ROS are described as reactive signal mediators produced by normal metabolism or external insults. In this review they are central to oxidative stress and tumour-associated immune dysfunction.
First-pass extracted concept
reactive oxygen species
Candidate: concept label9 source documents22 linked claims
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Aliases
H(2)O(2), ROS
Extracted Explainers
What the tool is doing
ROS are presented as a major class of free radicals arising from endogenous organelles and exogenous exposures. The review frames them as central drivers of oxidative stress.
The abstract describes ROS as normal products of plant metabolism that can act as second messengers or cause oxidative damage depending on cellular balance.
What problem it solves
What it does not solve
Evidence Snippets
Reactive oxygen species (ROS) are versatile determinants of cell fate, tipping the balance between survival and death.
There are common drivers of both immunosenescence and atherosclerosis; e.g. inflammation, reactive oxygen species (ROS), chronic viral infections, genomic damage...
Reactive oxygen species (ROS) and free radicals are produced intrinsically during normal cellular metabolic processes or extrinsically due to ionizing radiations, UV rays, xenobiotic insult, etc.
The free radicals, both the reactive oxygen species (ROS) and reactive nitrogen species (RNS), are derived from both endogenous sources ... and exogenous sources ...
Reactive oxygen species (ROS) were initially recognized as toxic by-products of aerobic metabolism. In recent years, it has become apparent that ROS plays an important signaling role in plants.
Reactive oxygen species are constantly produced in aerobic organisms as by-products of normal oxygen metabolism.
Reactive oxygen species (ROS) are produced as a normal product of plant cellular metabolism.
In this study, we describe the role of reactive oxygen species (ROS) as signaling molecules in starvation-induced autophagy. We show that starvation stimulates formation of ROS, specifically H(2)O(2).
The discovered reviews repeatedly describe ROS as the relevant damaging species within the free radical and mitochondrial aging theories.
Supporting Sources
Linked Claims
Nineteen distinct forms of cell death are shaped by reactive oxygen species as triggers, modulators, or inhibitors.
Reactive oxygen species promote crosstalk between death programs, enabling switches from one mode to another and influencing whether outcomes are inflammatory or non-inflammatory.
Reactive oxygen species are determinants of cell fate that can tip the balance between survival and death.
Across regulated cell death pathways, reactive oxygen species act as both gatekeepers and connectors of diverse death programs.
Reactive oxygen species can initiate, modulate, or suppress regulated cell death when they exceed critical thresholds or perturb compartment-specific signaling.
RNA viruses including HCV and HIV are described as inducing ROS generation, DNA damage, SASP, metabolic reprogramming, G1 cell-cycle arrest, telomere shortening, and epigenetic modification.
The review presents chronic viral infections as shared drivers of immunosenescence and atherogenesis through inflammation, sustained cytokine signaling, ROS generation, and DNA damage.
Reactive oxygen species are normal signaling mediators but, when not tightly balanced by antioxidant and enzyme systems, can drive oxidative stress that damages cellular components.
Knowledge of ROS action and antioxidant regulation may enable development of strategies to genetically engineer stress-tolerant plants.
Reactive oxygen species have an important signaling role in plants and control growth, development, and responses to biotic and abiotic environmental stimuli.
ROS production in plants is mainly localized in chloroplasts, mitochondria, and peroxisomes, with additional sites including the endoplasmic reticulum, cell membrane, cell wall, and apoplast.
Free radicals can damage nucleic acids, lipids, and proteins, altering redox status and increasing oxidative stress.
Quoted textsource-backed
Free radicals can adversely affect various important classes of biological molecules such as nucleic acids, lipids, and proteins, thereby altering the normal redox status leading to increased oxidative stress.
Reactive oxygen species and reactive nitrogen species arise from both endogenous sources such as mitochondria, peroxisomes, endoplasmic reticulum, and phagocytic cells, and exogenous sources such as pollution, alcohol, tobacco smoke, heavy metals, transition metals, industrial solvents, pesticides, certain drugs, and radiation.
Quoted textsource-backed
The free radicals, both the reactive oxygen species (ROS) and reactive nitrogen species (RNS), are derived from both endogenous sources (mitochondria, peroxisomes, endoplasmic reticulum, phagocytic cells etc.) and exogenous sources (pollution, alcohol, tobacco smoke, heavy metals, transition metals, industrial solvents, pesticides, certain drugs like halothane, paracetamol, and radiation).
Under environmental stress conditions, disturbed balance between ROS production and elimination causes oxidative damage to biomolecules and can lead to plant cellular death.
Whether reactive oxygen species function as signaling molecules or cause oxidative damage depends on the equilibrium between ROS production and scavenging.
Reactive oxygen species are produced as a normal product of plant cellular metabolism.
Reactive oxygen species at high concentrations or during long-term exposure damage DNA, proteins, and lipids and can lead to necrotic and apoptotic cell death.
Quoted textsource-backed
At low concentrations, reactive oxygen species serve as an important second messenger in cell signaling; however, at higher concentrations and long-term exposure, reactive oxygen species can damage cellular macromolecules such as DNA, proteins, and lipids, which leads to necrotic and apoptotic cell death.
Reactive oxygen species are well-described second messengers in plant cellular processes, including conferment of tolerance to environmental stresses.
Environmental stresses can cause excessive production of reactive oxygen species, leading to progressive oxidative damage and ultimately cell death in plants.
HsAtg4 is a direct target for oxidation by H2O2.
Starvation stimulates formation of reactive oxygen species, specifically H2O2, during starvation-induced autophagy.
Oxidative conditions are essential for autophagy because antioxidative treatment abolished autophagosome formation and protein degradation.