Evaluation of Efficacy of Mineral Oil, Charcoal, and Smectite in a Rat Model of Equine Cantharidin Toxicosis

Abstract

Background: The efficacy of orally administered therapeutics for the treatment of cantharidin intoxication has not been evaluated in controlled studies.Objective: To develop a model of acute cantharidin intoxication in laboratory rats and to evaluate in this model the relative efficacy of 3 gastrointestinal therapies used to treat equine cantharidin toxicosis.Animals: Sixty-four male Sprague-Dawley rats. Methods: A blinded, randomized, controlled study was performed on rats surgically implanted with telemetry transmitters for evaluating heart rate, locomotor activity, and body temperature. Orogastric administration of cantharidin was performed within 15 seconds before administration of mineral oil, activated charcoal, or smectite. Negative control groups received therapeutic agents alone. Urine was collected for cantharidin analysis. Rats were sacrificed 24 hours after intoxication, and tissues were collected for histopathologic evaluation. Data analysis included ANOVA procedures and contingency tables.Results: Six of 8 cantharidin-intoxicated rats treated with mineral oil died; bradycardia and hypothermia developed in the animals of this group 0-8 hours after intoxication. Rats treated with mineral oil had higher urine cantharidin concentrations than rats receiving cantharidin alone or with smectite (P = .04). The most severe hypothermia (30.6°C AE 1.0) developed in rats administered mineral oil at 4-8 hours after intoxication, whereas those treated with charcoal (35.2°C AE 0.8) had mean body temperatures higher than all other treatment groups (P = .03). Survival times in the charcoal (P = .16) and smectite (P = .12) treatment groups were not statistically different from negative controls.Conclusions and Clinical Importance: Mineral oil is often used in the treatment of equine cantharidin toxicosis. Our findings suggest that mineral oil increases cantharidin absorption, worsening morbidity and fatality in rats.

Activated charcoal: A natural protective measure against the lingual degenerative effect of tacrolimus immunosuppressant

“…In conclusion, the present study revealed that the charcoal-treated group showed enhancement in both epithelial and connective tissue architecture of the tongue, mucous and serous acini, which might be due to the protective action of charcoal in the treatment of toxicosis. Activated charcoal adsorbs ingested toxins within the gastrointestinal tract hindering the systemic absorption of that toxin [13,16]. Moreover, our observations suggest that the degenerative effects of tacrolimus were temporary.…”

“…Additionally, TAC has induced mucosal pigmentation on topical application [12]. Oral administration of activated charcoal (AC) has been evident in treating the side effects of immunosuppressants and many drug-induced toxicoses [13,14]. Production of AC commences by heating bamboo or wood and proceeds by its conversion into powder with micro-porosities to increase its surface area, attaining absorbent properties to the charcoal [15].…”