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At least 1,315 records · Page 73Linked to original sources
PubMed1999

Prenatal diagnosis of rhizomelic chondrodysplasia punctata due to isolated alkyldihydroacetonephosphate acyltransferase synthase deficiency.

Current practices in prenatal diagnosis of rhizomelic chondrodysplasia punctata (RCDP) are reviewed. A case is presented with a family having one daughter affected with RCDP due to alkyldihydroacetonephosphate acyltransferase synthase (DHAPAT synthase) deficiency, and three subsequent pregnancies. Biochemical test values are presented for the pregnancies and daughter. Post-mortem tests of one fetus of a terminated pregnancy showed that radiologic examination could not make the diagnosis of RCDP. We conclude that biochemical or molecular testing is necessary to accurately diagnose this type of RCDP prenatally.

Adult↗
PubMed1977

Studies on trimethylsilyl derivatives of 1-alk-1enyl-2-acyl glycerols by gas-liquid chromatography mass spectrometry.

Trimethylsilyl derivatives of 1-hexadec-1-enyl-2-decanoyl and -2-octadecenoylglycerols and 1-octadec-1-enyl-2-decanoyl and -2-octadecenoylglycerols were subjected to analysis by a gas chromatograph mass spectrometer system. The characteristic ions are as follows: (1) ions at [M-15]+ and [M-90]+- are observed, 2 or 16 mass units less than those of the corresponding 1-alkyl-2-acyl or 1,2-diacyl derivatives; (2) the base peak is m/e 129; (3) the ion at [M-R1CH=CHO]+ or [R2COO+130]+ is present in high abundance; (4) ions at m/e 311 and 339, characteristic of trimethylsilyl derivatives of 1-hexadec-1-enyl and 1-octadec-1-enylglycerols, are due to [R1CH-CHO-1)+73]+, also confirmed from studies on the perdeuteriotrimethylsilyl derivatives; (5) several ions based on one acyl group, [R2CO]+, [R2CO+74]+ and [R2COO+74]+ are also observed.

Acylation↗
PubMed2001

Chloroaluminum phthalocyanine tetrasulfonate delivered via acid-labile diplasmenylcholine-folate liposomes: intracellular localization and synergistic phototoxicity.

Folate-diplasmenylcholine (1,2-di-O-(Z-1'-hexadecenyl)-sn-glycero-3-phosphocholine; DPPlsC) liposomes have been shown to greatly enhance the potency of water-soluble antitumor agents via a selective folate-mediated uptake and acid-catalyzed endosomal escape mechanism (Rui et al. J. Am. Chem. Soc., 1998; 120:11213--18). This study describes an adaptation of this strategy for the delivery of chloroaluminum phthalocyanine tetrasulfonate ([AlPcS(4)](4-)), a water-soluble sensitizer used in photodynamic therapy, in a binary targeting scheme designed to enhance both its tumor selectivity and phototoxicity. [AlPcS(4)](4-)/DPPlsC:folate liposomes (9.8 microM bulk concentration, 2.5 mM intraliposomal concentration) were substantially more phototoxic to folate-deficient KB cells than 12.5 microM free [AlPcS(4)](4-) after a 30 min irradiation (630-910 nm). Considerable differences in phototoxicity were observed, however, between the commercially-available AlPcS(4)(4-) and an HPLC purified sample of [AlPcS(4)](4-) due to an increased tendency for the latter to aggregate. Experiments with [AlPcS(4)](4-)/DPPC:folate and folate-free [AlPcS(4)](4-)/DPPlsC liposomes (acid-insensitive and non-targeted controls, respectively) showed significantly reduced phototoxicities under the same illumination conditions. Our results imply that higher concentrations of water-soluble sensitizers can be delivered to target cells using the folate receptor-mediated pathway, which can change both the biodistribution and intracellular localization of the sensitizer when acid-labile DPPlsC liposomes are used as the delivery vehicle. Potential advantages of this approach include the use of lower bulk [AlPcS(4)](4-) concentrations, rapid plasma clearance of free [AlPcS(4)](4-), and better phototoxic responses, due to higher intracellular [AlPcS(4)](4-) concentrations combined with reduced collateral photodamage arising from misguided sensitizer accumulation, thereby enhancing the selective phototoxicity of PDT treatments.

Aluminum↗
PubMed2003

Internal residue loss produced by rearrangement of a novel cationic glycosphingolipid, glyceroplasmalopsychosine, in collision-induced dissociation.

A novel plasmal conjugate of galactosylsphingosine (psychosine), Gro1(3)-O-plasmal-O-6Galbeta-sphingosine (glyceroplasmalopsychosine), was analyzed by electrospray ionization and liquid secondary ion mass spectrometry with low- or high-energy collision-induced dissociation (CID). In the product ion spectra of the [M + H](+) ions, [M + H - glycerol](+) ions arising from the loss of a glycerol were predominant. Unexpectedly, CID of the [M + H - glycerol](+) ion produced an outstanding ion, [(M + H - glycerol) - Hex](+), which required the loss of the galactose from inside the molecule. This ion was greatly reduced in the spectra of N,N-dimethyl derivatives, indicating that the [(M + H - glycerol) - Hex](+) ion is formed from an intramolecular rearrangement with migration of the plasmal residue to the free amino group of sphingosine. It would be expected that the rearrangement occurs simultaneously with the elimination of glycerol or a rearranged [M + H](+) ion leads to the elimination of glycerol, to form a Schiff base-type [M + H - glycerol](+) ion, from which the terminal galactose could be removed by the normal mechanism of glycosidic cleavage. On the other hand, the [M + Na - glycerol](+) ion derived from the sodiated molecule did not produce an ion corresponding to the rearrangement reaction, possibly owing to a higher stability of the sodiated ions against conformational changes.

Animals↗
PubMed1994

Characterization of rabbit myocardial phospholipase A2 activity using endogenous phospholipid substrates.

We have developed an assay for studying myocardial phospholipase A2 activity by measuring accumulation of lysophospholipids resulting from hydrolysis of the endogenous choline glycerophospholipid pool. This assay was used to characterize phospholipase A2 activity in rabbit myocardium. Lyophilized rabbit myocardium was incubated at 37 degrees C in Tris-HCl buffer containing either ethylene glycol bis(beta-aminoethyl ether) N,N'-tetraacetic acid (EGTA)/EDTA or calcium, and palmitoyl-lysophosphatidylcholine (P-LPC), oleoyl-LPC, stearoyl-LPC, and 16:0-lysoplasmenylcholine were measured using a recently developed HPLC method. The identity of the individual species was confirmed by ion-spray LC-MS-MS. In the presence of EGTA/EDTA, incubation for up to 30 min caused a linear increase in all lysophospholipids. The main increases were found in P-LPC and 16:0-lysoplasmenylcholine, which increased by 37 +/- 3 (mean +/- SE, N = 8) and 48 +/- 3 nmol/g dry wt x min, respectively. The apparent phospholipase A2 activity was found to be calcium, temperature, and pH sensitive. The pH optimum was between 6.5 and 8.0, and incubation at room temperature and 45 degrees C decreased the activity by 80 and 40%, respectively. Studies of the metabolism of the formed lysophospholipids showed a substantial metabolism of the lysophospholipids that accounted for about 40% of the total phospholipase A2 activity. This method offers a novel approach to study phospholipase A2 activities by measuring accumulation of products resulting from hydrolysis of endogenous phospholipid pools.

Animals↗
PubMed2000

Elevation in phosphatidylethanolamine is an early but not essential event for cardiac cell differentiation.

The biosynthesis of phosphatidylethanolamine was examined during differentiation of P19 teratocarcinoma cells into cardiac myocytes. P19 cells were induced to undergo differentiation into cardiac myocytes by the addition of dimethyl sulfoxide to the medium. Immunofluorescence labeling confirmed the expression of striated myosin 10 days postinduction of differentiation. The content of phosphatidylethanolamine increased significantly within the first 2 days of differentiation. [1,3-(3)H]Glycerol incorporation into phosphatidylethanolamine was increased 7.2-fold during differentiation, indicating an elevation in de novo synthesis from 1, 2-diacyl-sn-glycerol. The mechanism for the increase in phosphatidylethanolamine levels during cardiac cell differentiation was a 2.8-fold increase in the activity of ethanolaminephosphotransferase, the 1,2-diacyl-sn-glycerol utilizing reaction of the cytidine 5'-diphosphate-ethanolamine pathway of phosphatidylethanolamine biosynthesis. Incubation of P19 cells with the phosphatidylethanolamine biosynthesis inhibitor 8-(4-chlorophenylthio)-cAMP inhibited the differentiation-induced elevation in phosphatidylethanolamine levels but did not affect the expression of striated myosin. The results suggest that elevation in phosphatidylethanolamine is an early event of P19 cell differentiation into cardiac myocytes, but is not essential for differentiation to proceed.

Animals↗
PubMed2003

Phenotypic variability (heterogeneity) of peroxisomal disorders.

Peroxisomes perform a multitude of biosynthetic and catabolic functions, many of which are related to lipid metabolism. Peroxisomal disorders result either from deficiency of a single peroxisomal enzyme or protein, or from a defect in the complex mechanism of peroxisomal biogenesis, resulting in deficiency of several or multiple peroxisomal functions. These can be assessed by a battery of biochemical assays, enabling a biochemical phenotype to be defined that is specific and diagnostic for each of the peroxisomal disorders. Some peroxisomal disorders have unique and specific clinical phenotypes, which may be diagnostic. Others share patterns of clinical abnormalities (particularly neurological dysfunction, craniofacial dysmorphism, skeletal defects, sensory deafness, retinopathy) consistent with defined clinical phenotypes, but with considerable overlap and heterogeneity. To a certain extent, the clinical features of a particular disorder reflect the accumulation or deficiency of specific metabolites. Thus, the same clinical phenotypes may be caused by both single enzyme defects and PBDs. Furthermore, the same defect may present with different clinical phenotypes. In general, the severity of the clinical phenotype correlates with the degree of biochemical dysfunction. The clinical heterogeneity of peroxisomal disorders constitutes a diagnostic challenge demanding a high index of suspicion on the clinician's part.

Chondrodysplasia Punctata, Rhizomelic↗