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Dihydroxycholestanoic acid

Alkyl PAT, alkyl-dihydroxy phosphate synthase Bif, bifunctional enzyme DHAPAT, dihydroxyphosphate acyltransferase deficiency DHCA, dihydroxycholestanoic acid N, normal nd, not determined Ox, acyl-CoA oxidase Rac, 2-methylacyl-CoA racemase RCDP, rhizomelic chondrodysplasia punctata Ref, Refsum s disease THCA, trihydroxycholestanoic acid VLCFA, very-long-chain fatty acid. [Pg.691]

Dihydroxycholestanoic acid CoA ester and trihydroxycholestanoic acid CoA ester IS d4-CA CoA ester Rat liver homogenate (0.1 g) extraction (ethyl acetate) RP-SPE Synergi HydroRP 80A (150 x 2.0 mm I.D., Phenomenex), isojHX>panol— acetonitrile—water adjusted to pH 2.7 with formic acid and 0.4 ml/min API 365 (Sciex), positive ESI, SRM ([M + p oduct ion) LOD 0.1 nmol [65]... [Pg.227]

Dihydroxycholestanoic acid, trihydroxycholestanoic acid and their taurine conjugates IS d4-CA and taurine conjugate of d4-CA Human plasma (50 pi) deproteinization (acetonitrile) AUtima Cig (250 x 2.1 mm I.D., AUtima), gradient (ethanol-5 mAf ammonium formate) and 0.3 ml/min Quattro II (Micromass), negative ESI, SRM ([M-H] — product ion, unconjugates), SIM ([M-H] , taurine conjugates) LOD 0.05 nmol/ml [67]... [Pg.227]

A, double bond at carbon number x UDCA, ursodeoxycholic acid (5(I-BA-3a,7p-diol) CDCA, chenodeoxycholic acid (5p-BA-3a,7a-diol) THCA, trihydrocholestanoic acid (5p-CA-3a,7a,12a-triol) DHCA, dihydroxycholestanoic acid (5p-CA-3a,7a-diol). [Pg.302]

FIGURE 14.7 Derivatization for ESI-MS/MS. (A) Preparation of the dimethylaminoethylester of dihydroxycholestanoic acid bis acetate. (B) Preparation of aminoethanesulfonate derivative of chenodeoxycholic acid. (C) Formation of sulfate ester of cholesterol. (D) Preparation of oxime of testosterone. [Pg.313]

Trihydroxycholestanoic acid (THCA) Dihydroxycholestanoic acid (DHCA) Phytanic acid Pristanic acid... [Pg.497]

Figure 4 Peroxisomal fatty-acid (FA) /3-oxidation pathways. While saturated long-chain fatty acids (LCFA) are preferentially degrade in mitochondria, saturated very-long-chain fatty acids (VLCFA) and some LCFA are shortened by peroxisomal /3-oxidation. Degradation of pristanic acid, the product of phytanic acid a-oxidation, and the conversion of the cholesterol-derived 27-carbon bile-acid precursors dihydroxycholestanoic acid (DHCA) and trihydroxycholestanoic acid (THCA) to 24-carbon bile acids also require this pathway. The mechanism by which these substrates enter peroxisomes is unknown. Four enzymatic reactions serve to shorten the substrates by either two (LCFA, VLCFA) or three (pristanic acid, DHCA, THCA) carbon atoms. The 2-methyl group of the latter substrates is shown in brackets. SCPx thiolase refers to the thiolase activity of sterol carrier protein x. Figure 4 Peroxisomal fatty-acid (FA) /3-oxidation pathways. While saturated long-chain fatty acids (LCFA) are preferentially degrade in mitochondria, saturated very-long-chain fatty acids (VLCFA) and some LCFA are shortened by peroxisomal /3-oxidation. Degradation of pristanic acid, the product of phytanic acid a-oxidation, and the conversion of the cholesterol-derived 27-carbon bile-acid precursors dihydroxycholestanoic acid (DHCA) and trihydroxycholestanoic acid (THCA) to 24-carbon bile acids also require this pathway. The mechanism by which these substrates enter peroxisomes is unknown. Four enzymatic reactions serve to shorten the substrates by either two (LCFA, VLCFA) or three (pristanic acid, DHCA, THCA) carbon atoms. The 2-methyl group of the latter substrates is shown in brackets. SCPx thiolase refers to the thiolase activity of sterol carrier protein x.
See other pages where Dihydroxycholestanoic acid is mentioned: [Pg.155]   
See also in sourсe #XX -- [ Pg.222 ]

See also in sourсe #XX -- [ Pg.313 ]



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