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Metabolism methyl

It is not presently known what phase I enzymes metabolize methyl parathion, and consequently, whether metabolism differs between children and human adults. There is some suggestive evidence for age-related differences in metabolism of methyl parathion in rats (Benke and Murphy 1975). [Pg.111]

The reduction in protein synthesis obviously has other ramifications, such as a deficiency in hepatic enzymes and a consequent general disruption of intermediary metabolism. Methylation reactions are presumably also affected. [Pg.361]

Choline is one of a few B Vitamins that participate in methyl group metabolism. Methyl groups (CHs) are components of numerous important biological compounds. [Pg.1772]

One of the problems faced by catechol compounds, such as noradrenaline, is the metabolic methylation of one of the phenolic groups. Since both phenol groups are involved in hydrogen bonds to the receptor, the masking of one of the phenol groups disrupts the hydrogen bonding and makes the compound inactive. [Pg.118]

Russo et al. followed the metabolism of labeled hordenine (o-hydroxy-N,N-dimethyl[13c]phenethylamine) by root homogenates with 13c NMR. They observed a decrease in the signal due to the dimethylamino group with a concomitant increase in a signal due to the methylamino group, but observed no signal due to the metabolized methyl group (30). [Pg.179]

DAET, diisopropyl aminoethanethiol DAEMS, diisopropyl aminoethyl methyl sulfide—resulting from the metabolic methylation of diisopropyl aminoethanethiol. [Pg.508]

Choline [(CH3)3N+-CHrCH2-OH]OH, a component of some phospholipids (see Membrane lipids) and of Acetylcholine (see). It is a metabolic methyl group donor. It decreases the deposition of body fat, lowers the blood pressure, and causes the uterus to contract. Under certain conditions it may be required in the diet, and is therefore sometimes accord the status of a vitamin. [Pg.116]

EA, GA, and the intestinal catabolites sutler an extensive phase II metabolism (methylation, glucuronidation, sulphation, or combination of them)... [Pg.93]

Hyperhomocysteinemia has long been identified as a risk factor for dementia including Alzheimer s disease (AD) and vascular dementia (VaD) (Morris 2003). The relationship of homocysteine metabolism (methylation and transsulfuration pathways) to deficiencies of the vitamin B complex suggests that hypervitaminosis (Bg, B12 and folate) could contribute to hyperhomocysteinemia (Gonzalez-Gross et al. 2001). [Pg.804]

Norlaudanosoline is metabolically methylated in the 6-position first. Hence it follows that a second 0-methyl group has to be introduced at position 4 of the tetra-hydrobenzylisoquinoline molecule on the way to norreticuline. One must postulate the existence of an enzyme which specifically methylates 6-0-methyl-norlaudanoso-line in the 4 -position with SAM serving as donor of the methyl group. Agmn,Berbers cell cultures (Hinz and Zenk 1981) proved to be an excellent plant source in the search for this new enzyme. Frenzel in our laboratory recently discovered this highly specific enzyme which catalyses the reaction depicted in Fig. 4. This enzyme should prove to be an interesting catalyst for specifically labelling norreticuline. [Pg.244]

Methionine and Cysteine Metabolism. Methyl groups play an important role in the biosynthesis of many substances, and methionine has turned out to be the methyl donor par excellence. Active methyl arises directly out of methionine and ATP it is a sulfonium compound (formula in Chapt. VI-5). We shall return to the active methyl group on occasion (cf. also Chapt. VI-5, XIII-2, XX-5), but now will discuss the demethylated methionine. Its name is homocysteine, because its carbon chain is longer than that of cysteine by one CH2 group. It can provide the sulfur for cysteine by condensing with serine the resultant thioether (cystathionine) breaks into homoserine and cysteine (formulas below). [Pg.166]


See other pages where Metabolism methyl is mentioned: [Pg.31]    [Pg.130]    [Pg.145]    [Pg.246]    [Pg.725]    [Pg.740]    [Pg.740]    [Pg.279]    [Pg.279]    [Pg.121]    [Pg.279]    [Pg.119]    [Pg.295]    [Pg.288]    [Pg.380]    [Pg.94]    [Pg.179]   
See also in sourсe #XX -- [ Pg.15 ]




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