Can Meat and Meat-Products Induce Oxidative Stress?

Abstract

High meat and meat-products consumption has been related to degenerative diseases. In addition to their saturated fatty acids and cholesterol contents, oxidation products generated during their production, storage, digestion, and metabolization have been largely implicated. This review begins by summarizing the concept of meat and meat-products by the main international regulatory agencies while highlighting the nutritional importance of their consumption. The review also dials in the controversy of white/red meat classification and insists in the need of more accurate classification based on adequate scores. Since one of the negative arguments that meat receives comes from the association of its consumption with the increase in oxidative stress, main oxidation compounds (malondialdehyde, thermaloxidized compounds, 4-hydroxy-nonenal, oxysterols, or protein carbonyls) generated during its production, storage, and metabolization, are included as a central aspect of the work. The review includes future remarks addressed to study the effects meat consumption in the frame of diet–gene interactions, stressing the importance of knowing the genetic variables that make individuals more susceptible to a possible oxidative stress imbalance or antioxidant protection. The importance of consumed meat/meat-products in the frame of a personalized nutrition reach in plant-food is finally highlighted considering the importance of iron and plant biophenols on the microbiota abundance and plurality, which in turn affect several aspects of our physiology and metabolism.

Formation of Lipid and Protein Oxidation Products during In Vitro Gastrointestinal Digestion of Dry-Cured Loins with Different Contents of Nitrate/Nitrite Added

“…During digestion, lipid oxidation products (LOP), such as malondialdehyde (MDA), 4-hydroxy-hexenal (4-HHE), or 4-hydroxy-nonenal (4-HNE), and protein oxidation products, such as carbonyls and oxidized forms of amino acids, are produced. Higher levels of these compounds are reached in the intestinal phase than are in the initial food, demonstrating that gastrointestinal digestion promotes lipid and protein oxidation [13][14][15].…”

Prevention by Dietary Polyphenols (Resveratrol, Quercetin, Apigenin) Against 7-Ketocholesterol-Induced Oxiapoptophagy in Neuronal N2a Cells: Potential Interest for the Treatment of Neurodegenerative and Age-Related Diseases

“…The accumulation of 7KC in the tissues mainly results from stress conditions (overproduction of reactive oxygen and nitrogen species (ROS, RNS), presence of metals (Fe 2+ , Cu 2+ , etc.) leading to the Fenton and Haber–Weiss reactions) [ 27 ]. Although the biogenesis pathway of 7KC by auto-oxidation is considered to be preponderant [ 28 ], 7KC can also be formed enzymatically by the enzyme 11β-HSD2 from 7β-hydroxycholesterol in some cells and from 7-dehydrocholesterol by the enzyme CYP7A1 [ 29 ].…”

Lipid Peroxidation and the Redox Effects of Polyherbal

“…Both natural and synthetic antioxidants compounds abound [21,27]. LPO products also result in deoxyribonucleic acid, cell membrane, and tissue damages in the human body [1,2]. The global demand for antioxidants is evident and has prompted scientific interests in searching for new and safe antioxidant substances of natural origin.…”

“…Lipid peroxidation (LPO) is one of the oldest risk factors for oxidative stress and its mechanistic processes in disease modulation were first observed during the oxidative deterioration of edible materials [1]. The independent works of scientists in the identification of membrane shedding formed the earliest breakthrough for the study of lipid peroxidation [1,2]. The biochemistry of oxygenase moiety was a light to the further understanding of the peroxidation of lipids [2].…”