Oxidative Stress and Lipid Peroxidation Products in Cancer Progression and Therapy
By G. Barrera. ISRN Oncology, 2012
812 citations recorded by the source corpus.
The generation of reactive oxygen species (ROS) and an altered redox status are common biochemical aspects in cancer cells. ROS can react with the polyunsaturated fatty acids of lipid membranes and induce lipid peroxidation. The end products of lipid peroxidation, 4-hydroxynonenal (HNE), have been considered to be a second messenger of oxidative stress. Beyond ROS involvement in carcinogenesis, increased ROS level can inhibit tumor cell growth. Indeed, in tumors in advanced stages, a further increase of oxidative stress, such as that occurs when using several anticancer drugs and radiation therapy, can overcome the antioxidant defenses of cancer cells and drive them to apoptosis. High concentrations of HNE can also induce apoptosis in cancer cells. However, some cells escape the apoptosis induced by chemical or radiation therapy through the adaptation to intrinsic oxidative stress which confers drug resistance. This paper is focused on recent advances in the studies of the relation between oxidative stress, lipid peroxidation products, and cancer progression with particular attention to the pro-oxidant anticancer agents and the drug-resistant mechanisms, which could be modulated to obtain a better response to cancer therapy.
Subfields: Biochemistry, Cancer Research, Organic Chemistry
View Paper: https://www.semanticscholar.org/paper/a2110d58ca55ff5c2b713c89cd77192313afd2c8
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Citations in the corpus
- Screening of Salt-Tolerant Rice Landraces by Seedling Stage Phenotyping and Dissecting Biochemical Determinants of Tolerance Mechanism (2020, background): “Under salt stress, molecular oxygen acts as an electron acceptor, giving rise to the accumulation of ROS in all plants (Abogadallah 2010), that causes the peroxidation of membrane lipids (Barrera 2012).”
- Targeting Free Radicals in Oxidative Stress-Related Human Diseases. (2017, background): “The occurrence of a free-radical mechanism is indicated by enhanced levels of lipid peroxidation [29] and decreased antioxidant status, in other words reduced concentrations of ascorbic acid, a-tocopherol, carotenoids, and GSH in the blood.”
- Lifestyle, Oxidative Stress, and Antioxidants: Back and Forth in the Pathophysiology of Chronic Diseases (2020, background): “Predominantly, these aggregates are made from proteins, with the remainder consisting of various lipids (Barrera, 2012; Takalo et al., 2013; Tsoukalas et al., 2019b).”
- Ferroptosis: a cell death connecting oxidative stress, inflammation and cardiovascular diseases (2021, background): “, which are capable of serving as “oxidative stress second messengers” because of their longed half-life and ability to diffuse from their formation site [30, 31].”
- Regulation of pyruvate metabolism and human disease (2013, background): “However, cancer cells are inherently pro-oxidative [161] and are unable to cope with the additional stress, which eventually leads to apoptosis [164, 165].”
- Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal (2014, background): “The differential effect of 4-HNE on cell proliferation in both malignant and nonmalignant cells may be the consequence of lower aldehyde-metabolizing enzymes, deregulation of antioxidant defenses, and mitochondrial metabolism alteration [132, 346], so that malignant cells are more vulnerable to furt”
- Shared Risk Factors in Cardiovascular Disease and Cancer (2016, background): “Oxidative Stress and Reactive Oxygen Species Accumulating evidence suggests that oxidative stress and its direct consequences, including lipid peroxidation, are involved in numerous pathological states including atherosclerosis, cancer, and inflammation.(15) Biological systems are constantly exposed”