Udilova Natalia, Jurek Daniela, Marian Brigitte, Gille Lars, Schulte-Hermann Rolf, Nohl Hans
Basic Pharmacology and Toxicology, Veterinary University of Vienna, A-1210 Vienna, Austria.
Food Chem Toxicol. 2003 Nov;41(11):1481-9. doi: 10.1016/s0278-6915(03)00164-9.
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.
促氧化剂的形成及由此导致的脂质过氧化被认为与包括癌症在内的各种疾病的发病机制有关。癌症风险可能受饮食结构的影响,高脂肪和红肉的高摄入量有害,而水果和蔬菜的高消费量具有保护作用。由于食用油可能含有潜在的促氧化剂,本研究的目的是证明:(i)生物膜中的氧化应激是否可由食用油诱导,以及(ii)其对培养的结肠(癌)细胞的活力和增殖有何影响。加热后,食用油中的脂质氢过氧化物含量增加。亚油酸氢过氧化物(LOOH)和/或具有不同氢过氧化物含量的油可诱导脂质体、红细胞影和结肠细胞中的脂质过氧化。与脂质体孵育时,只有在铁和抗坏血酸存在的情况下,LOOH和加热油才会诱导脂质过氧化。LOOH足以引发红细胞影的脂质过氧化。LOOH融入脂质双层,降低膜流动性并在脂质相中引发脂质过氧化。当培养的细胞(IEC18肠上皮细胞、SW480和HT29/HI1结肠癌细胞)暴露于LOOH时,它们会通过凋亡和坏死两种方式发生细胞死亡。膜不饱和程度较高的细胞更易受到影响,抗氧化剂(维生素E和亚硒酸盐)具有保护作用,表明氧化应激参与其中。因此,加热油中的脂质氢过氧化物可引发生物膜的过氧化。食用加热油可能导致结肠的氧化损伤和细胞死亡。这可能会因再生细胞增殖而增加患结肠癌的风险。