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1.
Perspect Biol Med ; 24(1): 1-14, Aut. 1980.
Artigo em Inglês | MedCarib | ID: med-9418

RESUMO

This article reviews the discovery of pyrrolizidine alkaloid poisoning in United States caused by the drinking of herbal tea and describes some of the difficulties involved in establishing a causal relationship between exposure to these alkaloids and the delayed appearance of toxic symptoms. In addition, some of the more general problems presented by the widespread use of herbs in various forms are addressed. First, however, a brief overview is given of the toxicity of this class of alkaloids. (AU)


Assuntos
Humanos , Lactente , Pré-Escolar , Pessoa de Meia-Idade , Masculino , Feminino , Bebidas/envenenamento , Medicina Herbária , Alcaloides de Pirrolizidina/envenenamento , Intoxicação por Plantas/epidemiologia , Contaminação de Alimentos , Jamaica , Hepatopatias/etiologia , Alcaloides de Pirrolizidina/administração & dosagem , Senécio
3.
Kingston; s.n; Dec. 1972. 185 p. ills, tab.
Tese em Inglês | MedCarib | ID: med-13707

RESUMO

With increasing interest in mutagenicity an array of agents such as chemicals and drugs are being defined as chromosome damaging agents. The activities of these agents were reviewed. An intensive investigation of the mutagenic potential of fulvine was undertaken for three reasons. 1. Fulvine is still widely consumed in Jamaica as a herbal remedy which causes a well defined pathological condition - veno - occlusive disease of the liver (VOD). 2. Fulvine was found to cause chromosome damage in previous screening experiments. 3. Fulvine is a member of the pyrrolizidine group of alkaloids which are known to have mutagenic effects. The mutagenic activities were investigated by in vivo studies in children who have recovered from VOD and experimentally in rats. Serial examination of 3 members of a family recently recovered showed a decline of the percentage of cells with damage to normal over a five month period. No abnormalities were detected in 7 recovered children. Fulvine was administered to rats at varying dosages of 0.08 mg/gm, 0.04 mg/gm, 0.02 mg/gm, 0.01 mg/gm, and repeated administrations of 0.04 mg/gm body weight. Chromosomal abnormalities were produced which included gaps, breaks, bivalent and quadriradial configurations, ring chromosomes, dicentrics, abnormal metacentrics and submetacentrics, chromatic exchanges. Tetraploidy was rarely detected. The abnormalities were comparable in type to those seen in human VOD. At all dosages exchanges predominated over other types of abnormalities. Abnormalities were induced within 48 hours after fulvine administration at a threshold dosage of 0.02 mg/gm. Mitotic inhibition and liver damage were more marked in 12 weanling rats treated with doses of 0.08 mg/gm body weight of fulvine. The model for investigation of fulvine as a mutagenic agent was evaluated (AU)


Assuntos
Humanos , Criança , Adolescente , Ratos , Masculino , Feminino , Alcaloides de Pirrolizidina/efeitos adversos , Cromossomos Humanos/patologia , Cromossomos/análise , Testes de Mutagenicidade , Hepatopatia Veno-Oclusiva , Histologia , Fígado , Mitomicinas , Alcaloides de Pirrolizidina/farmacologia
4.
West Indian med. j;21(3): 186-201, Sept. 1972.
em Inglês | MedCarib | ID: med-11027

RESUMO

The purpose of this experiment was to study the early structural and functional hepatic changes occurring in rats treated with a standardized dose of fulvine by gastric intubation. Histologic observationas and biochemical determinants were done at 1, 3, 6, 9, 18 and 32 hours after treatment. The results indicated that fulvine induced a wide spectrum of hepatic lesions that were detected as early as one hour after its administration. Some of the earliest lesions, such as the deterioration of hepatocytic endoplasmic reticulum and of the nuclei, progressed with time and suggested that the hepatocytes, rather than the vascular structures were the primary site of attack. Although single hepatocytic necrosis was detected at 3 hours and was only observed at the latest period (32 hours). This zonal necrosis was preceded by a prominent and progressive hepatocytic swelling in periportal and centrolobular areas and by increasing accumulation of cell debris and blood elements in the sinusoids. While fulvine or its metabolities appears to exert a direct necrotizing effect on the hepatocytes, the microcirculatory changes observed in our previous studies and suggested by the ultrastructural findings in the present one, may offer an explanation for the preferential location of the lesions that precede the occlusion of the terminal hepatic venules. (AU)


Assuntos
Humanos , Ratos , 21003 , Alcaloides de Pirrolizidina/toxicidade , Hepatopatia Veno-Oclusiva/fisiopatologia , Fígado/fisiopatologia , Plantas Medicinais/análise
6.
West Indian med. j ; 19(4): 258, Dec. 1970.
Artigo em Inglês | MedCarib | ID: med-6358

RESUMO

Some pyrrolizidine alkaloids have been shown to have nuclear toxicity in vitro. Fulvine was therefore investigated for its effect on mitotic chromosomes in the rat and in man. In vitro studies were performed on rat fibroblasts and human and rat peripheral blood cultures. In vivo studies were performed by injecting mature rats subcutaneously with 0.08mg/gm body weight in fulvine. Control animals received the identical dilutant. Blood cultures were established 24 and 48 hours, and 8 days later. Nine children with histologically proven veno-occlusive disease (VOD) and eight controls were studied by 48-hour blood cultures, for changes in chromosome number and morphology. The in vitro studies were negative. In vivo studies in rats showed marked mitotic depression at 24 and 48 hours. On the seventh day, breaks, gaps exchanges and rearrangements were seen in 24 percent of cells. VOD was found in 5 rats. Of the children, three sibs, and two others showed similar abnormalities marked in the former and less so in the latter. These findings are very suggestive of induction of chromosome abnormalities by fulvine or by VOD. The frequency of these changes may be related to dosage levels, intervals between ingestion and examination, or to familial reactions to the drug (AU)


Assuntos
Humanos , 21003 , Criança , Ratos , /efeitos adversos , Cromossomos/efeitos dos fármacos , Alcaloides de Pirrolizidina/efeitos adversos , Aberrações Cromossômicas/induzido quimicamente
7.
Ann Trop Med Parasitol ; 48(4): 386-96, Dec. 1954.
Artigo em Inglês | MedCarib | ID: med-8594

RESUMO

A study was made of 11 children suffering from "veno-occlusive disease of the liver" (V.O.D.). Clinically the disease was characterized by three overlapping phases, from the acute stage, with the sudden onset of hepatomegaly, with or without ascites, usually in infants from 18 months to three years of age, to the chronic stage, with the development of frank cirrhosis in later childhood. An attempt is made to outline the clinical natural history of V.O.D., as suggested by present information. The histology of V.O.D. is considered in outline. The primary lesion is a wide-spread occlusion of the smaller branches of the hepatic vein, the result of a primary endo-phlebitis; this is followed by the development of a non-portal type of cirrhosis radiating out from the central veins. The aetiology of V.O.D. is unknown, but it does not appear to be primarily or entirely nutritional; affected children are usually apparently adequately nourished. The possibility that V.O.D. is produced by the action of toxins, either bacterial or chemical, is considered, with special reference to "bush teas," which are widely used in Jamaica. Points of similarity are discussed between V.O.D. and serous hepatosis, Chiari's syndrome, senecio poisoning and Indian infantile cirrhosis (Summary)


Assuntos
Humanos , Lactente , Pré-Escolar , Criança , Masculino , Feminino , Hepatopatia Veno-Oclusiva/diagnóstico , Hepatopatia Veno-Oclusiva/etiologia , Jamaica , Hepatopatia Veno-Oclusiva/classificação , Fígado/patologia , Síndrome de Budd-Chiari , Alcaloides de Pirrolizidina/envenenamento , Cirrose Hepática
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