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Results for “FLUORIDE POISONING”

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At least 91 records · Page 5Linked to original sources
PubMed1993

[Effect of pollen extracts (cernitin preparation) on selected biochemical parameters of liver in the course of chronic ammonium fluoride poisoning in rats].

The aim of the paper has been the experimental evaluation of protracted exposure to ammonium-fluoride vapours exerted on selected biochemical parameters in serum as well as microsomal fraction of the liver in animals. An attempt was made to ameliorate eventual changes by using Cernitin preparation. The experiment was performed on male rats of Wistar strain. The rats were exposed to NH4F in a toxicological chamber with controlled parameters. Cernitin was added to standard diet and given to animals in the form of balls. The studies were carried out after 3 and 6 month-long exposure. The range of the performed studies covered: activity of enzymes (AspAT, AlAT, AP, ChE) and content of bilirubin as well as lipids were studied in the blood serum. Content of proteins, cholesterol and phospholipids was investigated in the liver homogenate. It has been shown that chronic exposure to NH4F vapours causes a rise in the activity of studied aminotransferases and alkaline phosphatase, and a decreases in activity of cholinesterase. The changes in activity were accompanied by an increase in the content of lipids. Prophylactic application of Cernitin preparation normalizes the disorder involving the studied enzymatic and lipid parameters.

Ammonium Compounds↗
PubMed1985

Experimental acute sodium fluoride poisoning in sheep: renal, hepatic, and metabolic effects.

Sheep received a single intragastric dose of 0.5, 1.0, 1.5, or 2.0 mmol F-/kg. Mild signs occurred at 1.5 mmol F-/kg and the animals recovered 2 days later. With the 2.0 mmol F-/kg dose all animals showed dullness, anorexia, and mild diarrhea which decreased from the third day. Dose-related congestion of duodenum, liver, kidney, and lung was observed in all animals. For the two higher doses kidney degeneration and tubular necrosis were associated with glomerular inflammation. Serum fluoride had a dose-related increase and was still significantly elevated on Day 7 for sheep given doses higher than or equal to 1.0 mmol F-/kg. Serum calcium and glucose levels were significantly lowered for all doses on the first day and the decrease was dose-related. In sheep given 2.0 mmol F-/kg total proteins and sodium were significantly lowered, whereas potassium and urea were increased (p less than 0.05); alkaline phosphatase (ALP) and lactic dehydrogenase (LDH) were both lowered (p less than 0.01) on the first day and ALP was still lowered on Day 7. For the highest dose glutamate dehydrogenase (GDH) was increased on Days 1 and 7 and gamma-glutamyl transferase (GGT) was increased on Day 1 and lowered on Day 7. Diuresis was increased for the two higher doses in Day 3 or 4 following dosage. A dose-related increase of daily fluoride excretion occurred for all doses on Day 1 and fluoride excretion was still significantly elevated on Day 7 except for the lowest dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed1996

Fatality due to acute fluoride poisoning following dermal contact with hydrofluoric acid in a palynology laboratory.

A fatal accident involving concentrated hydrofluoric acid in a palynological laboratory is described. Similar deaths due to dermal exposure to concentrated hydrofluoric acid have been reported in the literature. It is evident that rigorous control measures including proper personal protective equipment and first aid are of utmost importance in the prevention of death and injury when handling hydrofluoric acid. Possible factors that may have contributed to the accident are reviewed.

Accidents, Occupational↗
PubMed1985

The manipulation of potassium efflux during fluoride intoxication: implications for therapy.

Based on findings in 2 fluoride-toxic patients, it was suspected that hyperkalemia played a clinically important role in the etiology of sudden death from fluoride poisoning. Using fluoridated human erythrocytes as an in vitro model, it was confirmed that fluoride produced a marked potassium efflux from intact cells. Further, neither glucose and insulin in pharmacologic doses, nor various buffers could halt the efflux by shifting the potassium intracellularly. If these results can be extrapolated to the clinical situation, removal of potassium and fluoride via exchange resins or dialysis remains the only reasonable approach to this life threatening problem. Aside from sudden hyperkalemia and hypocalcemia, no serologic marker for fluoride toxicity has been identified. A high degree of clinical suspicion is therefore essential to the diagnosis.

Calcium↗
PubMed1980

Fluoridation: a clinician's experience.

In 1954 I described a case of chronic fluoride poisoning from artificially fluoridated water, in which the patient exhibited a multisymptomatic clinical picture without noticeable skeletal changes. Subsequently, others and I have confirmed this "nonskeletal phase" of the disease from fluoride in water and in air (in workers in fluoride-emitting factories and in people residing near such factories) and from fluoride-containing drugs. Further details on this disease are presented. In view of the constantly expanding use of fluoride in industry as well as its increase in food, water, and other hidden sources and because of the reactivity of the fluoride ion, the implications of these findings with respect to the etiology of several heretofore unexplained illnesses are discussed.

Adolescent↗
PubMed2003

Oral decontamination with calcium or magnesium salts does not improve survival following hydrofluoric acid ingestion.

Hydrofluoric acid (HF) ingestion may result in rapid death from systemic fluoride poisoning. Because fluoride binds calcium and magnesium, oral administration of calcium or magnesium salts has been suggested as useful therapy for HF ingestion. This study evaluates oral administration of calcium and magnesium salts for the prevention or attenuation of acute HF toxicity following oral exposure in a mouse model. Mixed breed CF-1 mice were randomized to treatment with a lethal-dose HF premixed with calcium chloride, magnesium sulfate, or deionized water by gavage. Average survival time for the three groups was the same. This study suggests that calcium- or magnesium-containing solutions do not alter the toxic effect of HF following oral exposure.

Animals↗