RESUMO
A recent article concluded that glutamic acid probably plays a central role in the vomiting and neurological features of ackee poisoning. The present article draws attention to misconceptions in the basis of that hypothesis, and reviews important evidence supporting a different view
Assuntos
Humanos , Intoxicação por Plantas , Acidose/induzido quimicamente , Vômito/induzido quimicamente , Ácido Aspártico/intoxicação , Ciclopropanos/intoxicação , Hipoglicinas/intoxicação , Glutamatos/intoxicaçãoRESUMO
An acute illness (Jamaican vomiting sickness) which affected two adults after eating unripe ackee fruit was investigated. Analyses of serum and urine samples were performed to compare the patterns of organic acidaemia and aciduria with those reported from childhood cases. The main conclusion from the comparison is that the toxic ackee constitutent, hypoglycin, produces essentially the same metabolic effects in adults as in children.
Assuntos
Ciclopropanos/toxicidade , Hipoglicinas/toxicidade , Intoxicação por Plantas/etiologia , Vômito/induzido quimicamente , Adulto , Ácidos Graxos/sangue , Ácidos Graxos/urina , Humanos , MasculinoRESUMO
We identified methylenecyclopropylacetic acid, a known metabolite of hypoglycin A, in the urine of two patients with Jamaican vomiting sickness. Excretion of unusual dicarboxylic acids such as 2-ethylmalonic, 2-methylsuccinic, glutaric, adipic and dicarboxylic acids with eight and 10 carbon chains were also detected in both patients. The amounts of these dicarboxylic acids were 70 to 1000 times higher than normal. These metabolites have also been identified in urine of hypoglycin-treated rats. This evidence links hypoglycin A to Jamaican vomiting sickness as its causative agent. Urinary excretion of short-chain fatty acids was also increased up to 300 times higher than normal. These results indicate that, despite their clinical and histologic similarities, the cause and biochemical mechanisms of Jamaican vomiting sickness differ distinctly from those of Reye's syndrome in which these abnormal urinary metabolites are not appreciably increased.
Assuntos
Doenças Transmitidas por Alimentos/metabolismo , Frutas/intoxicação , Vômito/etiologia , Animais , Pré-Escolar , Ciclopropanos/metabolismo , Diagnóstico Diferencial , Ácidos Dicarboxílicos/urina , Ácidos Graxos Voláteis/sangue , Ácidos Graxos Voláteis/urina , Feminino , Doenças Transmitidas por Alimentos/etiologia , Doenças Transmitidas por Alimentos/urina , Gluconeogênese , Humanos , Hidroxiácidos/urina , Hipoglicemia/etiologia , Jamaica , Ratos , Síndrome de Reye/diagnóstico , Toxinas Biológicas/metabolismo , Valeratos/urinaRESUMO
Large amounts of ethylmalonic acid have been identified in urines from two patients with the vomitting sickness of Jamaica. The amounts were 178 and 882 mug per mg creatinine which are 70 and 350 times, respectively, over control values. Other short and medium chain dicarboxylic acids including glutaric and adipic acids and those with eight and ten carbon chain, saturated and cis-unsaturated, were also detected in large quantities as in the case of hypoglycin treated rats; urine. However, the large increase of urinary ethylmalonic acid in these two human cases is in a sharp contrast to the findings in hypoglycin treated rats in which urinary ethylmalonic acid increased only 3 times over control. It appears that ethylmalonic acid is produced in the cases with the vomiting sickness of Jamaica by carboxylation of n-butyryl-CoA which is not oxidized further due to the inhibition by hypoglycin A. In case of hypoglycin-treated rats, n-butyryl-CoA is mainly conjugated with glycine or deacylated to free butyric acid.