Abstract
Maize seedlings of the genotype C I Sh Wx were fumigated with hydrogen fluoride gas (HF) continuously for 4, 6, 8 and 10 days. Miscrospore mitosis of the treated plants indicated the presence of fragments and bridges suggesting the occurrence of the phenomenon of breakage-fusion-bridge cycle of McClintock. This phenomenon was later confirmed by the production of endosperm mosaicisms. The period of fumigation was clearly related to the extent of the area resulting from the B-F-B cycle. Recombination values were estimated from F2 data for the regions C-sh and sh-wx. There was a significant increase in the frequency of crossing over for region I with maximum increase being for the 4 days duration. The recombination value for region II showed no significant deviation from the control. These findings indicate that HF in addition to being a mutagenic agent is also able to reduce crossing over in certain chromosome segments.
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The influence of atmospheric hydrogen fluoride on the frequency of sex-linked recessive lethals and sterility in Drosophila Melanogaster
The influence of hydrogen fluoride as an atmospheric contaminant was investigated in the Oregon-r strain of Drosophila melanogaster. Two principal parameters of mutagenicity were used: sex-linked recessive lethals and sterility. The flies were subjected to various levels of HF in fumigation chambers. Sex-linked recessive lethal mutation frequency increasd at each level
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Fluoride-induced genotoxicity in mouse bone marrow cells: effect of buthionine sulfoximine and N-acetyl-l-cysteine.
A significant level of reactive oxygen species generation was observed in sodium fluoride (NaF) treated mouse bone marrow cells (BMCs). Reduced glutathione (GSH) as a free radical scavenger could be an important determining factor in F-induced genotoxicity. We therefore attempted to monitor GSH to understand the mechanism of NaF-induced genotoxicity.
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Absence of DNA damage in multiple organs (blood, liver, kidney, thyroid gland and urinary bladder) after acute fluoride exposure in rats
Fluoride has been widely used in dentistry as a caries prophylactic agent. However, there has been some speculation that excess fluoride could cause an impact on genome integrity. In the current study, the potential DNA damage associated with exposure to fluoride was assessed in cells of blood, liver, kidney, thyroid
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Induction of micronuclei by sodium fluoride
More than 500 million people live in communities with artificially or naturally fluoridated drinking water that has been treated with 1 ppm or more of fluoride. Workers in aluminum plants, phosphate fertilizer plants and other fluoride-related factories are also exposed to high concentrations of fluoride. It is reported that workers
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Differential in vivo genotoxic effects of lower and higher concentrations of fluoride in mouse bone marrow cells.
In an in vivo genotoxicity investigation of the action of fluoride (F) on bone marrow cells, sodium fluoride (NaF) was administered through the drinking water of 2–3 month old Swiss albino mice for 30 days at lower (7.5, 15, and 30 mg/L) and higher concentrations (100 and 150 mg/L). Mitotic
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A Critique of Gelberg's Study on Fluoride/Osteosarcoma in New York
The case-control study by Gelberg, published first as a PhD dissertation and then later in two peer-reviewed journals, may represent the most substantive study on fluoride/osteosarcoma previous to Bassin’s 2001 analysis. In assessing Gelberg’s data, we were at first struck by the existence of several notable errors in both the thesis and papers. While these errors do raise questions about the study, our primary concern with Gelberg’s work relates to the methods she used to analyze her data.
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Micronucleus and Sister Chromatid Exchange Frequency in Endemic Fluorosis
The rise of sister chromatid exchange (SCE) and micronucleus (MN) in the peripheral blood lymphocytes of the fluorine-intoxicated patients indicates that fluorine is a mutagenic agent which can cause DNA and chromosomal damage.
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NTP Bioassay on Fluoride/Cancer (1990)
In 1977, the U.S. Congress requested that animal studies be conducted to determine if fluoride can cause cancer. The result of the Congressional request was an extensive animal study conducted in the 1980s by the National Toxicology Program (NTP) and published in 1990. The main finding of NTP's study was a dose-dependent increase in osteosarcoma (bone cancer) among the fluoride-treated male rats.
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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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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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