C-Fos expression in epileptogenic areas of nephropathic rats undergoing star fruit poisoning

Abstract Purpose Studies have demonstrated that star fruit consumption by nephropathic patients triggers severe neurotoxic effects that can lead to convulsions or even death. Brain areas likely susceptible to star fruit poisoning have not been investigated. The objective of the present study was to map possible epileptogenic areas susceptible to star fruit intoxication in nephropathic rats. Methods The study analyzed 25 rats (5 groups). Rats in the experimental group underwent bilateral ureteral obstruction surgery and orogastric gavages with star fruit juice. An electroencephalogram was used to confirm convulsive seizures. Urea and creatinine levels were used to confirm the uremia model. Immunohistochemical analysis was used to map cells with c-Fos protein (c-Fos+ cells) to identify brain areas with increased neuronal activity. Control groups included non-nephropathic and nephropathic rats that did not receive star fruit. Results A statistically significant increase (p<0.01) in c-Fos+ cells was noted in nephropathic animals receiving star fruit juice compared to control groups, in brain areas commonly related to epileptogenic neural circuits including the hippocampus, amygdala, rhinal cortex, anterior cingulate area, piriform area, and medial dorsal thalamus. Conclusion These data corroborate the neurotoxic capacity of star fruit in nephropathic patients.

Poisoning by the ingestion of seeds of the fruit of the "coteira" (Joanesia princeps)

A 15-year-old ingested the core of two seeds of a fruit of Joannesia princeps, a large tree sometimes found planted in sidewalks on streets in Brazilian towns. Four hours after the ingestion, he had several episodes of vomiting and diarrhea, but recovered spontaneously th same day. Poisoning by the ingestion of seeds of Joannesia princeps is possibly not rare, considering that the tree gives plenty of fruit and the seeds have an agreeable flavor, but is probably underestimated as mild cases are unlikely to be reported. Ingestion by small children, that could lead to potentially more severe cases, is in part probably prevented by the hardness of the shells coverning the seeds.

A re-examination of the mechanism of ackee-induced vomiting sckness

The hypoglycemia seen in ackee poisoning almost certainly results from the presence of hypoglycin A in the aril. However, the mechanisms underlying the vomiting and neurological disrders have not been properly established. We have, in thes review, re-examined the latter and proposed that the vomiting of glutamic and neurological feactures of ackee poisoning probably result from the excitotoxic properties of glutamic and aspartic acids derived directly and indirectly from ackee intake