Acute intentional self-poisoning with a herbicide product containing fenoxaprop-P-ethyl, ethoxysulfuron, and isoxadifen ethyl: a prospective observational study.

BACKGROUND: Herbicides are commonly ingested for self-harm, but relatively little has been published on poisoning with herbicides other than paraquat and glyphosate. We report here a case series of patients with acute exposure to a combination herbicide (brand name Tiller Gold or Whip Super) containing the selective phenoxy herbicide compounds fenoxaprop-P-ethyl and ethoxysulfuron and a safener isoxadifen ethyl. METHOD: Clinical data on all patients presenting with Tiller Gold or Whip Super poisoning to two General Hospitals in Sri Lanka from 2002-2008 were collected prospectively until discharge. RESULTS: Eighty-six patients with a history of Tiller Gold or Whip Super ingestion were included. The main clinical features were an epigastric burning sensation and vomiting; however, most of those who vomited had received gastric lavage or forced emesis. Eight patients had a reduced level of consciousness on admission (Glasgow coma scale 9-14) that resolved without intervention over several hours. Only symptomatic and supportive care was required. The median hospital stay was 1 day (IQR: 1-2) and the case fatality was zero (95% confidence interval: 0-4.2%). This low case fatality compared favorably with the case fatality of other common herbicides in our cohort: paraquat >40%, propanil >10%, 4-chloro-2-methylphenoxyacetic acid > 5%, and glyphosate >2%. CONCLUSION: This combination herbicide product appears to be safe in patients with acute self-poisoning, particularly in comparison with other herbicides, and causing few clinical features.

[Acute toloxatone poisoning. Apropos of 122 cases]. / Intoxication aiguë par la toloxatone. A propos de 122 observations.

Toloxatone is a new monoamine oxidase inhibitor. One hundred and twenty two cases of poisoning with this drug are reported. In this series, the minimal toxic dose was 2 g. The first symptoms appeared about one hour after ingestion. In most cases, only drowsiness and mild adrenergic effects were observed. In a few cases of massive overdose, coma, pyramidal irritation, and myoclonic jerks occurred. In 3 cases of severe poisoning, toloxatone was associated with tricyclic antidepressants. Symptoms were similar to those reported in intoxications associating classical monoamine oxidase inhibitors and tricyclic antidepressants: muscular rigidity, hyperthermia and cardiovascular collapse. Two of these patients died.

Non-NMDA receptor-mediated neurotoxicity in cortical culture.

The neurotoxicity of 3 non-NMDA glutamate receptor agonists--kainate, alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA), and quisqualate--was investigated quantitatively in dissociated murine cortical cultures. Five minute exposure to 500 microM kainate, but not AMPA, produced widespread acute neuronal swelling. Kainate-induced swelling was resistant to 2-amino-5-phosphonovalerate (APV) or replacement of extracellular sodium with choline but attenuated by either kynurenate or low concentrations of quisqualate. Unlike NMDA agonists, kainate or AMPA did not produce much late neuronal loss after a 5 min exposure. In contrast, 5 min exposure to 500 microM quisqualate produced both acute neuronal swelling and widespread late neuronal degeneration. This acute swelling was blocked by APV or by replacement of extracellular sodium by choline, consistent with mediation by NMDA receptors; we speculate that high concentrations of quisqualate may directly activate NMDA receptors or induce the release of endogenous glutamate. Quisqualate-induced late neuronal degeneration may be due to another unexpected process: cellular quisqualate uptake and delayed release, converting brief addition into prolonged exposure. Hours after thorough washout of exogenously added quisqualate, micromolar concentrations could be detected in the bathing medium by high performance liquid chromatography. With lengthy exposure (20-24 hr), all 3 non-NMDA agonists were potent neurotoxins, able to destroy neurons with EC50's of about 20 microM for kainate, 4 microM for AMPA, and 1 microM for quisqualate. Kynurenate and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), but not APV or L-glutamate diethyl ester, were effective in attenuating the neuronal degeneration induced by these agonists. CNQX was about 3 times more selective than kynurenate against kainate-induced neuronal injury, but CNQX was still nearly equipotent with APV against NMDA-induced injury. Gamma-D-glutamylaminomethyl sulfonate exhibited partial antagonist specificity for AMPA-induced toxicity.

Neuronal depletion of the amygdala resembles the learning deficits induced by low level lead exposure in rats.

The behavioral deficits observed after lead exposure have been related to limbic system dysfunction. In a previous study it was shown that the neurotoxicity of lead could not be explained by the damage of the hippocampus alone. The purpose of the present investigation was to use behavioral comparisons to test the hypothesis that the intrinsic neurons of several nuclei of the amygdala, where lead has been found to accumulate, can be a target of the effects of the metal as well. A group of rats were maternally and permanently exposed to lead (750 ppm in the diet as lead acetate). Another group of equally aged and housed rats, never experimentally exposed to lead, were injected ibotenic acid into the amygdala. All groups plus sham-operated and unoperated controls were tested in the open field, the radial arm maze, and a passive avoidance task. The results showed that lead exposure (both permanent and maternal) and amygdalectomy produced a) no effect on locomotor activity, b) impairments in the acquisition phase of the radial maze, and c) impairments in passive avoidance. These results suggest an involvement of the amygdala in the neurotoxic action of lead, but not as the only brain structure. The deficits in permanently lead-exposed rats are more pronounced than in only maternally-exposed animals suggesting a longlasting, but not totally irreversible effect of early lead exposure.

A fatality involving U4Euh, a cyclic derivative of phenylpropanolamine.

A fatality following ingestion of diazepam and 4,5-dihydro-4-methyl-5-phenyl-2-oxazolamine, a cyclic derivative of phenylpropanolamine known as U4EuH or 4-methyl aminorex, is described. Solid dosage samples of U4EuH were analyzed using gas chromatography, ultraviolet and infrared spectroscopy, nuclear magnetic resonance, and mass spectrometry. Physiological fluids were analyzed quantitatively by gas chromatography and qualitatively by gas chromatography-mass spectrometry. Concentrations of 4,5-dihydro-4-methyl-5-phenyl-2-oxazolamine were: in blood 21.3 mg/L; in urine 12.3 mg/L. Diazepam concentration in blood was 0.8 mg/L.

Biochemical changes in layer and broiler chickens when fed on a high-glucosinolate rapeseed meal.

Diets containing 500 g high-glucosinolate rapeseed meal/kg or an equivalent amount of soybean meal as the only protein supplement were fed to layer-type chickens and two broiler strains from 1 to 56 d of age. Additional groups of the former were maintained on the diets until they were 16 and 28 d old. The rapeseed meal produced thyroid hypertrophy in all strains but reduced the growth rate of only one of the broiler strains. The livers of chickens fed on rapeseed meal were enlarged and DNA analysis indicated hyperplasia, but no macroscopic lesions were found. The activities of aspartate transaminase, lactate dehydrogenase and alkaline phosphatase in the plasma were increased by rapeseed meal, suggesting liver damage. In all strains, feeding rapeseed meal increased plasma total protein, albumin and cholesterol and decreased urate. Hyperglycaemia accompanied by a decrease in plasma triglycerides occurred in the layer strain. Through its extra-thyroidal toxicity (-)5-vinyl-oxazolidine-2-thione (goitrin) was probably responsible for most of these changes.