Chemical lesions lipids

The chemical adducts formed by reaction of aldehydes with lysine residues form highly immunogenic epitopes, and antibodies have been prepared specific for malondialdehyde- and 4-hydroxynonenal-conjugated LDL (Gonen et al., 1987 Yla-Herttuala et al., 1989 Jurgens et al., 1990). These antibodies cross-react with material in atherosclerotic lesions but not normal tissue, thus supporting the central role of lipid peroxidation in the patho nesis of atherosclerosis (Yla-Herttuala et al., 1989, 1991). 

Bioactive peptides such as superoxide dismutase and interferon arc also hoped to be accumulated in the inflamed and vascular lesions. However, these active peptides cannot be incorporated in lipid microspheres. Instead of incorporating them into lipid microspheres, we devised a method to combine the bioactive peptides with a chemically modified lecithin. In this study, we also examined the tissue distribution of lecithinized IgG. 

The most direct mechanism of hepatotoxicity is through specific interaction of a chemical with a key cellular component and consequential modulation of its function. More common mechanisms, however, involve secondary effects of toxicant interaction. These include depletion of cellular molecules, such as ATP and GSH free radical and oxidant damage, in particular to membrane lipids covalent binding of reactive metabolites to critical cellular molecules and collapse of regulatory ion gradients. The following discussion will highlight how these cellular and molecular mechanisms contribute to specific types of chemically induced hepatic lesions. 

Steatosis, also known as fatty liver, results from the accumulation of excess lipid (more than 5% lipid by weight) in the liver. Many chemicals can cause this, and the lesions can be either acnte or chronic. Ethanol is a classic example, causing both acute and chronic lesions. It indnces large droplets of fat in the cell. On the other hand, snbstances snch as tetracycline and phosphorns produce many... 

In up to 5% of patients undergoing contrast-enhanced abdominal CT, an incidental adrenal mass is discovered (Korobkin et al. 1996). In order to differentiate a lipid-rich adrenal adenomas from pheochromocytomas and other masses such as metastases, patients have to either undergo additional NCCT or chemical-shift MR imaging (Israel et al. 2004). The diagnostic criterion at NCCT that is used to make the diagnosis of adrenal adenoma is low mean attenuation of the lesion <10-15 HU, which is caused by the presence of intracellular fat (Israel et al. 2004). In cases with... 

Hoff HP, O Neil J, Wu Z, Hoppe G, Salomon RL. Phospholipid hydroxyalkenals biological and chemical properties of specific oxidized lipids present in atherosclerotic lesions. Arterioscler Thromb Vase Biol 2003 23 275-282. 

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