期刊
FOOD RESEARCH INTERNATIONAL
卷 142, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.foodres.2021.110203
关键词
Acetaldehyde; Carbon disulfide; Inflammation; Lipid oxidation; Processed meat; Protein carbonyls; Nitrite salt; Oxidative stress
资金
- Research Foundation Flanders (FWO-Vlaanderen)
The mechanisms underlying the epidemiological associations between red (processed) meat consumption and chronic disease risk may involve oxidative reactions, microbial composition alterations, inflammation, and the formation of toxic bacterial metabolites. Experiment results demonstrated that nitrite salt could reduce protein carbonylation and inhibit lipid oxidation during digestion, while ascorbate enhanced the antioxidant effects. Consuming beef, compared to chicken, led to increased lipid oxidation and gut protein fermentation. Cured meat consumption showed effects on protein carbonylation, gut microbial composition, and fecal metabolite levels.
Mechanisms explaining epidemiological associations between red (processed) meat consumption and chronic disease risk are not yet elucidated, but may involve oxidative reactions, microbial composition alterations, inflammation and/or the formation of toxic bacterial metabolites. First, in vitro gastrointestinal digestion of 23 cooked beef-lard minces, to which varying doses of nitrite salt (range 0?40 g/kg) and sodium ascorbate (range 0?2 g/kg) were added, showed that nitrite salt decreased protein carbonylation up to 3-fold, and inhibited lipid oxidation, demonstrated by up to 4-fold lower levels of ?thiobarbituric acid reactive substances?, 32-fold lower 4hydroxynonenal, and 21-fold lower hexanal values. The use of ascorbate increased the antioxidant effect of low nitrite salt levels, whereas it slightly increased protein carbonylation at higher doses of nitrite salt. The addition of a low dose of ascorbate without nitrite salt slightly promoted oxidation during digestion, whereas higher doses had varying antioxidant effects. Second, 40 rats were fed a diet of cooked chicken- or beef-lard minces, either or not cured, for three weeks. Beef, compared to chicken, consumption increased lipid oxidation (2- to 4-fold) during digestion, and gut protein fermentation (cecal iso-butyrate, (iso-)valerate, and fecal indole, cresol), but oxidative stress and inflammation were generally not affected. Cured, compared to fresh, meat consumption significantly increased stomach protein carbonylation (+16%), colonic Ruminococcaceae (2.1-fold) and cecal propionate (+18%), whereas it decreased cecal butyrate (-25%), fecal phenol (-69%) and dimethyl disulfide (-61%) levels. Fecal acetaldehyde and diacetyl levels were increased in beef-fed rats by 2.8-fold and 5.9-fold respectively, and fecal carbon disulfide was 4-fold higher in rats consuming cured beef vs. fresh chicken. Given their known toxicity, the role of acetaldehyde and carbon disulfide in the relation between meat consumption and health should be investigated in future studies.
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