Prevention of Oral Dichlorvos Toxicity by Different Activated Charcoal Products in Mice

Study objective: To determine whether immediate treatment with oral activated charcoal (AC) products of differing surface areas prevents clinical toxicity of a lethal oral dose of dichlorvos in mice. Design: An in vivo, prospective, randomized, placebo-controlled study using 75 male albino mice. Interventions: Fasting mice were administered 57.5 mg/kg of a 0.55% dichlorvos solution via feeding tube. One minute later, groups of 15 mice each received 1 or 2 g/kg of Actidose-Aqua® AC or 1 or 2 g/kg of Sigma® AC or sterile water by feeding tube. In this way, all mice received 15 mL/kg of an AC suspension or sterile water. The animals were observed for 24 hours for seizures or death. Results: In all treatment groups, mice were found to have significantly fewer seizures and deaths (P.2). Conclusion: In this in vivo mouse model, all AC products tested decreased the incidence of seizures and death. Further studies should be done to investigate the clinical effects of AC products with different surface areas. [Tuncok Y, Gelal A, Apaydin S, Guven H, Fowler J, Gure A: Prevention of oral dichlorvos toxicity by different activated charcoal products in mice. Ann Emerg Med March 1995;25:353-355.]. © 1995 Mosby, Inc. All rights reserved

Methamphetamine causes depletion of glutathione and an increase in oxidized glutathione in the rat striatum and prefrontal cortex.

The administration of methamphetamine to experimental animals results in damage to dopaminergic neurons. The hypothesis that methampheta-mine-induced neurotoxicity is mediated by reactive oxygen species was evaluated. It was found that acute administration of methamphetamine (5 and 15 mg kg(-1)) resulted in production of oxidative stress as demonstrated by decreased glutathione and increased oxidized glutathione levels in the rat striatum and prefrontal cortex. These changes in glutathione and oxidized glutathione levels were dose-dependent in striatum, but not in prefrontal cortex. In conclusion, the results of present study provide further evidence in support of the notion that oxidative stress may play an important role in the metham-phetamine-induced neurotoxicity

Does cisplatin chemotherapy decrease the MDP uptake of normal bone? An experimental study

Objective Bone scan is the accepted initial imaging modality for skeletal metastases. Cisplatin is a cell-cycle nonspecific antineoplastic agent used in some chemotherapy regimens. Knowing that platinum reacts with phosphate compounds such as methylenediphosphonic acid (MDP), decreases bone resorption and new bone formation, it can be proposed that cisplatin chemotherapy may decrease Tc-99m MDP bone uptake. We aimed to demonstrate, if present, the decrease in bone uptake and to determine the duration of this effect