Abstract
Spent pot-liner (SPL) is a hazardous solid waste produced by the aluminum industry. Although its composition may vary, fluoride and cyanide salts as well as aluminum are predominant components. A seed-germination and root-elongation test was performed with Lactuca sativa seeds as a test system. SPL induced decrease of seed germination rate and root elongation. The concentration of 26.5 g/L SPL was established from a regression curve as the IC50 (inhibition concentration 50%). Through chemical analyses, the concentrations of fluoride, cyanide and aluminum in SPL solutions of 26.5 g/L (IC50), 39.75 g/L (1.5 IC50) and 13.25 g/L (0.5 IC50) were determined. Further, a cell-cycle test was conducted with root tips of L. sativa exposed to these same SPL solutions. All test chemicals presented toxic effects on meristematic cells of L. sativa. Aluminum was identified as the SPL component mainly responsible for reduction of the mitotic index. Chromosomal alterations resulted from the interactions among the three main chemical components of SPL, without a clear predominantly responsible agent. Induction of condensed nuclei was mainly due to effects of aluminum and fluoride, and may serve as an indicator of induced cell death.
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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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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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Lack of effect of prior treatment with fluoride on genotoxicity of two chemical agents in vitro
The goal of this study was to investigate the ability of fluoride to modulate the genotoxic effects induced by the oxidative agent hydrogen peroxide (H2O2) and the alkylating agent methyl methanesulfonate (MMS) in vitro by the single-cell gel (comet) assay. Chinese hamster ovary cells were exposed in culture for 1
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Curcumin supplementation protects from genotoxic effects of arsenic and fluoride
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)
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Chromosomal aberrations and sister-chromatid exchanges in Lithuanian populations: effects of occupational and environmental exposures
Cytogenetic analysis of chromosomal aberrations (CA) in 175,229 cells from 1113 individuals, both unexposed and occupationally or environmentally exposed to heavy metals (mercury and lead), organic (styrene, formaldehyde, phenol and benzo(a)pyrene) and inorganic (sulfur and nitrogen oxides, hydrogen and ammonium fluorides) volatile substances and/or ionizing radiation was performed. In addition,
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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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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's Mutagenicity: In vivo Studies
Consistent with dozens of in vitro studies, a number of in vivo studies, in both humans and animals, have found evidence of fluoride-induced genetic damage. In particular, research on humans exposed to high levels of fluoride have found increased levels of "sister chromatid exchange" (SCE). As noted in one study: "In
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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 & Liver Cancers in NTP Bioassay
On October 28, 1988, Battelle Columbus Laboratories submitted its Final Report to the NTP concerning the results of the Mouse study. The principal finding of Battelle's report was that a dose-dependent increase of a rare liver cancer (hepatocholangiocarcinoma) had occurred in the fluoride-treated male and female mice.
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