Diagnosis of Bromethalin Toxicosis in the Dog
| Autor: | Joseph Simon, William B. Buck, David C. Dorman, Karen A. Harlin |
|---|---|
| Rok vydání: | 1990 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Pathology 040301 veterinary sciences Metabolite Central nervous system Kidney Cerebral edema 0403 veterinary science 03 medical and health sciences chemistry.chemical_compound Dogs Internal medicine medicine Animals Dog Diseases Brain Chemistry Aniline Compounds Molecular Structure General Veterinary Poisoning Brain Rodenticides Optic Nerve Syndrome 04 agricultural and veterinary sciences medicine.disease Bromethalin Axons 030104 developmental biology medicine.anatomical_structure Endocrinology Adipose Tissue Liver Vacuolization chemistry Cerebrospinal fluid pressure Spongiosis |
| Zdroj: | Journal of Veterinary Diagnostic Investigation. 2:123-128 |
| ISSN: | 1943-4936 1040-6387 |
| Popis: | Dogs given a single oral dose of bromethalin at 6.25 mg/kg developed a toxic syndrome charac- terized by hyperexcitability, tremors, seizures, depression, and death within 15-63 hours after bromethalin administration. Gross lesions included mild cerebral edema (2/5) and mild pulmonary congestion (2/5). His- tologic lesions included diffuse white matter spongiosis (5/5), mild microgliosis (3/5), optic nerve vacuolization (3/5), mild thickening of Bowman's capsule (2/5), and occasional splenic megakaryocytes (2/5). Ultramicroscopic examination of midbrain stem revealed occasional swollen axons, intramyelinic vacuolization, and myelin splitting at the intraperiod line. Bromethalin was detected in kidney, liver, fat, and brain tissues, using gas chromatography with electron capture detection. Photodegradation of extracted bromethalin may limit accurate quantification of tissue residues. Acute, single-feeding rodenticides containing 0.01% bromethalin were introduced in 1985. a,b,c Bromethalin- based rodenticides are pelleted (tan or green color) grain- based products that contain 0.75-1.5 ounces (21-42 g) of bait in paper "place pack" enve1opes. l In the ex- posed animal, bromethalin is N-demethylated by he- patic microsomal enzymes (cytochrome P450) to form the desmethylbromethalin metabolite (Fig. 1). 2,11 The biochemical mechanism of action for bromethalin- based rodenticides differs from anticoagulant and cho- lecalciferol-based rodenticides and involves the un- coupling of oxidative phosphorylation. 2,11,12 Oxidative phosphorylation is dependent upon the normal func- tion of mitochondria1 cytochromes and is the primary means of ATP production in nervous tissues. Uncou- pling of oxidative phosphorylation by bromethalin and desmethylbromethalin, therefore, results in a lack of adequate ATP production and disruption of ATP de- pendent Na+-K+ ion channel pumps. 11 Disruption of normal ion pump activity in the central nervous system results in the development of cerebral edema and el- evated cerebrospinal fluid pressure (CSFP). Addition- ally, brain and spinal cord moisture and cation con- centrations are elevated in rats given a lethal oral dose of bromethalin. 11 |
| Databáze: | OpenAIRE |
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