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Open AccessJournal ArticleDOI

Antioxidants Maintain Cellular Redox Homeostasis by Elimination of Reactive Oxygen Species.

TLDR
The roles of cellular endogenous antioxidant systems as well as natural anti-oxidative compounds in several human diseases caused by ROS are summarized in order to illustrate the vital role of antioxidants in prevention against oxidative stress.
Abstract
Reactive oxygen species (ROS) are produced by living cells as normal cellular metabolic byproduct. Under excessive stress conditions, cells will produce numerous ROS, and the living organisms eventually evolve series of response mechanisms to adapt to the ROS exposure as well as utilize it as the signaling molecules. ROS molecules would trigger oxidative stress in a feedback mechanism involving many biological processes, such as apoptosis, necrosis and autophagy. Growing evidences have suggested that ROS play a critical role as the signaling molecules throughout the entire cell death pathway. Overwhelming production of ROS can destroy organelles structure and bio-molecules, which lead to inflammatory response that is a known underpinning mechanism for the development of diabetes and cancer. Cytochrome P450 enzymes (CYP) are regarded as the markers of oxidative stress, can transform toxic metabolites into ROS, such as superoxide anion, hydrogen peroxide and hydroxyl radical which might cause injury of cells. Accordingly, cells have evolved a balanced system to neutralize the extra ROS, namely antioxidant systems that consist of enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidases (GPxs), thioredoxin (Trx) as well as the non-enzymatic antioxidants which collectively reduce oxidative state. Herein, we review the recent novel findings of cellular processes induced by ROS, and summarize the roles of cellular endogenous antioxidant systems as well as natural anti-oxidative compounds in several human diseases caused by ROS in order to illustrate the vital role of antioxidants in prevention against oxidative stress.

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Journal ArticleDOI

Reactive Oxygen Species-Induced Lipid Peroxidation in Apoptosis, Autophagy, and Ferroptosis.

TL;DR: This review discussed how ROS propagate lipid peroxidation chain reactions and how the products of lipidperoxidation initiate apoptosis and autophagy in current models, and summarized lipid per oxidation in pathological conditions of critical illness.
Journal ArticleDOI

The role of cellular reactive oxygen species in cancer chemotherapy

TL;DR: In this paper, a review of the role of reactive oxygen species (ROS) in cancer cells during carcinogenesis and during chemotherapy, provides a critical analysis of the methods used for quantitative ROS detection and discusses the application of mathematical modeling in predicting treatment responses.
Journal ArticleDOI

A Review of the Role of Green Tea (Camellia sinensis) in Antiphotoaging, Stress Resistance, Neuroprotection, and Autophagy.

TL;DR: The reported anti-photoaging, stress resistance, and neuroprotective and autophagy properties of one of the most widely known functional foods—green tea are described.
Journal ArticleDOI

Regulation of Nrf2 by Mitochondrial Reactive Oxygen Species in Physiology and Pathology.

TL;DR: Mice transiently depleted of SOD2 or overexpressing skeletal muscle-specific UCP1 exhibit Nrf2-mediated antioxidant gene expression and PGC1α-mediated mitochondrial biogenesis, and these reports aid us in understanding the roles of NRF2 in pathophysiological alterations involving mtROS.
Journal ArticleDOI

Application of glutathione depletion in cancer therapy: Enhanced ROS-based therapy, ferroptosis, and chemotherapy.

TL;DR: In this article, various strategies for GSH depletion used in cancer therapy are comprehensively summarized and discussed, and functional materials with GSH consuming ability based on nanotechnology are elaborated due to their unique advantages and potentials.
References
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Journal ArticleDOI

Structure-antioxidant activity relationships of flavonoids and phenolic acids

TL;DR: The factors underlying the influence of the different classes of polyphenols in enhancing their resistance to oxidation are discussed and support the contention that the partition coefficients of the flavonoids as well as their rates of reaction with the relevant radicals define the antioxidant activities in the lipophilic phase.
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Ferroptosis: An Iron-Dependent Form of Nonapoptotic Cell Death

TL;DR: This paper identified the small molecule ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices, suggesting similarities between these two processes.
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Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach?

TL;DR: It is argued that modulating the unique redox regulatory mechanisms of cancer cells might be an effective strategy to eliminate these cells.
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ROS Function in Redox Signaling and Oxidative Stress

TL;DR: It is argued that redox biology, rather than oxidative stress, underlies physiological and pathological conditions.

superoxide production blocks three pathways of hyperglycaemic damage

TL;DR: This paper showed that hyperglycaemia increases the production of reactive oxygen species inside cultured bovine aortic endothelial cells and that this increase in reactive oxygen can be prevented by an inhibitor of electron transport chain complex II, an uncoupler of oxidative phosphorylation, by uncoupling protein-1 and by manganese superoxide dismutase.
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