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Results for “FLUORIDE POISONING”

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PubMed2002

[In vivo and in vitro study on the effect of excessive fluoride on type I collagen of rats].

In order to investigate the effects of excessive fluoride on type I collagen in rat bone, rat fluorosis model is induced by giving 221 mg/L NaF in drinking water for two months. The level of serum BGP, inorganic ingredient, the content of collagen and the degree of collagen cross-linking in fluorosis rat bone are determined. Rat calvaria osteoblasts are separated by enzyme digestion. After the treatment of 0.5 and 1.0 mmol/L NaF for 48 hour, effects of excessive fluoride on the expression level of type I collagen of the osteoblasts are detected through immunohistochemical method. The results show that after NaF treatment for two months, the serum BGP and inorganic ingredient content in fluorosis rat bone increase significantly in comparison to those of in control group (P < 0.05). On the contrast, the content of collagen and the degree of collagen cross-linking in fluorosis rat bone decrease significantly (P < 0.05) compared with control group. In in vitro study, the osteoblasts secrete less type I collagen after NaF treatment than they do in control group cells. The results suggest that excessive fluoride can inhibit the synthesis of type I collagen. The decrease of collagen may be one of causal factors to skeletal fluorosis.

Animals↗
PubMed1994

[Effectiveness of glutamate in the treatment of early manifestations of occupational fluorosis].

Efficiency of glutamic acid for therapy of early signs of occupational fluorosis was studied in workers engaged into cryolite production. The study proved that use of glutamic acid in occupational conditions prevents progressing of metabolic disorders. The results encourage recommendations to include glutamate into therapeutic and prophylactic nutrition of workers exposed to fluor compounds, into nutritive additions according to special recipe.

Adult↗
PubMed1985

Mortality and cancer morbidity after heavy occupational fluoride exposure.

A cohort of 431 male cryolite workers employed for at least six months between 1924 and 1961 was identified from personnel records at the Copenhagen cryolite factory. During this period, heavy fluoride exposure resulted in at least 74 cases of skeletal fluorosis. All workmen in the cohort were followed up in Denmark until July 1, 1981. During 1941-1981, 206 men died, while only 149.3 deaths were expected from national mortality statistics. Significant excesses were seen in the following causes of death: violent death and all cancers, in particular cancer of the respiratory system. When compared with specific mortality rates for the Copenhagen area, violent death (and suicide taken alone) remained in significant excess among employees hired before 1940. Cancer morbidity data for the 35-year period 1943-1977 showed 78 cases of malignant neoplasms in the cryolite workers against 53.2 expected for Denmark as a whole and 67.9 for Copenhagen. The excess was almost entirely due to an excess number of respiratory cancers. Cancer morbidity showed no apparent correlation with length of employment or time from first exposure. Because detailed information on predictors for respiratory cancer was unavailable, a possible residual effect of fluoride cannot be excluded. However, any major carcinogenic effect of heavy fluoride exposure would be very unlikely.

Denmark↗
PubMed2000

[Study on antagonistic effects of selenium and zinc on the renal impairments induced by fluoride in rats].

Wistar rats were provided with distilled water containing NaF(100 mg/L), and were administered through gavage with Na2SeO3[0.1 mg/(kgBW.d)] and/or ZnSO4[14.8 mg/(kg BW.d)]. The results of biochemical, pathological and ultrastructural examinations showed that fluoride could cause serious renal impairments. The major damage induced by fluoride was epithelia of proximal renal tubules. The lipid peroxidation might be one of the mechanisms of fluoride toxicity. Na2SeO3 and ZnSO4 could antagonize the renal impairments induced by fluoride through their antioxidation. The cooperative effect of Na2SeO3 and ZnSO4 was more powerful than either Na2SeO3 or ZnSO4 alone.

Animals↗
PubMed1993

[Promotive action of sodium fluoride on precancerous lesions of hepatocellular carcinoma induced by diethylnitrosamine (DEN) in rats--stereologic study of enzyme histochemistry].

In 10 Wistar male rats, partial hepatectomy was performed and followed by intraperitoneal injection of DEN (30 mg/kg) once and giving drinking water containing 80 ppm sodium fluoride (36 ppm F) for 14 weeks. By stereologic method of enzyme histochemistry, it was observed for the first time that the foci of hepatocytic precancerous enzyme alterations (gamma-GT positive, ATPase negative and G-6-Pase negative) were significantly increased in number and size compared with the negative control group. The results suggest that sodium fluoride promoted the growth of precancerous lesions of the liver induced by DEN in rats, and this has provided some data to the understanding of the relationship between fluorosis and neoplasms.

Animals↗
PubMed1994

Abnormal bone mineralization after fluoride treatment in osteoporosis: a small-angle x-ray-scattering study.

Sodium fluoride treatment of osteoporosis is known to stimulate bone formation and to increase bone mass, but recent clinical trials failed to prove its antifracture effectiveness. The formation of bone with abnormal structure and, therefore, increased fragility is discussed as a possible explanation. Until now, however, exact information on the mineral structure of osteoporotic bone after fluoride treatment has been lacking. Bone biopsies were taken from three patients with postmenopausal osteoporosis before and after fluoride treatment (60 mg NaF/day for 1-2 years), from one patient with iatrogenic fluorosis, as well as from three normal controls. The mineral in these samples was investigated by a combination of backscattered electron imaging and small-angle x-ray scattering. Depending on the total dose of fluoride, an increasing amount of new bone is laid down on the surface of preexisting trabeculae. Its mineral structure is identical to that of heavy fluorosis and is characterized by the presence of additional large crystals, presumably located outside the collagen fibrils. These large crystals, which are not present in the controls or in osteoporotic bone before fluoride treatment, contribute to increase the mineral density without significantly improving the biomechanical properties of the bone. The possible success of fluoride treatment depends not only on the amount of newly formed bone but also on the rate of bone turnover. Indeed, as soon as significant amounts of fluoride are present, bone turnover leads to the replacement of old (normal) bone by new (pathologically mineralized) bone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

[Influence of free radical inducer on the level of oxidative stress in brain of rats with fluorosis].

OBJECTIVE: To study changes in content of lipid peroxide and composition of fatty acids in the brain of rats affiliated with chronic fluorosis after treatment with free radical inducer (ferric ion). METHODS: Thirty-six Wistar rats were divided into three groups, fed with similar fodder and varied concentrations of fluoride in drinking water, and were killed five months after treatment. Lipid peroxidation was induced by ferric ions. Malondialdehyde content in brain was analysed by high-performance liquid chromatography; oxygen consumption was determined with an oxygen electrode and fatty acid composition was measured by gas chromatography in brain tissues of the rats. RESULTS: In the brain tissues, content of malondialdehyde and oxygen consumption increased, composition of polyunsaturated fatty acids decreased and that of saturated fatty acids decreased after treatment with free radical inducer in the treated group, as compared with those in control group. CONCLUSION: Over uptake of fluoride for a long term could cause potential increase in the level of oxidative stress in the brain tissue.

Animals↗