Tissue lipid peroxidation

AA233) Free radicals (cpm/mg) H202 (pmol)/mg tissue Lipid peroxidation... 

ZIDENBERG-CHERR AND KEEN Enhanced Tissue Lipid Peroxidation 57... 

Without doubt vitamin E is the most important lipid-soluble chain-breaking antioxidant in the human body. It is able to interact with lipid peroxyl radicals and is also able to react with singlet oxygen. The role of vitamin E as an antioxidant in vivo has been established several times by measuring tissue lipid peroxidation in vitamin E-deficient or in vitamin E-supplemented animals. 

These observations add emphasis to the caution that lipid peroxidation measurements be made on fresh tissue samples [700]. While no phenanthro-line-detectable copper, no loss of ceruloplasmin activity, and very little lipid peroxidation were found for samples stored for 4 weeks in the cold, there was a marked increase in phenanthroline-detectable copper, a loss in ceruloplasmin activity, and an increase in lipid peroxidation in these samples after 4 weeks of storage at 40 °C. Storage of these samples at - 20 °C or - 70 °C slowed but did not prevent these artifactual deteriorations in tissue samples. This may also provide some mechanistic insight into the observation that Cu-Zn-SOD-treated adjuvant arthritic rats experienced less paw swelling and tissue lipid peroxidations (/ < 0.001) [701]. 

Kumaraguraparan, R., Subapriya, R., Viswanathan, P., andNagini, S., Tissue lipid peroxidation and antioxidant status in patients with adenocarcinoma of the breast, Clinica Chimica Acta Int. J. Clinical Chem., 325, 165, 2002. 

Demling, R.H., Lalonde, C., Jin, L.J., Ryan, P. and Fox, R. (1986). Endotoxemia causes increased lung tissue lipid peroxidation in unanesthetized sheep. ]. Appl. Physiol, 60, 2094-2100... 

Gonzalez et al. (1995) evaluated EUK-8 in a highly stringent porcine model for sepsis-induced adult respiratory distress syndrome (ARDS). EUK-8 abrogated the increase in lung malondialdehyde, indicating that it prevented tissue lipid peroxidation. 

The effect of supplementation of black pepper or piperine for a period of 10 weeks on tissue lipid peroxidation and enzymic and nonenzymic antioxidants has been examined in rats fed a high-fat diet (20 % coconut oil and 2 % cholesterol). 

Following the action of extraordinary stimulants (hypoxic hypoxia, hypoxia + hyperoxia, hypodynamia + hyperthermia), animals demonstrate an accumulation of malonic dialdehyde with a simultaneous fall of antiradical activity of the liver tissue. A preliminary introduction to rats of acetylene amine 3,4,5-tris(morpho-linopropynyl)-l-methylpyrazole 103 and also of tocopherol antioxidant and gutumine antihypoxant averts activation of the lipid peroxidation processes. The inhibition of peroxidation with this agent is mediated by stabilization of ly-zosomal and mitochondrial membranes. Unsaturated amines prevent destruction of the organelle membranes provoked by UV irradiation and incubation at 37°C (pH4.7)(78MIl). 

The detection and quantification of one or more of the above lipid peroxidation produas (primary and/or secondary) in appropriate biofluids and tissue samples serves to provide indices of lipid peroxidation both in ntro and in vivo. However, it must be stressed that it is absolutely essential to ensure that the products monitored do not arise artifactually, a very difiScult task since parameters such as the availability of catalytic trace metal ions and O2, temperature and exposure to light are all capable of promoting the oxidative deterioration of PUFAs. Indeed, one sensible precaution involves the treatment of samples for analysis with sufficient levels of a chainbreaking antioxidant [for example, butylated hydroxy-toluene (BHT)] immediately after collection to retard or prevent peroxidation occurring during periods of storage or preparation. 

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). 

Nakaya, H., Tohse, N. and Kanno, M. (1987). Electrophysio-logical derangements induced by lipid peroxidation in cardiac tissue. Am. J. Physiol 253, H1089-H1097. 

Robak, J. and Sobanska, B. (1976). Relationship between lipid peroxidation and prostaglandin generation in rabbit tissues. Biochem. Pharmacol. 25, 2233-2236. 

The importance of vitamin E for maintenance of lipid integrity in vivo is emphasized by the fact that it is the only major lipid-soluble chain-breaking antioxidant found within plasma, red cells and tissue cells. Esterbauer etal. (1991) have shown that the oxidation resistance of LDL increases proportionately with a-tocopherol concentration. In patients with RA, synovial fluid concentrations of a-tocopherol are significantly lower relative to paired serum samples (Fairburn et al., 1992). The low level of vitamin E within the inflamed joint implies it is being consumed via its role in terminating lipid peroxidation and this will be discussed further in Section 3.3. 

NF-xB activation has been linked with atherosclerosis (Andalibi etal., 1993 Liao etui., 1993). Mice that were maintained on an atherogenic diet, which resulted in ox-LDL accumulation in the liver and arteries, showed NF-xB activation in hepatic tissues. Furthermore, inflammatory gene up-regulation corresponded to the concentration of accumulated lipid peroxides as well as genetic susceptibility to fetty-streak development. 

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