Is the Oxidative Stress Really a Disease?

Fogarasi, Erzsébet; Croitoru, Mircea Dumitru; Fülöp, Ibolya; Muntean, Daniela-Lucia

doi:10.1515/amma-2015-0070

Cited by 8 publications

(8 citation statements)

References 36 publications

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“…Free radicals are molecules with one or more unpaired electrons, extremely unstable and highly reactive. When produced in excess in the body, they become mediators of cell and tissue damage, resulting in a phenomenon called oxidative stress (1).…”

Section: Introductionmentioning

confidence: 99%

“…ROS, RNS, and CRS are molecules with free radicals or molecules without free radicals, but which can produce free radicals in certain conditions (reactive intermediates). Some free radicals, such as NO and the superoxide anion, are intentionally produced by the human body under certain conditions and at specific concentrations; they can serve as cell mediators with well-defined biological purposes (phagocytosis) (1).…”

Section: Introductionmentioning

confidence: 99%

“…A panel of biomarkers of oxidative stress have been established for evaluation of the oxidative stress in pregnancy, in the fetus and the newborn (6), grouped according to their nature as: lipid peroxidation products (including malondialdehyde, acrolein, isoprostanes), protein oxidation products (including protein carbonyl, tyrosine related groups), DNA oxidation products, stress response proteins, a novel biomarker (microRNAs) (6), and other biomarkers, such as enzymes (myeloperoxidase), thiols (glutathione) and metallothioneins (1). Furthermore, reduced and oxidized glutathione ratio (1) and non-protein-bound iron (6) have also been used as biomarkers in general analytical determinations (6).…”

Section: Introductionmentioning

confidence: 99%

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Oxidative stress and peripartum outcomes (Review)

et al. 2021

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Pregnancy, labor and childbirth are accompanied by excessive oxidative aggression. The excessive formation of free radicals [reactive oxygen species (ROS), reactive nitrogen species (RNS), chlorine reactive species (CRS)] causes cellular oxidative damage, which can be scavenged by enzymatic or non-enzymatic antioxidants in normal healthy pregnancy, physiological labor and delivery without any complications. An imbalance between the pro-oxidant and antioxidant factors may lead to oxidative stress, which contributes to the development of many diseases. This oxidative aggression can be a precursor for pathologies in the pregnant woman including eclampsia, miscarriage, preterm labor, and intrauterine growth retardation; in the offspring it may lead to bronchopulmonary dysplasia/chronic lung disease, necrotizing enterocolitis, retinopathy of prematurity, and periventricular leukomalacia. This review summarizes the studies conducted to identify the mechanisms of oxidative stress and the effect of cell membrane oxidation, the mechanisms that are behind oxidative stress-related diseases, and also those studies which have demonstrated the effect of antioxidants in preventing diseases or diminishing the effects of oxidative stress in the body, in obstetrics and neonatology.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Oxidative stress and peripartum outcomes (Review)

et al. 2021

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“…ROS are essential for cellular function and can be metabolized safely by antioxidant mechanisms; however, excessive ROS production causes oxidative stress 10 . Excessive ROS can stimulate free-radical chain reactions, which can damage lipids, proteins and DNA and ultimately cause adverse health effects 11 such as cardiovascular disease, neurodegenerative disorders, ageing, diabetes, cancer and metabolic syndromes 12 . In particular, the brain is known as one of the critical organs susceptible to the damaging effects of ROS.…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective effect of Ruminococcus albus on oxidatively stressed SH-SY5Y cells and animals

Park

Lee

Yeom

et al. 2017

Sci Rep

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Recent evidence shows that the gut microbiota has an important role in gut-brain crosstalk and is linked to neuronal disorders. The aim of this study was to investigate the effects of intestinal Ruminococcus albus with probiotic potential on neuroprotection in oxidatively stressed SH-SY5Y neuroblastoma cells and animals. To investigate these effects, conditioned medium was prepared using Caco-2 cells cultured with heat-killed R. albus (CRA-CM). Caco-2 cells cultured with heat-killed R. albus showed increased BDNF expression and BDNF protein levels increased in CRA-CM. CRA-CM up-regulated the protein expression levels of SRF, C-fos and CDK2. In addition, CRA-CM protected SH-SY5Y cells from H2O2-induced cell death. CRA-CM significantly decreased the Bax/Bcl-2 ratio in oxidatively stressed SH-SY5Y cells. Animal experiments showed that oral administration of heat-killed R. albus for 15 days attenuated the oxidative stress induced by sodium arsenate. Treatment with heat-killed R. albus reduced the level of ROS, and the levels of SOD and GSH increased in oxidatively stressed brains. In conclusion, the secretome prepared from Caco-2 cells cultured with heat-killed R. albus might promote neuronal proliferation through the activation of cell proliferation-related proteins, and heat-killed R. albus protects neurons from oxidative damage by reducing ROS levels and increasing SOD and GSH levels.

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“…Furthermore, free radicals are chemical species that have one or more unpaired electrons, which can act as acceptors of other electrons belonging to other molecules. As a result, they produce oxidation and cause a chain of molecular damage [12]. Free radicals come from sources that are endogenous the own metabolism of the cell, mainly carried out during the respiratory chain in the internal membrane of the mitochondria) and exogenous environmental pollution, tobacco, smoke, drugs, xenobiotics, or radiation) [13].…”

Section: Reactive Oxygen Species and Antioxidant Defensesmentioning

confidence: 99%

Oxidative Stress, Inflammation, and Formation of Beta‐ Amyloid 1‐42 in Brain

Rivas‐Arancibia¹,

Rodrı́guez-Martı́nez²,

Méndez‐García³

et al. 2016

Free Radicals and Diseases

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Alzheimer's disease is characterized by the pathognomonic presence of intracellular neuroibrillary tangles containing hyperphosphorylated tau protein and extracellular senile plaques primarily formed by -amyloid. Both the neuroibrillary tangles and the plaques formed by -amyloid 1-42 are the inal result of a chain of events that progressed along with the disease for a long time. Oxidative stress plays a fundamental role among those events as proven by the experiments carried out using animal models. This can be demonstrated since there are studies indicating that, although the formation ofamyloid is inhibited through diferent mechanisms using drugs or speciic antibodies), cognitive deicit is not prevented. In this chapter, we will focus on reviewing the role the chronic state of oxidative stress plays in the development of Alzheimer's disease and how the loss of redox balance induces a vicious cycle that may change normal signaling. As a consequence, there are alterations in multiple metabolic pathways that end up in the formation of hyperphosphorylated tau and insoluble -amyloid, leading to the advance of a progressive neurodegeneration process. This is characterized by neuronal dead, astrocytic changes, microglia activation, and the loss of brain repair.Keywords: oxidative stress, Alzheimer's disease, -amyloid 1-42, ozone, neurodegeneration © 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. . IntroductionDespite a great deal of studies and the eforts of researchers in the ield, the physiopathology of Alzheimer's disease AD) is not yet clear. There is neither an accurate early diagnosis nor an efective treatment that allows the patients to have beter life expectancies [1]. Perhaps one of the most important problems to solve is understand that when the diagnosis is made, the symptoms and the signs of Alzheimer's disease are the result of a long chain of events that took place during an extended period of time and that such symptoms and signs change with time [2].One can assume that intracellular signaling and metabolic changes found during the early stages of the disease are not the same as the ones found at more advanced stages. For this reason, recent postmortem studies fail to completely clarify the physiopathology of this disease. . Changes at cellular level caused by chronic oxidative stressAcute oxidative stress is reversible and it is present in a number of physiological and pathological mechanisms that are reversible as well. These mechanisms play a defensive role ...

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Is the Oxidative Stress Really a Disease?

Cited by 8 publications

References 36 publications

Oxidative stress and peripartum outcomes (Review)

Oxidative stress and peripartum outcomes (Review)

Neuroprotective effect of Ruminococcus albus on oxidatively stressed SH-SY5Y cells and animals

Oxidative Stress, Inflammation, and Formation of Beta‐ Amyloid 1‐42 in Brain

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