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Biomedical subjects

A Curley

Publications and source records attributed to A Curley.

36 records · Page 2Linked to original sources
PubMed1971

Organic mercury identified as the cause of poisoning in humans and hogs.

Atomic absorption spectrophotometry and neutron activation analysis showed the presence of mercury in organic extracts of seed grain and in tissues of hogs fed the contaminated grain. Mercury was also found in the urine, serum, and cerebrospinal fluid of humans who ate the contaminated pork. Mass spectral analysis confirmed the presence of organic mercury. This paper reports the first documented episode of indirect mercury poisoning in humans in the United States caused by the ingestion of contaminated meat from animals that had consumed mercury in their food supply.

Activation Analysis↗
PubMedDate not supplied

Two acute human poisoning cases resulting from exposure to diazinon transformation products in Egypt.

Two spraymen working in public health occupations in Alexandria, Egypt, experienced acute toxicity resulting from exposure to diazinon. Symptomatology was similar to that previously reported for exposure to parathion or other organophosphorus insecticides. Plasma and red blood cell cholinesterase activity values were determined in blood samples obtained from both individuals at various times after the incident. Cholinesterase activity showed a marked reduction up to 18 days after exposure. Blood cholinesterase activity recovered to approximately 90% of the normal level of activity 28 days after the poisoning incident in one individual. This activity recovered to about the same level in the other individual, but after only 20 days from the poisoning date. Experimental results suggested that this acute toxicity resulted from unsuitable storage conditions of the emulsifiable concentrate formulation of diazinon. The diazinon that was applied was stored in "tin" containers made of tin-plated sheet steel. The emulsifiable concentrate (60%) was not in compliance with the World Health Organization's standard specifications regarding the emulsion stability tests because of the presence of crystals in the emulsifiable concentrate. A sample of this crystalline material was analyzed. Gas chromatographic analysis combined with mass spectrometric techniques failed to identify intact diazinon in samples of that material. The sample represented virtually complete conversion of diazinion into transformation products. Sulfotepp and monothiono-TEPP were two of the identified products in the sample, both of which are much more toxic than diazinon.

Adult↗
PubMedDate not supplied

Assay of chicken brain neurotoxic esterase activity using leptophosoxon as the selective neurotoxic inhibitor.

Hen brain microsomal preparation has phenyl valerate-hydrolyzing activity associated with neurotoxic esterase activity. Part of that activity is due to paraoxon-insensitive esterases and a sub-part of this is sensitive to neurotoxic organophosphates, i.e., mipafox and leptophosoxon. This neurotoxic agent sensitive esterase activity is referred to as neurotoxic esterase (NTE). Because of the commercial unavailability and high toxicity of mipafox, which is usually used as the selective inhibitor for assaying NTE, leptophosoxon was used as an alternative to mipafox. Results indicated that the NTE fraction of hen brain microsomal PV-hydrolyzing activity is the same target for either mipafox or leptophosoxon. The inhibitory effect of leptophosoxon against that fraction was much higher than that of mipafox. The availability of leptophos/leptophosoxon makes this assay very useful for screening organophosphorus esters for neurotoxic effects.

Animals↗
PubMedDate not supplied

A kinetic study on the inhibition of hen brain neurotoxic esterase by mipafox.

A direct method of assaying neurotoxic esterase (NTE) activity, using 4-nitrophenyl valerate, has been described. The technique was used to determine the bimolecular rate (ki), phosphorylation (k2), and affinity (Kd) constants for the reaction of hen brain microsomal NTE with mipafox. Results indicate that the new technique for assaying NTE makes detailed kinetic studies of NTE inhibition possible. The affinity and phosphorylation constants, Kd and k2, for the reaction of hen brain microsomal NTE with mipafox, were found to be 6.72 x 10(-5) M and 3.23 min-1, respectively. The bimolecular rate constant (ki) for this reaction was obtained by interpreting the results according to two different linear equations. The obtained values for ki by these interpretations were 4.8 x 10(4) and 4.0 x 10(4) M-1 min-1, respectively.

Animals↗
PubMedDate not supplied

In vivo inhibition of chicken brain acetylcholinesterase and neurotoxic esterase in relation to the delayed neurotoxicity of leptophos and cyanofenphos.

An equimolal single dose (1 mmole/kg) of leptophos or cyanofenphos was given orally to chickens to assay the clinical and biochemical neurotoxic effects of these two organophosphorus insecticides. Parathion and TOCP at 2 and 1000 mg/kg of chicken body weight were tested in the same manner as negative and positive neurotoxicants, respectively. Three birds of each of five groups tested were sacrificed 1,2,3,7,14,21 and 28 days after treatment and the brains were taken for the biochemical tests. Acetylcholinesterase (AChE) and neurotoxic esterase (NTE) activities were determined in the brain microsomal fractions. In addition, the AChE activity in the brain soluble fractions was measured. Clinical observations indicated that leptophos-, cyanofenphos- and parathion-treated chickens became acutely poisoned but recovered from the typical cholinergic signs in a day or two. However, about 10 to 15 days later leptophos- and cyanofenphos-treated chickens developed the characteristic leg weakness and unrecoverable ataxia seen in birds given TOCP. The biochemical results indicated that cyanofenphos followed by leptophos and parathion produced more in vivo AChE inhibition than that produced by TOCP in both chicken brain soluble and microsomal fractions. Results suggested that there are no correlations between the in vivo effect of TOCP, leptophos and cyanofenphos on AChE and phenyl valerate-total hydrolyzing activities and the ability of these chemicals to produce neuropathy in hens. The results obtained from this study of the in vivo effect of the tested compounds on chicken brain NTE activity present an acceptable correlation between the inhibition of this enzyme and the ability of these chemicals to induce neuropathy. The mechanism and explanation for this correlation are presented. The in vivo effect of the tested compounds on the chicken brain NTE activity was determined using the indirect and a new direct method. The data presented in this report suggested that the new direct technique of assaying NTE activity using 4-nitrophenyl valerate (4-NPV) as substrate, can be useful in the in vivo screening studies of organophosphates for their ability to induce neuropathy in hens.

Acetylcholinesterase↗
PubMedDate not supplied

Delayed neurotoxicity induced by organophosphorus compounds in the wild mallard duckling: effect of leptophos.

Feeding of 260 ppm of leptophos to mallard ducklings caused delayed neurotoxicity similar to that reported for hens. Thus leptophos caused ataxia, with subsequent paralysis, loss of appetite, and slow-down in the growth rate of the treated birds. Spinal lesions were identical in morphology and distribution to those seen in hens following leptophos administration. The severity of histologic changes correlated both with the clinical condition and the duration of intoxication.

Animals↗