Fatal cases of acute suicidal sodium and accidental zinc fluorosilicate poisoning. Review of acute intoxications due to fluoride compounds

Lech, Teresa

doi:10.1016/j.forsciint.2010.06.027

Cited by 15 publications

(7 citation statements)

References 27 publications

(46 reference statements)

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“…Occupational and accidental exposure of F -has always posed a high risk to human health. Acute F -toxicity can occur through dermal exposure, accidental or suicidal ingestion of hydrofluoric acid, ammonium fluoride or sodium fluoride [2]. F -exposure has a direct toxic effect on the cardiovascular system but the specific mechanism is still unclear.…”

Section: Introductionmentioning

confidence: 99%

Single oral acute fluoride exposure causes changes in cardiac expression of oxidant and antioxidant enzymes, apoptotic and necrotic markers in male rats

et al. 2015

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Section: Introductionmentioning

confidence: 99%

Single oral acute fluoride exposure causes changes in cardiac expression of oxidant and antioxidant enzymes, apoptotic and necrotic markers in male rats

et al. 2015

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“…Abbreviations: F, Fluoride; Pr, protein; OSI, organo-somatic index; TPr, total protein; ALB, albumin; AKP, alkaline phosphatase; MDA, malondialdehyde; SOD, superoxide dismutase; GSH-Px, glutathione peroxidase; SGOT, serum glutamic-oxaloacetic transaminase; SGPT, serum glutamic. membranes and accumulate in diverse soft tissues such as stomach, small intestine, liver, kidney, and brain pyruvic transaminase (Lech, 2011), threatening the health of human and animal. Further investigation revealed F tendentiously alters the activity of many mitochondria-rich cells like hepatocyte (Dabrowska et al, 2004), which accorded with the result of a study on organ-specific toxicological response to F by Chattopadhyay et al (2011).…”

Section: Introductionmentioning

confidence: 99%

Ameliorative effect of protein and calcium on fluoride-induced hepatotoxicity in rabbits

Liang¹,

Niu²,

Wang³

et al. 2012

Afr. J. Biotechnol.

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To investigate whether protein (Pr) or calcium (Ca) supplementation could ameliorate hepatic damage induced by excessive fluoride (F); thirty-two 30-day-old healthy New Zealand rabbits were randomly divided into four groups (female: male = 1:1). The four groups were maintained on distilled water and fed the following diets for 120 days: (1) a malnutrition control (MC) diet (8.58% Pr, 0.49% Ca); (2) the MC diet plus HiF (high fluoride in their diet, 200 mg F ion/kg from NaF); (3) a Ca deficient MC diet plus HiPr+HiF (0.46% Ca, 18.41% Pr, plus HiF); and (4) a Pr deficient MC diet plus HiCa+HiF (2.23% Ca, 8.35% Pr, plus HiF). Results show that in HiF group, the serum total Pr (TPr) and albumin (ALB) content significantly decreased, whereas both Pr and Ca rich diets significantly enhanced their levels. In liver, low superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, high malondialdehyde (MDA) content, and evident mitochondria lesions in HiF group indicated a significant oxidative stress, while Pr or Ca supplementation brought an ultrastructural repair and a recovery antioxidant defense in liver. The findings in the present work implied the ameliorative effects of Pr or Ca supplementation on F-induced hepatotoxicity in rabbits.

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“…Hsps are among the major defensive stress proteins, which play an important role in the pathophysiology of various xenobiotic-induced cardiotoxicity models (Shan et al 2003;Yu et al 2012). Acute F − poisoning is known to cause sudden cardiac failure in both humans (Vohra et al 2008;Lech 2011) and experimental animals (McIvor et al 1987). Our previous study showed that acute F − exposure impairs cardiac dysfunction through increased mitochondrial oxidative damage, apoptosis, and necrosis in rat myocardium .…”

Section: Resultsmentioning

confidence: 99%

“…Acute F − exposure always posed a high risk to human health during occupational and accidental exposure of hydrofluoric acid, ammonium bifluoride, or sodium fluoride (Lech 2011). Apart from the groundwater contamination of F − , over fluoridation of public water system plays a major concern in many parts of the world (Gessner et al 1994;Penman et al 1997).…”

Section: Introductionmentioning

confidence: 99%

Differential expression of myocardial heat shock proteins in rats acutely exposed to fluoride

Panneerselvam

Raghunath

2017

Cell Stress and Chaperones

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Acute fluoride (F − ) toxicity is known to cause severe cardiac complications and leads to sudden heart failure. Previously, we reported that increased myocardial oxidative damage, apoptosis, altered cytoskeleton and AMPK signaling proteins associated with energy deprivation in acute F − induced cardiac dysfunction. The present study was aimed to decipher the status of myocardial heat shock proteins (HspsHsp27, Hsp32, Hsp40, Hsp60, Hsp70, Hsp90) and heat shock transcription factor 1 (Hsf1) in acute F − -intoxicated rats. In order to study the expression of myocardial Hsps, male Wistar rats were treated with single oral doses of 45 and 90 mg/kg F − for 24 h. The expression levels of myocardial Hsps were determined using RT-PCR, western blotting, and immunohistochemical studies. Acute F − -intoxicated rats showed elevated levels of both the transcripts and protein expression of Hsf1, Hsp27, Hsp32, Hsp60, and Hsp70 when compared to control. In addition, the expression levels of Hsp40 and Hsp90 were significantly declined in a dosedependent fashion in F − -treated animals. Our result suggests that differential expression of Hsps in the rat myocardium could serve as a balance between pro-survival and death signal during acute F − -induced heart failure.

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Fatal cases of acute suicidal sodium and accidental zinc fluorosilicate poisoning. Review of acute intoxications due to fluoride compounds

Cited by 15 publications

References 27 publications

Single oral acute fluoride exposure causes changes in cardiac expression of oxidant and antioxidant enzymes, apoptotic and necrotic markers in male rats

Single oral acute fluoride exposure causes changes in cardiac expression of oxidant and antioxidant enzymes, apoptotic and necrotic markers in male rats

Ameliorative effect of protein and calcium on fluoride-induced hepatotoxicity in rabbits

Differential expression of myocardial heat shock proteins in rats acutely exposed to fluoride

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