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What Do the Heart Arteries Do When They Are Damaged? The Infinite Insults and Finite Responses in CHD
Published in Mark C Houston, The Truth About Heart Disease, 2023
In conclusion, oxidative stress is an imbalance of radical oxygen species (ROS) and radical nitrogen species (RNS) (the bad guys) with a decrease in antioxidant defenses (the good guys) that contributes to CHD and MI in humans based on genetics and environment. Oxidative stress is like having too much fire in the arteries but no fire extinguishers to put out the fire, i.e., not having enough antioxidants. The oxidative stress will damage cells to the point that they do not function or they die. If this happens in the coronary arteries, the result is CHD or MI. It is important to balance the oxidative stress and the oxidative defense. The predominant ROS produced by cells is called superoxide anion and is part of our normal metabolism with oxygen and the breakdown of our food to make energy or ATP. In addition, the superoxide anion reduces nitric oxide and produces other downstream ROS and RNS, which leads to endothelial and glycocalyx dysfunction and CHD. Our antioxidant defense is supplied by various compounds (enzymes) that will break down the ROS and also by the intake of vitamins, minerals, and antioxidants in our diet or in supplements.
Metabolic Syndrome
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Metabolic syndrome is a risk factor for cardiac events even with other risk factors such as dyslipidemia, coagulopathy, and hypertension. This may be due to the link with endothelial dysfunction. Nitric oxide production is sufficient when the endothelium is healthy. It allows the arteries to vasodilate, provides surfaces that are not sticky so that clots do not attach, and suppresses atheromas from forming due to stopping leukocytes from breaching the endothelium. With metabolic syndrome’s inflammation, excessive superoxide is produced, leading to increased atheroma formation, thrombosis, and vasoconstriction.
Antioxidant Effects of Peptides
Published in Mesut Karahan, Synthetic Peptide Vaccine Models, 2021
Rümeysa Rabia Kocatürk, Fatmanur Zehra Zelka, Öznur Özge Özcan, Fadime Canbolat
Under normal physiological conditions, human beings have a balance between the produced reactive oxygen species (ROS) and antioxidants. Cells and tissues in our bodies constantly create free radicals due to metabolism, as well as environmental factors, for example, radiation, pollution, microorganisms, allergens, cigarettes, smoke, and pesticides increase the number of exposed free radicals that the body encounters (Hekimi, Lapointe, and Wen 2011). With increasing ROS types, the body’s balance is disturbed, superoxide radicals begin to accumulate in the cells and an endogenous defense system is inadequate. This accumulation and increase of free radicals, for example superoxide radicals, is defined as oxidative stress and oxidative stress is not beneficial for body composition. It causes many distortions at the molecular level. The increase in ROS is toxic to the cell, damaging the proteins, lipids, and nucleic acids (DNA and RNA) inside the cell, disrupting the intracellular signaling pathways and adversely affecting health (Aslankoç et al. 2019).
Toxic effect of carpet dust on the biochemical indices and histological structure of the lung in rats: the potential role of cytochrome P450 2E1 and extracellular signal-regulated kinase/mitogen-activated protein kinase pathways
Published in Biomarkers, 2023
Abeer Salama, Rania Elgohary, Noha Mowaad, Doaa Sadek, Walaa Abdelhamid
Another hypothesised mechanism for carpet dust-induced lung inflammation could be the significant NO content elevation. NO is mostly produced from alveolar macrophages and neutrophils. Our study demonstrated the involvement of induced NO by carpet dust in inflammatory responses in the lung. In addition, its overproduction could result in deleterious effects as it combines with superoxide to form peroxynitrite, which is a cytotoxic free radical that causes severe lung damage (El-Agamy et al.2014). Furthermore, endotoxin, one of the most common components of carpet dust, is potentially known to cause lung injury, through ROS and NO production. NO can also induce apoptosis and necrosis (Gerald et al.2019). Conversely, ROS modulates intracellular signalling pathways with subsequent expression of nuclear transcription factors as NF-κB. Therefore, carpet dust-exposed rats exhibited a significant elevation in NF-κB contents. Our study suggested that NF-κB plays a significant role in regulating various cytokine production because IL-6 exhibited a significant elevation in carpet dust-treated rats, especially those receiving high dose tufted dust (5 mg/kg). This provides insight into the role of NF-κB and IL-6 in the progression of lung inflammation in our rat model.
Hyperglycaemia and the risk of post-surgical adhesion
Published in Archives of Physiology and Biochemistry, 2022
Gordon A. Ferns, Seyed Mahdi Hassanian, Mohammad-Hassan Arjmand
Hyperglycaemia increases superoxide production (Nishikawa et al.2000). Under hyperglycaemic conditions, there is increased glucose entering the glycolytic pathway (important biochemical pathway in the cells for glucose metabolism) that produced two molecules of pyruvate. In aerobic conditions, pyruvates are converted to acetyl-CoA by pyruvate dehydrogenase. Acetyl-CoA produced by pyruvate entered to the Krebs cycle in mitochondria. Three molecules of NADH are produced by each Krebs cycle (Sabri 1984). NADH is an electron carrier to transport electron in complex 1 of the electron transport chain in mitochondria for ATP synthesis. An excessive amount of NADH causes reductive stress by intracellular production of superoxide O2– (Liu et al.2002) (Figure 3). Superoxide is one of the most important ROS factors and can damage biomolecules and increase of inflammation (McCord 1980). Increase of ROS such as superoxide causes excessive production of proinflammatory cytokines and growth factors by immune cells which are associated with adhesion formation post-surgical (Fortin et al.2015).
Aortic dysfunction by chronic cadmium exposure is linked to multiple metabolic risk factors that converge in anion superoxide production
Published in Archives of Physiology and Biochemistry, 2022
Celeste Santamaria-Juarez, Fausto Atonal-Flores, Alfonso Diaz, Victor E. Sarmiento-Ortega, Miguel Garcia-Gonzalez, Patricia Aguilar-Alonso, Gustavo Lopez-Lopez, Eduardo Brambila, Samuel Treviño
In summary, Wistar rats exposed to a LOAEL dose of Cd (32.5 ppm) in drinking water develop a metabolic disorder similar to metabolic syndrome. This pathological condition constitutes a risk factor which has been related to hypertension and vascular damage. Metabolic changes developed by Cd administration produces insulin resistance and atherosclerotic environment that increase oxidative stress in the endothelium. Oxidative stress associated with high levels of superoxide produced by the NADPH oxidase complex activity, diminish NO availability, which could be part of the mechanism by which rats exposed to Cd develop hypertension. This hypothesis is supported by the fact that both apocynin and SOD produce the relaxation of aortic rings in rats exposed to Cd, at the same level as rats non-exposed to Cd. Therefore, the reduction of superoxide could be an exploring strategy to reduce the risk of endothelial damage and cardiovascular diseases, at least in situations of Cd exposure.