Toxicology of Fluorine-Containing Monomers

Gl, Kennedy

doi:10.3109/10408449009089877

Cited by 48 publications

(17 citation statements)

References 55 publications

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“…Epidemiologically, the risk of fluorosis is now well recognized all over the world with greater emphasis on environmental fluoride (Lu et al, 2000;Ando et al, 2001;Griffin et al, 2002) and its misuse in consumer items, particularly oral hygiene products (Bottenberg et al, 2001). There is also clinical evidence suggesting that a high intake of fluoride provokes nephrotoxic changes in humans (Kennedy, 1990;Cittanova et al, 1996) and animals (Dote et al, 2000) and can lead to urolithiasis and high serum levels of thiobarbituric acid reactive substances (TBARS) in the human (Singh et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

The effect of Pycnogenol on fluoride induced rat kidney lysosomal damage in vitro

Arhima¹,

Gulati²,

Sharma³

2004

Phytotherapy Research

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Pycnogenol (PYC) is a procyanidin-rich extract of the bark of French maritime pine (Pinus pinaster) with a potent ability to scavenge free radicals. Lysosome-rich fractions from rat renal cortices were incubated with varying amounts of PYC and challenged with noxious doses of fl uoride. Controls were also included. The release of N-acetyl-beta-D-glucosaminidase (NAG) isozymes in the supernatant was estimated by spectrophotometric methods. The protein content of the renal cortex was also determined. Our results show that fluoride in unhealthy doses can cause a concentration dependent release of N-acetyl-beta-D-glucosaminidase (NAG) isozymes from the renal lysosomes. This may be related to its known ability to initiate free radical formation or direct damaging effects on the lysosomal membrane. As a blend of bio flavonoids pycnogenol has a potent ability to scavenge free radicals. In our study PYC was effective in preventing fluoride induced release of NAG isozymes from the renal lysosomes.

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Section: Introductionmentioning

confidence: 99%

The effect of Pycnogenol on fluoride induced rat kidney lysosomal damage in vitro

Arhima¹,

Gulati²,

Sharma³

2004

Phytotherapy Research

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“…These neurological effects were not observed in the 90-day trans-DCE study in rats (Kelly et al, 1999), although a similar effect was observed in the acute study wherein cis-DCE, at very high concentrations (i.e., 13,500 and 15,700 ppm), produced some neurotoxic effects during the exposure (Kelly et al, 2000). No neurological effects were reported in the 2-wk PFBE inhalation study in rats (Kennedy, 1990), although these neurotoxicity-related parameters may not have been evaluated during that study, which was conducted in 1980.…”

Section: Discussionmentioning

confidence: 96%

“…In a 2-wk subchronic inhalation study with PFBE, groups of 10 male and 10 female rats were exposed 6 h/day, 5 days/wk, to 500, 5000, or 50,000 ppm of PFBE (Kennedy, 1990). At 500 ppm PFBE, no clinical signs of toxicity or compound-related pathological changes were seen.…”

Section: Discussionmentioning

confidence: 99%

4-Week Inhalation Toxicity Study With a Mixture of Dichloroethylene and Perfluorobutylethylene in Rats

Malley

Hansen

Everds

et al. 2002

Inhalation Toxicology

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Inhalation studies were conducted to determine the potential subchronic toxicity of a mixture of trans-1,2-dichloroethylene (70%), cis-1,2-dichloroethylene (5%), and perfluorobutylethylene (25%). Groups of rats were exposed to 0, 400, 2000, or 8000 ppm concentrations of the mixture vapor 6 h/day, 5 days/wk, for a total of 20 exposures. Subgroups of rats were further observed during a 1-mo recovery period. Functional observational battery (FOB) and motor activity (MA) behavioral tests were conducted prior to initiation of the exposures, during exposure wk 4, and after a 1-mo postexposure recovery period. Clinical pathology evaluations were conducted at the end of the exposure period and after a 1-mo recovery period. At the end of the 4-wk exposure period, tissues from rats were collected, histologically processed, and evaluated by light microscopy. Test substance-related, biologically significant decreased body weights and body weight gains occurred in male and female rats exposed to 8000 ppm. In addition, test substance-related, statistically significant decreases in food consumption and/or food efficiency were observed in male rats exposed to 8000 ppm. During exposures to 8000 ppm, some rats exhibited tremors and ataxia. Usually tremors and ataxia were observed within 1 h after initiation of the daily exposure period and were observed during each exposure day. Tremors were also observed during 1 exposure day in the 2000 ppm animals. In addition to the tremors and ataxia, rats exposed to 2000 ppm or 8000 ppm had a diminished and/or no alerting response to a sharp, sound stimulus during each of the daily exposure periods. These effects were transient since no clinical observations of compromised neurological function were detected when the rats were evaluated upon return to the animal room following exposure. Daily reoccurrence of this apparently acute effect in the 8000 ppm group did not produce enduring neurological changes since there were no test substance-related effects on FOB parameters or on MA conducted the day following the last exposure or during the recovery period. In addition, there were no toxicologically significant changes in hematology, clinical chemistry, or urinalysis parameters in either males or females for any exposure concentration; and there were no test substance-related gross or microscopic morphological changes in males or females administered any exposure concentration. Under the conditions of the study, the no-observed-effect level (NOEL) was 400 ppm in males and females based on clinical signs of toxicity during exposure to 2000 or 8000 ppm.

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“…Tetrafluoroethene, chlorotrifluoroethene, and 2-(fluoromethoxy)-1,1,3,3,3-pentafluoro-1-propene are selective nephrotoxins in experimental animals (24)(25)(26)(27). Although rats exposed to chlorotrifluoroethene excrete fluoride, a known nephrotoxin, the amount of fluoride formed was considered to be too low to account for the observed nephrotoxicity (24,28).…”

Section: Thioacyl Halidesmentioning

confidence: 99%

Chemical Toxicology of Reactive Intermediates Formed by the Glutathione-Dependent Bioactivation of Halogen-Containing Compounds

Anders

2007

Chem. Res. Toxicol.

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The concept that reactive intermediate formation during the biotransformation of drugs and chemicals is an important bioactivation mechanism was proposed in the 1970s and is now accepted as a major mechanism for xenobiotic-induced toxicity. The enzymology of reactive intermediate formation as well as the characterization of the formation and fate of reactive intermediates are now well-established. The mechanism by which reactive intermediates cause cell damage and death is, however, still poorly understood. Although most xenobiotic-metabolizing enzymes catalyze the bioactivation of chemicals, glutathione-dependent biotransformation has been largely associated with detoxication processes, particularly mercapturic acid formation. Abundant evidence now shows that glutathione-dependent biotransformation constitutes an important bioactivation mechanism for halogen-containing drugs and chemicals and has for many compounds been implicated in their organ-selective toxicity and in their mutagenic and carcinogenic potential. The glutathione-dependent biotransformation of haloalkenes is the first step in the cysteine S-conjugate beta-lyase pathway for the bioactivation of nephrotoxic haloalkenes. This pathway has been a rich source of reactive intermediates, including thioacyl halides, alpha-chloroalkenethiolates, 3-halo-alpha-thiolactones, 2,2,3-trihalothiiranes, halothioketenes, and vinylic sulfoxides. Glutathione-dependent bioactivation of gem-dihalomethanes and 1,2-, 1,3-, and 1,4-dihaloalkanes leads to the formation of alpha-chlorosulfides, thiiranium ions, sulfenate esters, and tetrahydrothiophenium ions, respectively, and these reactions lead to reactive intermediate formation.

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Toxicology of Fluorine-Containing Monomers

Cited by 48 publications

References 55 publications

The effect of Pycnogenol on fluoride induced rat kidney lysosomal damage in vitro

The effect of Pycnogenol on fluoride induced rat kidney lysosomal damage in vitro

4-Week Inhalation Toxicity Study With a Mixture of Dichloroethylene and Perfluorobutylethylene in Rats

Chemical Toxicology of Reactive Intermediates Formed by the Glutathione-Dependent Bioactivation of Halogen-Containing Compounds

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