Lipid-linked sources

Molecular fossils have been successfully identified in younger Precambrian rocks and linked to certain classes of biological source material. In organic analyses of ancient sediments the cleaned, pulverized rocks are treated with organic solvents to extract a soluble fraction containing the less complex and more easily identifiable compounds. However, this fraction is more subject to contamination since it is not locked within the rock matrix. Normal alkanes have been identified in extracts of the 3 billion year old Fig Tree Shale. These alkanes have a probable biological origin in cellular lipids. The odd and even-numbered alkanes are evenly distributed, a characteristic of alkanes from ancient rocks. It is uncertain, however, whether these compounds were present at the time of deposition or derived from a later source [24]. 

The structural components encountered in E. coli are also present in lipid A of other bacterial sources. Thus, a survey of the structures analyzed shows that lipid A, in general, contain two g/wcoconfigured and pyranosidic D-hexosamine residues (2-amino-2-deoxy-D-glucose, GlcpN, or 2,3-diamino-2,3-dideoxy-D-glucose, GlcpN3N, also termed DAG (49,50)], which are present as a ) -(l — 6)-linked disaccharide (monosaccharide backbones have also been identified, but the respective lipid A lack endotoxic activity). The disaccharide is phosphorylated by one or, in most cases, two phosphate... 

The role of protein kinase C in many neutrophil functions is undisputed and has been recognised for some time. For many years it was believed that the source of DAG, the activator of protein kinase C, was derived from the activity of PLC on membrane phosphatidylinositol lipids. Whilst this enzyme undoubtedly does generate some DAG (which may then activate protein kinase C), there are many reasons to indicate that this enzyme activity is insufficient to account for all the DAG generated by activated neutrophils. More recently, experimental evidence has been provided to show that a third phospholipase (PLD) is involved in neutrophil activation, and that this enzyme is probably responsible for the majority of DAG that is formed during cell stimulation. The most important substrate for PLD is phosphatidylcholine, the major phospholipid found in neutrophil plasma membranes, which accounts for over 40% of the phospholipid pool. The sn-1 position of phosphatidylcholine is either acyl linked or alkyl linked, whereas the sn-2 position is invariably acyl linked. In neutrophils, alkyl-phosphatidylcholine (1-0-alky 1-PC) represents about 40% of the phosphatidylcholine pool (and is also the substrate utilised for PAF formation), whereas the remainder is diacyl-phosphatidylcholine. Both of these types of phosphatidylcholine are substrates for PLD and PLA2. 

Lipid metabolism in the liver is closely linked to the carbohydrate and amino acid metabolism. When there is a good supply of nutrients in the resorptive (wellfed) state (see p. 308), the liver converts glucose via acetyl CoA into fatty acids. The liver can also take up fatty acids from chylomicrons, which are supplied by the intestine, or from fatty acid-albumin complexes (see p. 162). Fatty acids from both sources are converted into fats and phospholipids. Together with apoproteins, they are packed into very-low-density lipoproteins (VLDLs see p.278) and then released into the blood by exocytosis. The VLDLs supply extrahepatic tissue, particularly adipose tissue and muscle. 

Lipid peroxidation is one of the major sources of free-radical mediated injury that directly damages membranes and generates a number of secondary products. In particular, markers of lipid peroxidation have been found to be elevated in brain tissues and body fluids in several neurodegenerative diseases, and the role of lipid peroxidation has been extensively discussed in the context of their pathogenesis. Peroxidation of membrane lipids can have numerous effects, including increased membrane rigidity, decreased activity of membrane-bound enzymes (e.g., sodium pumps), altered activity of membrane receptors, and altered permeability [Anzai et al., 1999 Yehuda et al., 2002], In addition to effects on phospholipids, lipid-initiated radicals can also directly attack membrane proteins and induce lipid-lipid, lipid-protein, and protein-protein cross-linking, all of which obviously have effects on membrane function. 

Sources for specific omics studies are also available. For instance, tools such as the RNA-Seq Atlas [17], Human Protein Atlas (HPA) [18], and the Human Metabolome Database (HMDB) [19] are useful for systemic genomic, proteomic, and metabolo-mics studies of human beings. LIPID Metabolites and Pathways Strategy (LIPID MAPS) [20] is a lipidomics gateway, an integrative platform for studies in lipid biology. More resources and updated links can be found at the Biomarkers portal (see Table 1). 

Hatcher et al. (1981) pointed out that the aliphatic region of terrestrial humic acids is very similar to that of marine humic acids and that the only difference is the presence of aromatic bands in the terrestrial humic acid spectra. In previous work, Hatcher (1980) and Hatcher et al. (1980b) concluded from the H/C ratio of 1.5 and presence of a strong terminal methyl band at 0.9 ppm that marine humic acids have highly branched and cross-linked paraffinic carbon atoms. These structures appear to arise from algal and microbial lipids. The similarity in the aliphatic region in terrestrial humic acids suggests that soil microbial lipids may be the source of the aliphatic structures in terrestrial humic acids. 

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