Induction of lipid peroxidation in biomembranes by dietary oil components.
Prooxidant formation and resulting lipid peroxidation are supposed to be involved in the pathogenesis of various diseases including cancer. Cancer risk is possibly influenced by the composition of diet with high intake of fat and red meat being harmful and high consumption of fruits and vegetables being protective. Since dietary oils may contain potential prooxidants, the aim of the present study was to prove (i) whether oxidative stress in biomembranes may be induced by dietary oils and if, (ii) which impact it has on the viability and proliferation of cultured colon (carcinoma) cells. Lipid hydroperoxide content in dietary oils increased after heating. Linoleic acid hydroperoxide (LOOH) and/or oils with different hydroperoxide contents induced lipid peroxidation in liposomes, erythrocyte ghosts and colon cells. Upon incubation with liposomes, both LOOH and heated oil induced lipid peroxidation only in the presence of iron and ascorbate. LOOH was sufficient to start lipid peroxidation of erythrocyte ghosts. LOOH incorporates into the lipid bilayer decreasing membrane fluidity and initiating lipid peroxidation in the lipid phase. When cultured cells (IEC18 intestinal epithelial cells, SW480 and HT29/HI1 colon carcinoma cells) were exposed to LOOH, they responded by cell death both via apoptosis and necrosis. Cells with higher degree of membrane unsaturation were more susceptible and antioxidants (vitamin E and selenite) were protective indicating the involvement of oxidative stress. Thus, peroxidation of biomembranes can be initiated by lipid hydroperoxides from heated oils. Dietary consumption of heated oils may lead to oxidative damage and to cell death in the colon. This may contribute to the enhanced risk of colon cancer due to regenerative cell proliferation.
Udilova
Natalia
N
Basic Pharmacology and Toxicology, Veterinary University of Vienna, A-1210 Vienna, Austria.
Jurek
Daniela
D
Marian
Brigitte
B
Gille
Lars
L
Schulte-Hermann
Rolf
R
Nohl
Hans
H
D000818:Animals; D000975:Antioxidants / Q000737:chemistry / Q000494:pharmacology; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D003110:Colonic Neoplasms / Q000473:pathology; D004042:Dietary Fats, Unsaturated / Q000032:analysis / Q000494:pharmacology*; D004578:Electron Spin Resonance Spectroscopy; D004910:Erythrocyte Membrane / Q000187:drug effects; D005227:Fatty Acids / Q000737:chemistry; D006358:Hot Temperature; D006801:Humans; D007501:Iron / Q000737:chemistry; D008041:Linoleic Acids / Q000737:chemistry; D015227:Lipid Peroxidation / Q000187:drug effects*; D008054:Lipid Peroxides / Q000737:chemistry; D008081:Liposomes / Q000737:chemistry; D008566:Membranes / Q000737:chemistry / Q000187:drug effects; D016877:Oxidants / Q000737:chemistry / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D014407:Tumor Cells, Cultured; D014810:Vitamin E / Q000737:chemistry / Q000494:pharmacology
D000975:Antioxidants; D004042:Dietary Fats, Unsaturated; D005227:Fatty Acids; D008041:Linoleic Acids; D008054:Lipid Peroxides; D008081:Liposomes; D016877:Oxidants; D014810:Vitamin E; C008285:linoleic acid hydroperoxide; D007501:Iron