Laboratory for Animal Nutrition and Animal Product Quality, Department of Animal Sciences and Aquatic Ecology, Ghent University, Coupure Links 653, B-9000 Ghent, Belgium.
Center for Microbial Ecology and Technology (CMET), Ghent University, Coupure Links 653, B-9000 Gent, Belgium.
Food Res Int. 2021 Apr;142:110203. doi: 10.1016/j.foodres.2021.110203. Epub 2021 Feb 10.
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 4-hydroxynonenal, 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.
目前,尚不清楚解释红(加工)肉消费与慢性病风险之间的流行病学关联的机制,但可能涉及氧化反应、微生物组成改变、炎症和/或有毒细菌代谢物的形成。首先,对 23 种不同剂量亚硝酸盐盐(0-40g/kg)和抗坏血酸钠(0-2g/kg)添加到煮熟的牛肉-猪油肉末中的体外胃肠道消化显示,亚硝酸盐盐使蛋白质羰基化减少了高达 3 倍,并抑制了脂质氧化,表现为“硫代巴比妥酸反应物质”降低了高达 4 倍,4-羟基壬烯醛降低了 32 倍,己醛降低了 21 倍。抗坏血酸钠的使用增加了低亚硝酸盐盐水平的抗氧化作用,而在较高剂量的亚硝酸盐盐下,它略微增加了蛋白质羰基化。添加低剂量的抗坏血酸钠而不添加亚硝酸盐盐在消化过程中稍微促进了氧化,而较高剂量则具有不同的抗氧化作用。其次,40 只大鼠连续 3 周喂食煮熟的鸡肉或牛肉-猪油肉末,或不腌制的肉末。与鸡肉相比,牛肉消费在消化过程中增加了脂质氧化(2-4 倍)和肠道蛋白质发酵(盲肠异丁酸、(异)戊酸和粪便吲哚、苯酚),但氧化应激和炎症通常不受影响。与新鲜肉相比,腌制肉消费显著增加了胃蛋白羰基化(增加 16%)、结肠瘤胃球菌科(增加 2.1 倍)和盲肠丙酸(增加 18%),但降低了盲肠丁酸(减少 25%)、粪便苯酚(减少 69%)和二甲基二硫(减少 61%)水平。牛肉喂养的大鼠粪便乙醛和二乙酰的水平分别增加了 2.8 倍和 5.9 倍,而摄入腌制牛肉的大鼠粪便碳二硫化物比新鲜鸡肉高 4 倍。鉴于它们已知的毒性,在未来的研究中应该研究乙醛和碳二硫化物在肉消费与健康之间的关系中的作用。