Thermal dietary oxidation and malondialdehyde-deoxyguanosine

835

Epidemiological studies have suggested an association between high-temperature cooking methods, including frying, and increased risk of cancer at different sites, including gastric, colon, breast and lung cancer. Relevant amount of hydroperoxides, aldehydes and reactive oxygen species can arise from thermally oxidation of polyunsaturated fatty acids contained in animal fat and vegetable oils used for frying. Oxidized dietary fat can cause lipid peroxidation and endogenous damage.

One of the main groupof endogenous adducts includes the exocyclic malondialdehyde (MDA)-dG, the major adduct generated by reaction ofMDA-dG with deoxyguanosine. MDA-dGis a product of lipid peroxidation and eicosanoid biosynthesis. MDA-dG can be also formed via site-specific free radical attack on the DNA, through base propenals.MDA-dG has been shown to block DNA replication and induce frameshift and base pair substitutionmutations. In the most recent literature, lipid peroxidation related adducts are considered to be a reliable indicator of “oxidant status” in the whole organism, possibly associated to genetic instability and to an increased propensity for tumor progression.

Here, we have undertaken a study to investigate the lifestyle and dietary determinants of the production of MDA-dG in 89 subjects living in Thailand using the ³²P-DNA postlabelling assay. As far as fried food consumption was considered, an increased frequency of endogenous MDA-dG formation was found in frequent consumers of all fried foods (FR = 1.74 for highest level, 95% CI = 1.11 - 2.75, P < 0.05). When fried chicken intake was analyzed, a linear trend was also found (P < 0.05). MDA-dG level was borderline higher in current smokers than in non-smokers (FR = 1.45 95% CI = 0.94 - 2.23, P = 0.094). Furthermore, frequent consumption of fresh fruit was associated to a reduction in MDA-dG frequency (FR = 0.54 95% CI = 0.30 - 0.96, P < 0.05).

The increased level of exocyclic DNA adduct in frequent consumers of fried foods shows that high-temperature cooking, e.g. frying cooking, is a relevant determinant of endogenous damage. Consumption of fat-containing foods, such as chicken, was associated with MDA-dG mean frequency indicating that the type of food being fried can also influence the production of MDA-dG. Our findings are in keeping with previous studies reporting that the level of endogenous DNA damage can be modulated from fatty acid, but show that the thermal oxidation of culinary oils and animal fat can exert an important contribute to oxidative stress.

Our study shows that an increment of endogenous DNA damage over the “background” level can be induced from increased intake of oxidative by-products induced by thermal oxidation of culinary oils and animal fat. Higher level of MDA-dG can be also reflective of impairments in genes that control levels of cellular oxidative damage, including by antioxidant and DNA repair mechanisms.