Citation

Dousset E, Carrega L, Steinberg JG, Clot-Faybesse O, Jouirou B, Sauze N, Devaux C, Autier Y, Jammes Y, Martin-Eauclaire MF, Guieu R. Comp. Biochem. Physiol. C Toxicol. Pharmacol. 2005; 140(2): 221-226.

Affiliation

Laboratoire des Déterminants Physiologiques de l'Activité Physique (UPRES EA 3285), Institut Fédératif de Recherche E-J Marey (IFR 107), Faculté des Sciences du Sport, Université de la Méditerranée (Aix-Marseille II), Marseille, France.

Copyright

(Copyright © 2005, Elsevier Publishing)

DOI

10.1016/j.cca.2005.02.003

PMID

15907767

Abstract

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.

Language: en