INVESTIGADORES
CHOLICH Luciana Andrea
artículos
Título:
Hepatic encephalopathy induced by seeds and pods of Senna occidentalis in pigs
Autor/es:
CHILESKI GABRIELA; RIOS ELVIO E; LERTORA WALTER J; GIMENO, E.J.; CHOLICH LUCIANA A
Revista:
REVISTA CIENTíFICA
Editorial:
UNIV ZULIA
Referencias:
Lugar: Zulia; Año: 2018 vol. 28 p. 343 - 348
ISSN:
0798-2259
Resumen:
Senna occidentalis is a toxic plant that affects different animalspecies. The predominant lesion found in most of the intoxicatedanimals is skeletal muscle degeneration. However, in horsesand humans, this poisoning is primarily characterized by hepaticencephalopathy. The aim of this paper was to determine whether,in addition to this myodegeneration, the seeds and pods of S.occidentalis induce toxic hepatic encephalopathy in pigs. Ten pigswere divided into two groups (of five animals each), one of whichwere fed with a ration containing 20 % of S. occidentalis podsand seeds, and the other with a commercial ration (control) for14 days. Poisoned animals had a sudden onset of symptoms,characterized by incoordination, ataxia, disorientation andhead pressing, depression and lateral recumbency. Aspartateaminotransferase and Creatine phosphokinase serum activitiesincreased along with an increasement of serum bilirubin inintoxicated animals with S. occidentalis. Histopathologicalstudies of the poisoned pigs showed hepatocellular swellingand centrilobular necrosis in the liver, vacuolization of the whitematter and Alzheimer type II astrocytes in the cerebral cortex ofthe brain. Electron microscopy revealed mitochondrial lesions inliver. These results showed that in this study, the muscle injurypreviously reported was not observed, most probably becausethe toxic hepatic encephalopathy reproduced in the evaluatedanimals were produced before skeletal muscle degenerationoccurred. On the other hand, the animals of the present studydeveloped clinical signs and histological lesions that were similarto those observed in cases of accidental poisoning. Besides,further studies are needed to identify the specific toxin responsiblefor acute liver failure, observed in the animals of this study.