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Side 1 fra 79 resultater
Antagonistic effect of melatonin against cyanide-induced seizures and acute lethality in mice.
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The effect of melatonin on potassium cyanide-induced neurotoxicity was investigated in vivo. The ED50 value of potassium cyanide, as measured by induction of tonic and clonic seizures, was significantly increased by 1.5- or 1.8-fold by s.c. preinjection of melatonin (20, 100 or 345 mg/kg) in mice.
Preventive effect of melatonin against cyanide-induced seizures and lipid peroxidation in mice.
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Subcutaneous injection of potassium cyanide (6, 8, and 9 mg/kg) caused a severe tonic seizure in a dose-dependent manner. However, the incidence of seizures induced by potassium cyanide was significantly inhibited by preadministration of melatonin (20 mg/kg, s.c.) Lipid peroxidation in homogenates
Alpha-lipoic acid protects against potassium cyanide-induced seizures and mortality.
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This study was proposed to investigate the potential protective effect of alpha-lipoic acid (α-LA) against potassium cyanide (KCN)-induced seizures and lethality in mice. The intraperitoneal ED(50) value of KCN, as measured by induction of clonic and tonic seizures was increased by pretreatment of
Protective effect of NG-nitro-L-arginine (N5-[imino(nitroamino)methyl]-L-ornithine) against cyanide-induced convulsions in mice.
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The effects of NG-nitro-L-arginine (NNA; an inhibitor of the oxidative L-arginine pathway) on convulsions induced by cyanide were investigated in mice. NNA prevented cyanide-induced convulsions in a dose-dependent manner. Furthermore, the inhibitory effect against convulsions induced by cyanide with
Protective effect of calmodulin inhibitors against acute cyanide-induced lethality and convulsions in mice.
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The ED50 value of cyanide as measured by induction of convulsions (tonic seizure) was significantly increased by 80% or 69% when trifluoperazine (TFP) or chlorpromazine (CHP), a specific calmodulin inhibitor was preinjected intracerebroventricularly (i.v.t.) at a dose of 0.09 mumol/body of mice.
Seizures and selective CA-1 hippocampal lesions induced by an excitotoxic cyanide metabolite, 2-iminothiazolidine-4-carboxylic acid.
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Excitatory amino acid (EAA)-like and excitotoxic properties of the secondary metabolite of cyanide, 2-iminothiazolidine-4-carboxylic acid, (2-ICA) were evaluated because of its possible role in cyanide-induced neurotoxicity. Intracerebroventricular (i.c.v.) injections of 2-ICA in mice produced
A hypothesis for cyanide-induced tonic seizures with supporting evidence.
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A possible relationship among cyanide-induced convulsions, calmodulin, nitric oxide and protein kinase C was investigated in mice. The ED50 value of cyanide as measured by induction of tonic seizures was significantly increased in a dose-dependent manner when mercuric chloride (0.5 or 5.0
Citrus peel extract attenuates acute cyanide poisoning-induced seizures and oxidative stress in rats.
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The primary aimed of this study was to investigate the potential protective effects of methanolic extract of citrus peel (MECP) on acute cyanide (KCN) poisoning-induced seizures and oxidative stress in rats. The intraperitoneal LD50 value of KCN (6.3 mg/Kg bwt), based on 24 hrs mortality, was
Protection against cyanide-induced convulsions with alpha-ketoglutarate.
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Protection against convulsions induced by cyanide was observed after treatment with alpha-ketoglutarate, either alone or in combination with sodium thiosulfate, a classical antagonist for cyanide intoxication. However, sodium thiosulfate alone did not protect against cyanide (30 mg/kg)-induced
Repeated cyanide convulsions without central nervous pathology.
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Antagonism of cyanide poisoning by dihydroxyacetone.
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Dihydroxyacetone (DHA) effectively antagonized the lethal effect of cyanide in mice and rabbits, particularly if administered in combination with thiosulfate. Oral DHA (2 and 4 g/kg) given to mice 10 min before injection (i.p.) of cyanide increased the LD50 values of cyanide from 5.7 mg/kg to 12 and
Acute cyanide poisoning.
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OBJECTIVE
Cyanide intoxication is an extremely rare event. We report a case of a teenager presenting with unresponsiveness, hemodynamic instability, and profound anion gap metabolic acidosis secondary to elevated lactate levels. It was later confirmed that he was a victim of cyanide
Acute cyanide poisoning: clinical spectrum, diagnosis, and treatment.
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Cyanide poisoning presents in many forms. Industrial intoxications occur due to extensive use of cyanide compounds as reaction products. Smoke inhalation, a polyintoxication, is most often responsible for domestic cyanide poisonings. Suicidal poisonings are rare. Cyanogenic compounds may produce
Cyanide toxicity from acetonitrile-containing false nail remover.
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A patient presented without symptoms 30 minutes after ingesting acetonitrile, also known as methylacyanide. He had prompt gastric lavage and activated charcoal administration. Hours later, the onset of clinical toxicity was heralded by mental status abnormalities and vomiting prior to a generalized
Cyanide intoxication in Macaca mulatta. Physiological and neuropathological aspects.
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Sodium cyanide was infused intravenously in 11 lightly anaesthetised and spontaneously breathing M. mulatta. In most, the EEG, ECG, respiratory rate, blood pressure, cerebral venous sinus pressure, end-tidal pCO2 and body temperature were recorded. Blood gases, pH, lactate and pyruvate were
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