Oxidative Stress and Diet: The Health Implications of Advanced Glycation and Lipid Oxidation End-Products

Topic Information

Dear Colleagues,

Activation of oxygen to reactive oxygen species (ROS) is the primordial process for initiation in foods of oxidized dietary proteins, lipids, and glycation/lipid-oxidation end-products (AGEs/ALEs). Lipid and protein oxidation is one of the major degradative processes responsible for losses in food safety and quality. The oxidation of unsaturated fatty acids and reducing sugars results in significant generation of dietary ALEs and AGEs, which are in part cytotoxic and genotoxic compounds. The gastrointestinal tract is constantly exposed to dietary oxidized food compounds; following digestion, a small proportion of them is absorbed into the lymph or directly into the bloodstream. After ingestion of oxidized fats and proteins, animals and humans have been shown to have increased amounts of lipophilic carbonyl and electrophilic compounds in their blood and urine. Oxidized cholesterol in the diet was found to be a source of oxidized lipoproteins in human serum. Some dietary ALEs/AGEs, which are absorbed from the gut into the circulatory system, appear to act as harmful chemicals that activate an inflammatory response that affects not only the circulatory system but also organs such as the liver, kidney, lung, and the gut itself. We believe that repeated consumption of oxidized fat and proteins as a part of one’s diet poses a chronic threat to human health. High concentrations of dietary antioxidants could prevent lipid oxidation and ALE/AGE generation not only in foods but also in certain gastrointestinal conditions and thereby potentially decrease their absorption from the gut. This could explain the health benefits of diets containing large amounts of dietary antioxidants such as those present in fruits and vegetables or products such as red wine or tea consumed during a meal.

Prof. Dr. Joseph Kanner
Prof. Dr. Ron Kohen
Topic Editors

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Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Antioxidants antioxidants	6.6	12.4	2012	17.4 Days	CHF 2900	Submit
Cancers cancers	4.4	8.8	2009	20.3 Days	CHF 2900	Submit
Gastroenterology Insights gastroent	0.7	2.7	2009	28.9 Days	CHF 1800	Submit
Life life	3.4	6.0	2011	19.3 Days	CHF 2600	Submit
Nutrients nutrients	5.0	9.1	2009	12.9 Days	CHF 2900	Submit

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Open AccessReview

Ferroptosis: The Initiation Process of Lipid Peroxidation in Muscle Food

by Joseph Kanner, Adi Shpaizer and Oren Tirosh

Antioxidants 2025, 14(10), 1157; https://doi.org/10.3390/antiox14101157 - 24 Sep 2025

Viewed by 563

Abstract

Animal slaughtering causes the cessation of oxygen delivery and that of nutrients such as cystine, glucose and others to muscle cells. In muscle cells, the changes in oxygen level and pH cause mitochondria, the endoplasmic reticulum, xanthine oxidase and uncoupled NOS to increase [...] Read more.

Animal slaughtering causes the cessation of oxygen delivery and that of nutrients such as cystine, glucose and others to muscle cells. In muscle cells, the changes in oxygen level and pH cause mitochondria, the endoplasmic reticulum, xanthine oxidase and uncoupled NOS to increase the level of O₂^•−, affecting the generation of H₂O₂ and the release of iron ions from ferritin. The activation of enzymes that remove and dislocate fatty acids from the membrane affects the sensitivity of muscle cells to peroxidation and ferroptosis. Increasing PUFAs in membrane phospholipids, by feeding animals a diet high in w-3 fatty acids, is a driving factor that increases lipid peroxidation and possible muscle ferroptosis. The activation of lipoxygenases by ROS to Fe³⁺-lipoxygenase increases hydroperoxide levels in cells. The labile iron pool generated by a “redox cycle” catalyzes phospholipid hydroperoxides to generate lipid electrophiles, proximate executioners of ferroptosis. Ferroptosis in food muscle cells is protected by high concentrations of vitamin E and selenium. In fresh muscle cells, glutathione peroxidase (GSH-PX) and other endogenous antioxidant enzymes are active and prevent lipid peroxidation; however, muscle heating eliminates enzymatic activities, making cells prone to high non-enzymatic lipid peroxidation. In muscle cells, coupled myoglobin and vitamin E act as a hydroperoxidase, preventing the generation of lipid electrophiles. Free iron ion chelators or effectors such as deferoxamine, EDTA, or ceruloplasmin are strong inhibitors of muscle cell lipid peroxidation, proving that muscle ferroptosis is mostly dependent on and catalyzed by the labile iron redox cycle. Full article

(This article belongs to the Topic Oxidative Stress and Diet: The Health Implications of Advanced Glycation and Lipid Oxidation End-Products)

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