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AnyGenes

WHAT IS OXIDATIVE STRESS?

Oxidative stress OS arises from an imbalance between reactive oxygen species (ROS) production and antioxidant defenses. While ROS are critical for cell signaling and immune defense, excessive levels can damage DNA, proteins, and lipids, contributing to various diseases such as cancer, neurodegeneration, and cardiovascular disorders. Free radicals derived from OS are required at low concentrations for many important physiological functions, such as muscle contraction and drug detoxification.

Why choose anygenes® for OS research?

At AnyGenes®, we provide advanced qPCR arrays tailored for studying oxidative stress pathways. Our solutions empower researchers to:

  • Investigate key ROS-regulating genes such as SODs, GPXs, and CAT.
  • Explore OS biomarkers like HMOX1, NRF2, and NOX enzymes.
  • Examine interactions between OS and signaling pathways, including PI3K/Akt and MAPK.

Our qPCR arrays are designed for precision, reliability, and reproducibility, enabling breakthroughs in understanding OS mechanisms.

AnyGenes Oxidative Stress Array for gene expression analysis and ROS research.

Discover our advanced qPCR arrays for Oxidative Stress research.

Model of how a favorable redox environment prevents vascular endothelial dysfunction and reduces cardiovascular disease risk.

A proposed model of how a favorable redox environment prevents vascular endothelial dysfunction and possibly the risk
for cardiovascular disease in an uncontrolled and controlled redox environment 
.

KEY MECHANISMS OF OXIDATIVE STRESS

OS is driven by complex molecular processes:

  • Reactive Oxygen Species (ROS) Production: Generated by mitochondria, NADPH oxidase, and external sources like UV radiation or pollution.  However, factors such as environmental toxins, inflammation, and unhealthy dietary habits can lead to excessive ROS production, overwhelming the body's antioxidant defenses.
  • Antioxidant Defense: Enzymes such as SOD, CAT, and GPX detoxify ROS to maintain cellular balance.
  • Cellular Damage: Excess ROS can cause oxidative damage DNA, proteins, and lipids, contributing to cellular dysfunction and death. This damage is particularly pronounced in tissues with high metabolic rates, such as the brain.
  • Signaling Roles: ROS serve as signaling molecules in pathways like NRF2/KEAP1 and HIF-1α under controlled conditions.
  • Link to Inflammation: Elevated ROS levels can activate inflammatory pathways, creating a vicious cycle that exacerbates tissue damage and contributes to disease progression.

KEY COMPONENTS OF THE OXIDATIVE STRESS PATHWAY

  1. Reactive Oxygen Species (ROS):
    • Includes superoxide anion (O₂⁻), hydrogen peroxide (H₂O₂), and hydroxyl radical (•OH).
  2. Antioxidant Defense Systems:
    • Enzymatic: Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx).
    • Non-Enzymatic: Glutathione (GSH), vitamins C and E.
  3. Pro-Oxidant Enzymes:
    • NADPH oxidases (NOX) and xanthine oxidase (XO).
  4. Mitochondria: Major source of ROS during energy production.
  5. Key Regulators:
    • NRF2: Activates antioxidant defenses.
    • NF-κB: Mediates inflammation linked to OS.
  6. OS Biomarkers:
    • Malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG).

This pathway highlights the balance between ROS production and antioxidant defenses crucial for maintaining cellular health.

SIGNALING PATHWAYS INVOLVED IN OS

Several key signaling pathways are activated in response to OS:

  • Nuclear Factor kappa B (NF-κB): This transcription factor is activated by ROS, leading to the expression of pro-inflammatory cytokines and further promoting OS.
  • Forkhead Box O (FoxO) Proteins: FoxO transcription factors regulate the expression of antioxidant genes in response to OS. For instance, FoxO3a enhances the expression of SOD2, protecting cells from oxidative damage.
  • Mitogen-Activated Protein Kinases (MAPK): These pathways are involved in cellular responses to stress, regulating apoptosis and inflammation in response to ROS levels.

CLINICAL SIGNIFICANCE

Dysregulated OS contributes to a range of health conditions:

  • Neurodegenerative Diseases: ROS are implicated in Alzheimer's, Parkinson's, and Huntington's diseases.
  • Cancer: Oxidative damage promotes mutations, tumor progression, and therapy resistance.
  • Cardiovascular Disorders: ROS contribute to atherosclerosis, hypertension, and heart failure.
  • Aging and Metabolic Disorders: Chronic oxidative stress accelerates aging and is linked to obesity and diabetes.

Researching OS mechanisms is crucial for developing antioxidants, therapeutics, and preventive strategies.

(1) Pruchniak MP, Aražna M & Demkow U. Biochemistry of Oxidative Stress. Adv Exp Med Biol. (2016) 878:9-19.
(2) Ihsan AU & al. Role of oxidative stress in pathology of chronic prostatitis/chronic pelvic pain syndrome and male infertility and antioxidants function in ameliorating oxidative stress. Biomed Pharmacother. (2018) 106:714-723.
(3) Peña-Oyarzun D & al. Autophagy and oxidative stress in non-communicable diseases: A matter of the inflammatory state?. Free Radic Biol Med. (2018) 20;124:61-78.
(4) Liguori I & al. Oxidative stress, aging, and diseases. Clin Interv Aging. (2018) 26;13:757-772.
(5) Simioni C & al. Oxidative stress: role of physical exercise and antioxidant nutraceuticals in adulthood and aging. Oncotarget. (2018) 30; 9(24): 17181–17198.
(6) Varadharaj S & al. Role of Dietary Antioxidants in the Preservation of Vascular Function and the Modulation of Health and Disease. Front Cardiovasc Med. (2017) 1;4:64.

OXIDATIVE DAMAGE SIGNALING PATHWAY BIOMARKER LIST

Customize your own signaling pathways (SignArrays®) with the factors of your choice!
Simply download and complete our Personalized SignArrays® information file and send it at [email protected] to get started on your project.

You can check the biomarker list included in this pathway, see below: