Abstract
The acute toxicity of hydrofluoric acid (HFA) was investigated in a 24-hour lethal dose study of intravenous injection in rats. The LD50 and LD90 were 17.4 and 23.0 mg/kg, respectively. Harmful systemic effects were also studied 1 hour after acute sublethal exposure to HFA. Rats were injected with HFA (1.6, 3.2, 6.4, or 9.6(LD5) mg/kg) or saline. Blood samples were obtained from the carotid artery. BUN and Cr were significantly increased in response to HFA concentrations greater than 3.2 mg/kg. Acute glomerular dysfunction also occurred at HFA concentrations greater than 3.2 mg/kg. PCO2, HCO3– and base excess were significantly decreased in the 6.4 and 9.6 mg/kg groups. Total and ionized calcium was significantly decreased, and potassium was increased in the 9.6 mg/kg group. Ionized fluoride exposure directly affected serum electrolytes. Mortality was thought to be due to cardiac arrhythmia resulting from hypocalcemia and hyperkalemia. Metabolic acidosis and renal failure were severe in response to HFA exposure. Even low exposure to HFA can cause acute renal dysfunction, electrolyte abnormalities and metabolic acidosis. These complications result in a poor prognosis.
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Evaluation of serum lipoprotein and tissue antioxidant levels in sheep with fluorosis
The aim of this study was to evaluate serum lipoprotein and tissue antioxidant levels of sheep with and without fluorosis living in a volcanic area of Turkey. Fifteen Akkaraman sheep with fluorosis in the A?ri region north of Lake Van and 10 Akkaraman sheep without fluorosis in the Van region
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Toxicokinetics and metabolism deteriorated by acute nephrotoxicity after a single intravenous injection of hydrofluoric acid in rats
OBJECTIVES: This study was designed to investigate the early dynamic state of hydrofluoric acid (HFA) in blood and urine as a model of accidental occupational exposure to a subtoxic dose of HFA. It was also aimed at determining the relationship between the kinetics and harmful effects of HFA on the
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Author Correction: Sodium fluoride induces nephrotoxicity via oxidative stress-regulated mitochondrial SIRT3 signaling pathway.
Accumulation of mitochondrial reactive oxygen species (mROS) has been implicated in the pathogenesis of fluorosis. As the main mitochondrial deacetylase, SIRT3 is closely associated with oxidative stress. To investigate the role of SIRT3 in response to sodium fluoride (NaF)-induced nephrotoxicity. Our results showed that NaF treatment impaired mitochondrial ultrastructure, decreased
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Effects of melatonin and epiphyseal proteins on fluoride-induced adverse changes in antioxidant status of heart, liver, and kidney of rats
Several experimental and clinical reports indicated the oxidative stress-mediated adverse changes in vital organs of human and animal in fluoride (F) toxicity. Therefore, the present study was undertaken to evaluate the therapeutic effect of buffalo (Bubalus bubalis) epiphyseal (pineal) proteins (BEP) and melatonin (MEL) against F-induced oxidative stress in heart,
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The Influence of fluoride on chronic kidney disease of uncertain aetiology (CKDu) in Sri Lanka.
Fluoride is an element that is widely distributed in the environment. The involvement of fluoride in pathogenesis of Chronic Kidney Disease of uncertain aetiology (CKDu) in Sri Lanka is a much-debated topic. This study aimed to investigate the fluoride concentration in drinking water in CKDu affected areas in Sri Lanka
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