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Aging esterase

This process of aging is believed to be critical in the development of delayed neuropathy, after NTE has been phosphorylated by an OP (see Chapter 10, Section 10.2.4). It is believed that most, if not all, of the B-esterases are sensitive to inhibition by OPs because they, too, have reactive serine at their active sites. It is important to emphasize that the interaction shown in Fignre 2.11 occurs with OPs that contain an oxon group. Phosphorothionates, which contain instead a thion group, do not readily interact in this way. Many OP insecticides are phosphorothionates, but these need to be converted to phosphate (oxon) forms by oxidative desulfuration before inhibition of acetylcholinesterase can proceed to any significant extent (see Section 2.3.2.2). [Pg.39]

A few OP compounds cause delayed neuropathy in vertebrates because they inhibit another esterase located in the nervous system, which has been termed neuropathy target esterase (NTE). This enzyme is described in Chapter 10, Section 10.2.4. OPs that cause delayed neuropathy include diisopropyl phosphofluoridate (DFP), mipafox, leptophos, methamidophos, and triorthocresol phosphate. The delay in the appearance of neurotoxic symptoms following exposure is associated with the aging process. In most cases, nerve degeneration is not seen with initial inhibition of the esterase but appears some 2-3 weeks after commencement of exposure, as the inhibited enzyme undergoes aging (see Section 16.4.1). The condition is described as OP-induced delayed neuropathy (OPIDN). [Pg.300]

In the peel strong immunological depositions of acetyl esterase were found in epidermis, the small cells of the exocarp and in the oil cavities (Fig. 3 A,B,C). In the mesocarp and endocarp the immunological depositions were more moderate (Fig. 3 D), but strong immunological depositions were found in the vascular bundles, especially in xylem. The immunological depositions in the peel seem to be correlated with cell size or cell age. The small cytoplasma rich cells have a higher content of acetyl esterase. [Pg.728]

Aspirin serum esterase activity is species dependent.194 In man it is sex linked since it was found to be higher in men than women.195 It also seems to be age dependent.196... [Pg.33]

The enzymes used by these workers were cholinesterase, prepared from horse serum, and horse-liver esterase. Parallel experiments were carried out with twice crystallized ovalbumin, and with an aged, dialysed specimen of horse serum with negligible esterase activity. [Pg.91]

Nitromethane was administered intraperitoneally (200 mg/kg bw) to male Wistar rats (three months of age) as a 10% solution in olive oil. The effects of nitromethane in the liver were detected only 48 h after administration and included a decrease in NADPH-cytochrome c reductase activity with proliferation of the smooth endoplasmic reticulum. Nitromethane also caused an increase in brain acid proteinase (4 h after injection) and acetylcholine esterase activities (4, 24 and 48 h after injection) (Zitting etal, 1982). [Pg.493]

Section D,5, Fig. 11-8, and Chapter 19). Demethylation occurs by hydrolysis, which is catalyzed by esterases. Carboxylmethylation also occurs in eukaryotic cells but is often substoichiometric and part of a mechanism for repair of isomerized or racemized aspartyl residues in aged proteins (Box 12-A). However, the major eukaryotic protein phosphatase 2A is carboxylmethylated at its C terminus,131 as are the Ras proteins discussed in Section D,3. [Pg.548]

In 86 intensively treated patients with type 1 diabetes aged 7-18 years, the incidence of severe hypoglycemia correlated with the serum activity of acetylcholine esterase. Patients with acetylcholine esterase activity at the median or above reported 3.0 events/year and those with acetylcholine esterase activity below the median reported 0.5 events/year, suggesting that a genetic factor may play a role in the emergence of severe hypoglycemia (46). [Pg.395]

Plata, M. C., Mauricio, J. C., Millan, C., and Ortega, J. M. (1998). In Vitro activity of alcohol acetyltransferase and esterase in two flor yeast strains during biological aging of sherry wines. J. Ferment. Bioeng. 85, 369-374. [Pg.39]

Age in 1984, years Anticholin- esterases Anticholin- ergics Cholinesterase Reactivators Semvl Irritants- Vesicants Canna- binoids LSD None fNCn Totala ... [Pg.55]

However, a small study of younger women (16-59 years of age) presenting with a history of two symptoms - dysuria and frequency - but dipstick negative for both leucocyte esterase and nitrites, demonstrated that treatment with short-course trimethoprim significantly decreased the median time to resolution of dysuria (76% of women in trimethoprim group were free of dysuria by day 3 compared with 26% of placebo group). The authors concluded that their results supported the use of symptoms alone to diagnose and treat UTI without urinalysis (Richards et al., 2005). [Pg.118]

Cheese/hutter flavor. Pregastric lipases, have, been used for years to intensify flavor in Menzyme-modified cheese , and for an intensified butter flavor in lipolyzed butter. Generally the fatty acid residues that need to be split off (to generate the right flavor) are the short chain fatty acids, especially the C to C-jq acids typical of Italian cheeses. The butyric acids are produced from butterfat more specifically by newly developed lipases (really esterases) from Mucor meihei and a very new one, from Aspergillus oryzae, especially for cheddar cheese flavor development. The latter enzyme is marketed under the name Flavor Age (4). Flavors produced in this manner are used widely in cheese-flavored snack foods the value of the intensified cheese flavors is on the order of 50 million, but the. value of the enzymes employed is only about 2-3 million. [Pg.174]

OPs are known to induce time-delayed neurotoxicity. This is due to the inhibition of an esterase in nerve tissue, neuropathy target esterase (NTE), that is also found in muscle and blood cells. The NTE level in the blood is an indicator of the inhibition of the enzyme. Inhibition of NTE and aging, the process of following the OP binding to an active esterase site that prevents the reactivation of the site, is important for selection of an antidote against certain OP nerve agents. It is of primary concern for Novichok agent. There is little information available on OP-caused neurotoxicity and the cardiac toxicity. [Pg.499]


See other pages where Aging esterase is mentioned: [Pg.868]    [Pg.945]    [Pg.868]    [Pg.945]    [Pg.39]    [Pg.86]    [Pg.197]    [Pg.206]    [Pg.377]    [Pg.164]    [Pg.103]    [Pg.52]    [Pg.362]    [Pg.430]    [Pg.217]    [Pg.327]    [Pg.132]    [Pg.348]    [Pg.486]    [Pg.23]    [Pg.128]    [Pg.567]    [Pg.38]    [Pg.43]    [Pg.271]    [Pg.271]    [Pg.314]    [Pg.47]    [Pg.47]    [Pg.695]    [Pg.762]    [Pg.763]    [Pg.770]    [Pg.771]    [Pg.799]   
See also in sourсe #XX -- [ Pg.28 , Pg.92 , Pg.526 , Pg.826 , Pg.868 , Pg.869 , Pg.937 , Pg.938 , Pg.939 , Pg.944 , Pg.945 ]




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Aging neuropathy target esterase

Aging serine esterase

Esterase

Esterases

Esterases esterase

Serine esterases aging

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