious as a single dose and in the time course study. The beneficial effect of Ocimum sanctum is possibly due to the synergistic action of constituents like polyphenols, triterpenoids, and flavonoids.
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Evaluation of multi-endpoint assay to detect genotoxicity and oxidative stress in mice exposed to sodium fluoride
Fluoride compounds are naturally present in soil, water and food. The objective of this study was to investigate the genotoxic and oxidative damage induced by chronic fluoride exposure on mammalian cells in vivo. For this purpose, the genotoxic potential was investigated in bone marrow cells by the micronucleus test, chromosome
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Toxicity assessment of sodium fluoride in Drosophila melanogaster after chronic sub-lethal exposure
Sodium fluoride (NaF), one of the most frequently used fluoride compound is composed of Na+ and F-. Apart from its use in water fluoridation, NaF also acts as a major component for different dental products like toothpastes, gels and mouth rinses etc. The present study was carried out to explore the toxic impact of chronic
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Ameliorative effects of N-acetylcysteine on fluoride-induced oxidative stress and DNA damage in male rats' testis
This study was to elucidate DNA damage in rats treated with sodium fluoride (NaF) by performing 8-Hydroxy-2-deoxyguanosine (8-OHdG) immunohistochemical staining assays on seminiferous tubules of rats' testis, and also to evaluate the protective effects of N-acetylcysteine (NAC) on spermatogenesis. Male Sprague Dawley (SD) rats were exposed to a single dose
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DNA damage, apoptosis and cell cycle changes induced by fluoride in rat oral mucosal cells and hepatocytes
AIM: To study the effect of fluoride on oxidative stress, DNA damage and apoptosis as well as cell cycle of rat oral mucosal cells and hepatocytes. METHODS: Ten male SD rats weighing 80-120 g were randomly divided into control group and fluoride group, 5 animals each group. The animals in
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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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Fluoride & Osteosarcoma: A Timeline
Several human epidemiological studies have found an association between fluoride in drinking water and the occurrence of osteosarcoma (bone cancer) in young males. These studies are consistent with the National Toxicology Program's (NTP) cancer bioassay which found that fluoride-treated male rats had an dose-dependent increase in osteosarcoma. Although a number of studies have failed to detect an association between fluoride and osteosarcoma, none of these studies have measured the risk of fluoride at specific windows in time, which based on recent results, is the critical question with respect to fluoride and osteosarcoma.
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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/Osteosarcoma Link Is Biologically Plausible
The "biological plausiblility" of a fluoride-osteosarcoma link is widely acknowledged in the scientific literature. The biological plausibility centers around three facts: 1) Bone is the principal site of fluoride accumulation, particularly during the growth spurts of childhood; 2) Fluoride is a mutagen when present at sufficient concentrations, and 3) Fluoride can stimulate the proliferation of osteoblasts (bone-forming cells).
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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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Fluoride's Mutagenicity: The "Oral Health Research Institute's" Studies
Although many in vitro and in vivo studies have detected mutagenic effects from fluoride exposure, the Oral Health Research Institute at Indiana University's School of Dentistry has repeatedly failed to find any such effect in multiple studies on the subject.
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