Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the retinal changes in occupationally exposed pesticide workers, 79 subjects exposed to an organophosphate, fenthion, and 18 exposed to an organochlorine pesticide DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl) ethane], were subjected to a detailed study, including history taking, physical examination and ophthalmic evaluation. Fluorescein angiography was performed in selected cases. Serum cholinesterase level in 22 workers and serum DDT residue in 17 workers of the respective groups were also estimated. Fifteen workers (19%), who were exposed to fenthion had macular changes (P less than 0.01). The macular lesions were characterized by perifoveal irregularity of pigmentation and areas of hypopigmentation of 1/8-1/3 disc diameter. Mean age of the subjects having macular involvement was 30.6 years and mean duration of exposure 7.9 years. The symptoms reported by them were diminution of vision (8), dislike for bright light, flash of light, black dots in front of the eyes (2 each) and visual blurring (1). Paracentral scotoma and constriction of peripheral field were present in three workers each. Fluorescein angiography suggested pigment epithelium defect. Other causes of macular involvement in these workers were excluded; a possible role of pesticides in the genesis of these macular changes is suggested.
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PMID:Some observations on the macula of pesticide workers. 400 78

Alzheimer's disease (AD) is associated with a reduction in cholinergic activity as a result of specific neuronal loss. Current potential treatments for the disease include both cholinomimetic drugs and anticholinesterase inhibitors. One of the drugs approved by the FDA is tacrine (9-amine-1,2,3,4 tetrahydroacridine; THA), a strong acetylcholinesterase (AChE) inhibitor. We have studied the effects of tacrine on glial and neuronal cells in culture assessing cell survival and viability and morphology. Lactate dehydrogenase (LDH) activity and methylthiazol-diphenyl-tetrazolium (MTT) reduction were used as toxicity indicators. We found that tacrine toxicity on rat B12 glial cells and mouse Neuro 2A cells was strongly dependent on its concentration (up to 500 microM) and time of exposure. The toxic effect was not prevented by serum factors nor by bovine serum albumin. Fluorescein-conjugated phalloidin was used to examine the arrangement of actin filaments at substrate adhesion regions and cell-cell contacts. Primary events following exposure to tacrine included changes in cell morphology, disappearance of actin filament bundles, and disruption of focal adhesion contacts. At concentrations between 10 and 50 microM, tacrine induced neurite outgrowth in Neuro 2A cells, an effect that was not observed in B12 cells, suggesting that certain tacrine effects could be specific for neuronal cells. Although similar trends of response were observed for both cell types, some differences between undifferentiated and differentiated cells were apparent.
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PMID:Responses induced by tacrine in neuronal and non-neuronal cell lines. 958 88

Low doses of the acetylcholinesterase-inhibiting carbamate nematicides disrupt chemoreception in plant-parasitic nematodes. Fluorescein isothiocyanate (FITC)/dextran conjugates up to 12 kDa are taken up from the external medium by certain chemosensory neurons in Caenorhabditis elegans. Similar chemoreceptive neurons of the non-feeding infective stage of Heterodera glycines (soybean cyst nematode) fill with FITC and the nuclei of their cell bodies selectively stain with bisbenzimide. The widely used nematicide aldicarb disrupts the chemoreceptive response of H. glycines with 50% inhibition at very low concentrations (ca 1 pM), some 10(-6)-fold lower than required to affect locomotion. Similarly, the anthelmintic levamisole had this effect at 1 nM. Peptides selected as mimetics of aldicarb and levamisole also disrupt chemoreception in H. glycines and Globodera pallida at 10(-3)-fold or lower concentration than required to inhibit locomotion. We propose an uptake pathway for aldicarb, levamisole, peptide mimetics and other soluble molecules by retrograde transport along dendrites of chemoreceptive neurons to the cell bodies and synapses where they act. This may prove to be a general mechanism for the low-dose effects of some nematicides and anthelmintics.
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PMID:Neuronal uptake of pesticides disrupts chemosensory cells of nematodes. 1255 75