Lipid peroxidation cell culture

Igarashi, M. and Miyazawa, T., Do conjugated eicosapentaenoic acid and conjugated docosahexaenoic acid induce apoptosis via lipid peroxidation in cultured human tumor cells Biochem. Biophys. Res. Commun., 270, 649, 2000. 

Tse SYH, Mak IT, Weglicki WB, et al. 1988. Chlorinated hydrocarbons enhance lipid peroxidation in cultured endothelial cells and smooth muscle cells. In Proceedings of the 10th International Society for Heart Research Annual Meeting, Williamsburg VA, June 26-29, 1988. J Mol Cell Cardiol 20(Suppl 3) S36. 

Negre-Salvayre A, Alomar Y, Troly M, Salvayre R. Ultraviolet-treated lipoproteins as a model sy stem for the study of the biological effects of lipid peroxides on cultured cells. III. The protective effect of antioxidants (probucol, catechin, vitamin E) against the cytotoxicity of oxidized LDL occurs in two different ways. Biochim Biophy Acta 1991 1096 291-300. 

The generation of radicals from lipids appear to be dependent on the abstraction of hydrogen by other radicals. Consistent with this idea is the observation that either lipid peroxidation or anoxia can cause a release of free arachidonic acid fix>m culture cells, and this release can be blocked by antioxidants (Braughler et al., 1985, 1988). 

During ischaemia, NOS is activated by calcium influx or by cytokines like tumour necrosis factor (TNF) or by lipopolysaccharide (LPS) and NO is produced in excess. It has been proposed that the excitotoxic effect of glutamate, which contributes to ischaemia-induced neuronal damage, is mediated by increased production of NO via a chain of events that includes increases in intracellular calcium (via glutamate activation of NMDA receptors), calcium activation of NOS, production of NO and peroxynitrite, and induction of lipid peroxidation. In fact, N-nitro-L-atginine, a selective inhibitor of NOS, has been shown to prevent glutamate-induced neurotoxicity in cortical cell cultures (Dawson rf /., 1991). 

Kaneko et al. (1993) have described a group of lipophilic ascorbic-acid analogues that have been studied in cultured human umbilical vein endothelial cells that were first incubated with test drug and then exposed to lipid hydroperoxides. Although ascorbate itself did not protect the endothelial cells, derivatives like CV3611 protected. Pretreatment was necessary. CV3611 was synergistic with vitamin E. The authors concluded that these lipophilic antioxidants incorporate into endothelial cell membranes where they are effective inhibitors of lipid peroxidation. In contrast, lipophobic antioxidants were not effective in their hands (Kaneko et al., 1993). 

Matos, HR, P Di Mascio, and MHG Medieros. 2000. Protective effect of lycopene on lipid peroxidation and oxidative DNA damage in cell culture. Arch Biochem Biophys 383(1) 56—59. 

The above findings are supported in the other studies of the inhibitory effects of flavonoids on iron-stimulated lipid peroxidation. Quercetin was found to be an inhibitor of iron-stimulated hepatic microsomal lipid peroxidation (/50 = 200 pmol I ) [134]. Flavonoids eriodictyol, luteolin, quercetin, and taxifolin inhibited ascorbate and ferrous ion-stimulated MDA formation and oxidative stress (measured by fluorescence of 2,7,-dichlorodihydro-fluorescein) in cultured retinal cells [135]. It should be mentioned that in recent work Heijnen et al. [136] revised the structure activity relationship for the protective effects of flavonoids against lipid peroxidation. 

Vohra and Hui [352] showed that the pretreatment of cultured neutrons with taurine suppressed lipid peroxidation and the loss of glutathione peroxidase activity induced in these cells by carbon tetrachloride. 

Antioxidant activity. Aqueous extract of the husk fiber, in cell culture, was active vs 2,2-diphenyl-1-picryl-hydrazyl-hydrate radicals . Juice, in cell culture, was active vs l,l-diphenyl-2-picrylhydrazyl, 2,2 -azino-bis(3-ethylbenz-thiazoline-6-sulfonic acid) and superoxide radicals but promoted the production of hydroxyl radicals and increased lipid peroxidation. The activity... 

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