Evidence that free radical generation occurs during scorpion envenomation.
Comp Biochem Physiol C Toxicol Pharmacol
; 140(2): 221-6, 2005 Feb.
Article
en En
| MEDLINE
| ID: mdl-15907767
Although it is well established that symptomatology, morbidity and death following scorpion envenomation are due to increases in neurotransmitter release secondary to toxins binding to voltage-sensitive sodium channels, the mechanism by which venom action is involved in damaging heart, liver, lungs and kidneys remains unclear. We hypothesized that scorpion toxins could induce the generation of high levels of free radicals responsible for membrane damage in organs targeted by venom action. We have investigated lipid peroxidation in different organs, through the evaluation of thiobarbituric acid reactive substances (TBARS), after experimental envenomation of rats by toxic fractions of Androctonus australis Hector venom. We have shown that scorpion toxins cause considerable lipid peroxidation in most vital organs. We also evaluated the protective effects of antioxidants in mice injected with lethal doses of toxins. Among the drugs tested, N-acetylcysteine (NAC) was effective in protecting the mice when injected prior to toxin application. However, the free radical scavenging properties of NAC seem less implicated in these protective effects than its ability to increase the fluidity of bronchial secretions. We therefore conclude that free radical generation only plays a minor role in the toxicity of scorpion venom.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Venenos de Escorpión
/
Picaduras de Escorpión
/
Radicales Libres
/
Neurotoxinas
Límite:
Animals
Idioma:
En
Revista:
Comp Biochem Physiol C Toxicol Pharmacol
Asunto de la revista:
FARMACOLOGIA
/
TOXICOLOGIA
Año:
2005
Tipo del documento:
Article
País de afiliación:
Francia
Pais de publicación:
Estados Unidos