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Results for “FLUORIDE POISONING”

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At least 145 records · Page 8Linked to original sources
PubMed1984

Hydrofluoric acid poisoning.

A case of suicidal ingestion of hydrofluoric acid is presented. Death of the victim while in police custody was one of the more unique aspects of the case. This is the sixth case of poisoning of this type reported in Dade County. Clinical, pathological, and toxicological aspects of fluoride poisoning are discussed.

Adult↗
PubMed1993

Effect of long-term administration of sodium fluoride on plasma calcium level in relation to intestinal absorption and urinary excretion in rabbits.

The present study was undertaken to determine the effect of chronic fluoride toxicity on calcium metabolism. Rabbits (n = 10) were orally administered an aqueous solution of 10 mg NaF/kg body wt daily for 18 months. Equal numbers (n = 10) of age-, sex- and weight-matched rabbits kept under identical laboratory conditions, but not treated, with NaF solution, served as control. The fasting plasma calcium concentrations of fluoride-treated rabbits were significantly lower (P < 0.001) than those of control animals. In contrast to the decrease in plasma calcium level, and increase in intestinal radioactive calcium (45Ca) absorption was observed (P < 0.001) in all fluoride-treated animals. However, urinary calcium excretion levels were found to be reduced (P = not significant) in fluoride-treated rabbits. It is therefore concluded that long-term fluoride poisoning alters the calcium homeostatic mechanism, thereby affecting calcium metabolism.

Animals↗
PubMed1989

Studies on the treatment of hydrofluoric acid burn.

Changes in serum and tissue and urinary levels of fluoride, calcium and other biochemical consequences were investigated in rats after experimental hydrofluoric acid (HF) burns, to obtain adequate method of emergency treatment for the injury. Increases in ionized fluoride and decreases in total and ionized calcium, in the sera were observed after contact with HF. Hyponatremia and hyperkalemia were observed over a 24 hour period. Parathyroid hormone (PTH) concentrations were elevated in the sera taken within 24 hours after burn and fell to reference range once the calcium concentration had been raised. Electrocardiographic changes including severe bradycardia were observed. These results indicate that an HF skin burn results in systemic fluoride poisoning followed by hypocalcemia, hypersecretion of PTH, hyponatremia, hyperkalemia and other electrolytes imbalance. Flushing with running water was effective for HF burns. By applying 2.5% calcium gluconate jelly, concentrations of fluoride in the urine and the tissues surrounding the injured region were reduced. Thus, the present results proved that the irrigation with running water and the jelly applications was evaluated as the most effective therapy among various methods tested for the HF burn.

Animals↗
PubMed1991

Incidental cardiac rhabdomyomas: a significant finding necessitating additional investigation at the time of autopsy.

Cardiac rhabdomyomas are rare lesions forming part of the tuberous sclerosis complex that may be responsible for sudden death. As well as remaining clinically occult for variable periods of time, they may, along with other manifestations of tuberous sclerosis, be quite difficult to detect clinically and pathologically. A patient is described in whom multiple cardiac rhabdomyomas were an incidental finding at autopsy following fatal potassium fluoride poisoning. Other gross pathological lesions typical of tuberous sclerosis were present but were quite subtle in appearance. Awareness of the association of cardiac rhabdomyomas with tuberous sclerosis is important so that full examination of organ systems for characteristic lesions can be undertaken during the autopsy, and so that fresh and frozen tissue can be obtained at the time of dissection for further investigation.

Cerebral Cortex↗
PubMed1988

Hydrofluoric acid-induced hypocalcemia.

Among patients exposed to hydrofluoric acid the potentially lethal effect of calcium depletion induced by binding with fluoride ion has not been well reported. Three patients exposed to hydrofluoric acid had acute fluoride poisoning with serum calcium levels equal to or below 4.1 mgm/dl. Treatment included administration of large amounts of calcium, both intravenously and by subsechar injection, to replenish the biologically active calcium and to bind fluoride. This report describes successful treatment of two survivors, apparently the first two, of severe hypocalcemia caused by hydrofluoric acid.

Adult↗
PubMed1985

The production of DNA strand breaks in human leukocytes by superoxide anion may involve a metabolic process.

H2O2 is known to be capable of inducing strand-break damage in intracellular DNA, but whether O2- also can do so in the absence of H2O2 is uncertain. The difficulty in distinguishing the effects of the two is that, under physiological conditions, dismutation of O2- to H2O2 can readily occur. When human leukocytes are stimulated with phorbol 12-myristate 13-acetate (PMA), they release O2-, and within a few minutes strand breakage in intracellular DNA can be observed. We have attempted to determine whether the O2- produced is itself capable of causing DNA damage or whether H2O2 alone, or in combination with O2-, is responsible for the observed damage. Addition of catalase (up to 250 micrograms/ml) to remove H2O2 prevented no more than about 50% of the DNA damage. The majority of the remaining damage could be blocked, in a dose-dependent manner, by superoxide dismutase (SOD) or a SOD-mimetic copper complex, identifying a fraction of damage to intracellular DNA dependent upon extracellular O2-. We studied this O2(-)-specific fraction through the use of three metabolic poisons (fluoride, 2-deoxyglucose, and A23187). These agents largely blocked DNA damage, while affecting extracellular O2- levels only slightly. For comparison, H2O2-induced DNA damage was studied with glucose oxidase to generate a flux of H2O2. The first two metabolic poisons had little effect, whereas A23187 did inhibit H2O2-induced DNA damage. We conclude that O2(-)-induced damage occurs through a mechanism that differs, at least in part, from the H2O2 damage pathway and that the former may involve one or more metabolic steps.

Calcimycin↗
PubMed1999

Fluoride-induced depletion of polyphosphoinositides in rat brain cortical slices: a rationale for the inhibitory effects on phospholipase C.

Fluoride, which is used commonly as a pharmacological tool to activate phosphoinositide-phospholipase C coupled to the heterotrymeric Gq/11 proteins, inhibited the phosphorylation of phosphatidylinositol (PtdIns) to polyphosphoinositides (PtdIns4P and PtdIns4,5P2) in membranes from rat brain cortex. Fluoride enhanced basal production of 3H-inositol phosphates in membranes prepared from brain cortical slices that had been prelabeled with [3H]inositol, but inhibited the stimulation elicited by carbachol in the presence of GTPgammaS. However in both cases fluoride depleted [3H]PtdIns4P content by 95%. The inhibitory effects of fluoride on the release of 3H-inositol phosphates in slices were not apparent in a pulse [3H]inositol-labeling strategy, but became dramatic in a continuous labeling protocol, particularly at long incubation times. Prelabeling slices with [3H]inositol in the presence of fluoride precluded polyphosphoinositide labeling, and eliminated phospholipase C responsiveness to carbachol under normal or depolarizing conditions, and to the calcium ionophore ionomycin. The lack of response of 3H-polyphosphoinositide-depleted slices to phospholipase C stimuli was not due to fluoride poisoning, unaccessibility of the [3H]inositol label to phospholipase C or desensitization of Gq/11, as the effect of carbachol and GTPgammaS was restored, in the presence of ATP, in membranes prepared from slices that had been labeled in the presence of fluoride. In conclusion, our data show that fluoride, at a concentration similar to that used to stimulate directly Gq/11-coupled phospholipase C, effectively blocks the synthesis of phospholipase C substrates from PtdIns.

Animals↗
PubMedDate not supplied

[Evoluation of biologic balance as a function of radiologic status in a population living in a endemic fluoride zone of southern Algeria].

Chronic fluoride intoxication in subjects living in an endemic South Algerian zone: El Oued (drinking water fluor: 3 to 5 mg/l), provokes some blood and urinary levels modifications, when compared to normals living in Algiers (drinking water fluor: 0,6 mg/l). These modifications are the more often present in stade 0 (normal radiologic aspect) and do not increase with radiological evolution (stades I, II, III). Fluoremy and fluorury increase. Phosphocalcic metabolism is altered. Tubular reabsorption coefficient, particularly, decreases strongly. Using renal functional exploration, a pretty soon tubular failure is founded, which preceeds glomerular failure. Blood levels of certain products and enzymes are studied.

Adolescent↗
PubMed2000

Effect of long term fluoride exposure on lipid composition in rat liver.

Chronic fluorosis can severely damage many systems of human body, but its pathogenesis is unclear. Normal composition and structure of cellular membrane lipids are a basic factor to maintain cell function. In this investigation, cellular membrane lipids of the liver were analysed after a long term fluoride treatment for rats and the results are discussed in order to give an explanation for the pathogenesis of this disease. Wistar rats were supplied with drinking water containing either 30 or 100 ppm fluoride (NaF) for seven months. Contents of phospholipid and neutral lipid in rat liver were analyzed by high-performance liquid chromatography, and fatty acid composition from individual phospholipids was measured by gas chromatography. Results showed that the total liver phospholipid content decreased in the rats treated with high dose of fluoride due to a lower content of phosphatidylethanolamine (PE), phosphatidylcholine (PC) and phosphatidylserine (PS). Among the fatty acid compositions of PE and PC in the livers of fluoride poisoned animals, the proportion of polyunsaturated fatty acids (20:4 and 22:6) decreased, whereas saturated fatty acids (16:0 and 18:0) increased. No changes could be detected in the amounts of liver cholesterol and dolichol. Total ubiquinone contents in rat liver were reduced by 11% in the group treated with 30 ppm fluoride and by 42% in the group treated with 100 ppm fluoride. In the subclasses of ubiquinone, both ubiquinone-9 and ubiquinoine-10 amounts decreased after fluoride treatment. These modifications of membrane lipids might be induced by oxidative stress, which might be an important factor in the pathogenesis of chronic fluorosis.

Animals↗
PubMed1973

Secondary hyperparathyroidism in patients with endemic skeletal fluorosis.

Investigation of 20 patients with skeletal fluorosis showed that five had clear evidence of secondary hyperparathyroidism. The hyperactivity of the parathyroid glands in skeletal fluorosis in the presence of decreased solubility of the bone mineral (fluoroapatite) strongly suggests that it is a compensatory attempt to maintain a normal extracellular ionized calcium equilibrium. Further study of the parathyroid glands and of bone lesions in skeletal fluorosis is in progress.

Adult↗