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)

Patients with atopic dermatitis have abnormal autonomic responses of the arterioles, pilomotor smooth muscle, and sweat glands. Their lesions have been reported to contain increased amounts of the neurohumors, acetylcholine and norepinephrine, as well as increased activity of acetylcholinesterase and catechol-O-methyltransferase. In vitro studies of epidermis show that beta adrenergic agonists fail to evoke the normal inhibition of mitosis of basal cells of patients with atopic dermatitis. Epidermis removed not only from the lesions, but also from normal-appearing skin, responded abnormally. The increase in intracellular levels of cAMP after exposure to catecholamines was similar in normal and atopic epidermis. Lymphocytes and PMN leukocytes isolated from patients with atopic dermatitis show both a decreased physiologic response (glycogenolysis and inhibition of lysosome enzyme release) and a decreased rise in intracellular levels of cAMP upon incubation with beta agonists, but a normal response to PGE1. Cortisol increases the response of lymphocyte adenyl cyclase to both agonists and, in the case of the patients with atopic disease, more than overcomes the depressed response to beta agonists. Because the leukocytes respond normally to PGE1 and because others have reported normal activities of skin and adenyl cyclase, phosphodiesterase, and protein kinases, we conclude that the step responsible for the diminished beta adrenergic response lies antecedent to the catalytic site of adenyl cyclase.
J Invest Dermatol 1976 Sep
PMID:Adrenergic mechanisms and the adenyl cyclase system in atopic dermatitis. 0 56

This is a review of historical facets of research in cutaneous neurohistology. The silver stains, used for some 150 years, led to the discovery of the neurone theory and to contemporary comparative studies. The cholinesterase methods, used since 1950, are the most convenient for general studies of nerves. The fluorescence technique of Falck (1962) is valuable for the study of adrenergic fibers. The electron microscope techniques used since 1950 have allowed the comprehensive description of myelinated and unmyelinated nerve fibers and of corpuscles. The most important unsettled questions pertain to the physiology of cutaneous nerves and precise definitions of cutaneous sensibility.
J Invest Dermatol 1976 Jul
PMID:Cutaneous innervation. 5 52

Acetylcholinesterase (Ache) and pseudocholinesterase (BUche) activities were studied quantitatively in healthy skin by spectrophotometric methods and qualitatively by polyacrylamide gel electrophoresis. The results were compared to those obtained in plasma. The substrates used to reveal enzyme activities were acetylthiocholine (ATC) iodide and butyrylthiocholine (BTC) iodide, respectively. A linear relationship exists between the values of BUche and Ache activities in plasma and those in skin. Six isoenzymes of different electrophoretic mobility were observed in the skin. One of them, which is never found in plasma extracts, appears to be specific to the skin. On gradient gel electrophoresis, with both substrates (ATC and BTC), a single band of enzyme activity, corresponding to a molecular weight of 600,000 was observed. These results suggest that in the skin there is only one enzyme, most probably butyryl cholinesterase, which cleaves BTC somewhat faster than ATC. This methodology, when applied to the study of dermatoses in which abnormalities of cutaneous nerve terminals are suspected, should furnish precise functional pathophysiological details.
J Invest Dermatol 1979 Sep
PMID:Cholinesterases isoenzymes: a comparative study in the skin and plasma. 46 77

At the same temperature and with adequate circulation of blood or receptor solution beneath it the permeability of the stratum corneum of the rabbit ear to T2O or to 32P-TPP was the same in vivo as in vitro. When skin permeability was measured in vitro, the subcutaneous adipose tissue present in the full-thickness skin of the rat delayed the penetration of CR, a lipophilic substance with a low water solubility, and decreased the permeability constant by nearly 3x. The retardant solvent PEG 300 did not penetrate the stratum corneum; it formed a hydrogen-bonded complex with the cholinesterase inhibitor VX, thereby reducing the thermodynamic activity and penetration rate of this compound through the stratum corneum. The accelerant solvent DMSO removed protein components from the stratum corneum; electron microscope studies showed that the cells of stratum corneum so treated became separated from one another, and their contents became stainable in bulk with Pb++, indicating the creation of new diffusion pathways. When the temperature, clearance of penetrant from the lower surface of the stratum corneum and penetrant formulation were the same in vivo as in vitro, and the surface of the stratum corneum was saturated with the penetrant or its solution, the results of permeability measurements made in vivo were similar to those made in vitro.
Curr Probl Dermatol 1978
PMID:Factors affecting the permeability of skin. The relation between in vivo and in vitro observations. 75 61

S-(2-diisoproplaminoethyl) 0-ethyl methylphosphonothioate (VX), an anticholinesterase liquid of low volatility, was applied to the skin of 139 men at environmental temperatures of -18 degrees, 2 degrees, 18 degrees, or 46 degrees C. The skin was decontaminated after 3 hr and the men spent the next 21 hr at about 27 degrees C. The amount of VX penetrating the skin was estimated from the inhibition of red blood cell cholinesterase. The decimal fraction of the dose that penetrated in 3 hr ranged from 0.04 at -18 degrees C to 0.32 at 46 degrees C for the cheek and from 0.004 at +18 degrees C to 0.029 at 46 degrees C for the forearm. Further increase in cholinesterase inhibition after decontamination was evidence of a deposit of VX in the skin. The amount of VX remaining in the skin after decontamination was greater in the forearm and less in the cheek at higher temperatures.
J Invest Dermatol 1977 Jun
PMID:Environmental temperature and the percutaneous absorption of a cholinesterase inhibitor, VX. 86 76

Eccrine sweat collected from the human skin surface contains at least five different esterases. One of them is a cholinesterase. A non-specific carboxylesterase with the electrophoretic mobility of an alpha-globulin appears to be a serum protein. Besides this, there are two isoenzymes of human origin migrating with the same electrophoretic mobility as gamma-globulins. These two isoenzymes are immunologically identical with a non-specific carboxylesterase occurring in numerous organs and body fluids. Lipase activity could not be demonstrated.
Br J Dermatol 1976 Jul
PMID:Immunological demonstration of multiple esterases in human eccrine sweat. 95 42

Allergenic and photosensitizing effects of organophosphorus pesticides (OPP) have been detected, as well as their destructive effect on the skin cell ultrastructure, on the body metabolism and enzymic systems, and the inhibitory effect on cholinesterase activity. Pesticide-induced changes in polyunsaturated fatty acids (PUFA) are significant in the mechanism of dermatoses development. The complex of treatment-and-prophylaxis measures includes regular dermatologic check-ups and limitation of the number of subjects handling OPP. Subjects in whom premorbid shifts have been detected, should be followed up. The therapy and prevention of the dermatoses developing as a result of exposure to pesticides may be effectively carried out with antioxidants, amino acids, vitamins, etc.; diets with the optimal PUFA-tocopherol ratio are advisable. Overalls with multiple protective physicochemical characteristics, filtering respirators and such are recommended.
Vestn Dermatol Venerol 1989
PMID:[Measures for the combined therapy and prevention of dermatoses occurring in workers in contact with organophosphorus pesticides]. 253 Jul 19

Four patients with aquagenic pruritus (AP), one patient with polycythemia rubra vera, one patient with cold urticaria, and three normal control volunteers were studied to better understand the pathophysiology of water-induced itching. Punch biopsy specimens were taken before and after water contact; the specimens were immediately frozen, sectioned, and stained histochemically for acetylcholinesterase (AChE) activity. This was localized in the nerve fibers surrounding eccrine sweat glands and was quantified by microspectrophotometry. In AP and polycythemia rubra vera after water exposure a significantly increased AChE activity suggesting acetylcholine release was observed, whereas in the patient with cold urticaria and the controls, a significant decrease was noted. Two related patients with AP had an inherited abnormality of serum cholinesterase, which, however, had no obvious correlation with their particular disease. The proof of AChE activation might support the clinical diagnosis and indicate a hypothetical involvement of eccrine sweat glands in the pathogenesis of AP.
Arch Dermatol 1988 Jan
PMID:Aquagenic pruritus. Water-induced activation of acetylcholinesterase. 333 47

We observed the autonomic nerve plexuses in the skin of an erythermalgic patient and a normal individual using the methods of acetylcholinesterase (AChE) histochemistry, catecholamine histofluorescence, and electron microscopy. The density of both AChE-positive and catecholamine-containing nerve terminals in the periarterial and sweat glandular plexuses was greatly reduced in the erythermalgic foot skin compared with those in unaffected skin from the same patient and in the foot skin of a normal individual. Ultrastructurally, the terminal axons containing either agranular (cholinergic) or small dense-cored (adrenergic) vesicles were present in the periarterial and periglandular regions of the erythermalgic skin, but the occurrence of these nerve terminals in the involved skin appeared to be much reduced in frequency compared with uninvolved skin and the skin of a normal individual.
Arch Dermatol 1983 Jan
PMID:Autonomic innervation of the skin in primary erythermalgia. 633 30

We previously reported that normal human keratinocytes express muscarinic receptors, and that acetylcholine induces attachment of these cells to each other. We have now studied the ability of human keratinocytes to synthesize, secrete, and degrade acetylcholine. To detect and localize the synthesizing enzyme choline acetyltransferase and degrading enzyme acetylcholinesterase, cultured cells and cryostat sections of normal human skin were pre-incubated with specific monoclonal antibodies and stained with an avidin-biotin complex/alkaline phosphatase. The choline acetyltransferase activity was assessed by the conversion of [3H]acetyl CoA to [3H]acetylcholine, and newly synthesized [3H]acetylcholine was detected using thin-layer chromatography. The acetylcholinesterase activity was measured spectrophotometrically. Both cholinergic enzymes were present in cultured keratinocytes, and in basal, spinous and granular epidermal cell layers. Choline acetyltransferase was visualized in the vicinity of cell nuclei, and acetylcholinesterase was observed in or near cell membranes. Newly synthesized acetylcholine was detected in both cell homogenates and culture supernatants. The estimated Vmax of the synthesis of labeled acetylcholine by homogenized keratinocytes was about 20 pmoles acetylcholine produced/mg protein/min at 37 degrees C. A single keratinocyte synthesized a mean of 2 x 10(-17) moles, and released 7 x 10(-19) moles acetylcholine per minute. Both cell homogenates and culture supernatants exhibited similar acetylcholinesterase activities indicating that human keratinocytes secrete acetylcholinesterase, too. Thus, we have demonstrated that normal human keratinocytes possess choline acetyltransferase and acetylcholinesterase, and synthesize, store, release, and degrade acetylcholine. Because human keratinocytes can also respond to acetylcholine, we believe that keratinocyte acetylcholine works in the epidermis as a local hormone.
J Invest Dermatol 1993 Jul
PMID:Human keratinocytes synthesize, secrete, and degrade acetylcholine. 833 Dec 94


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