Oxidative Stress
Response Genes
Free radicals are generated constantly by metabolism, exercise, and pollution. While systemic blood panels measure cellular damage, transcriptomics allows us to quantify the cell's active defense mechanisms against oxidative stress.
Quantifying Cellular Defense
When reactive oxygen species (ROS) accumulate, they damage DNA, proteins, and lipid membranes, accelerating aging and cellular decay.
Cells defend themselves by stabilising NRF2 protein that is already being made and continuously destroyed, which then coordinates a suite of cytoprotective genes (PMID 29717933). Transcriptomic profiling measures NFE2L2 alongside antioxidant enzyme genes including HMOX1, SOD1, SOD2, GPX1, GPX4 and CAT.
This describes which antioxidant genes were being transcribed when the sample was taken.
Key Pathway Targets
Nuclear Factor Erythroid 2-Related Factor 2
Master transcription factor directing the cellular antioxidant response.
Superoxide Dismutase 1 and 2
Enzymes that dismutate toxic superoxide radicals into oxygen and hydrogen peroxide.
Glutathione Peroxidase 1 and 4
Enzymes reducing organic hydroperoxides and hydrogen peroxide, protecting lipid membranes.
Catalase
Converts hydrogen peroxide into water and molecular oxygen, protecting cells from oxidative damage.
Heme Oxygenase 1
Inducible stress protein with potent anti-inflammatory and cytoprotective properties.
Why DNA Tells Only Half the Oxidative Stress Story
Your static DNA contains genetic variants (SNPs) in primary antioxidant genes like SOD2 or glutathione transferases. These SNPs indicate your baseline susceptibility to cellular aging and mitochondrial degradation from free radical damage, but they represent a static prediction.
Transcriptomics (RNA) measures whether your cellular antioxidant defense systems are actively meeting the current environmental and physical demands of your body. Because transcription responds to conditions rather than inheritance, a transcript panel reflects the state of these genes at the moment the sample was taken.
Protein Panels vs. Transcriptomics
Protein and metabolite panels measure the products of oxidative chemistry. Transcriptomics measures the antioxidant genes being transcribed. The two describe different layers of the same biology.
| Protein Marker | What It Measures | RNA Target |
|---|---|---|
| 8-OHdG | Urinary marker of oxidative DNA base modification and repair excision. | NFE2L2 (NRF2) |
| Lipid Peroxides | Marker of ongoing lipid peroxidation. | GPX1 / GPX4 |
| Erythrocyte Glutathione | Total erythrocyte glutathione pool. | GCLC / GCLM |
WHAT A TRANSCRIPTIONAL PANEL DOES NOT TELL YOU
- × That you have, or do not have, any medical condition. This panel reports gene activity, not diagnoses.
- × Whether a therapy is working. Transcript levels move for many reasons — sleep, a recent infection, the time of day, how long since you last ate or trained — and a change in them is not evidence that any intervention succeeded or failed.
- × What your results will be next month. Every value describes the moment the sample was drawn. Single-timepoint transcript measurements carry substantial within-person variability.
- × What is happening in a tissue the sample did not come from. These panels run on a blood sample. A blood transcript level is not a muscle, liver, brain or adipose measurement.
The Keap1-Nrf2 Antioxidant Cascade
Cells possess an elegant sensor system to neutralize oxidative strain. The central regulator of this pathway is Nrf2, which resides in the cytoplasm bound to its inhibitor protein, Keap1. Under normal conditions, Nrf2 is continually degraded.
Oxidative Stress
Reactive Oxygen Species (ROS) build up, modifying specific cysteine residues on Keap1.
Nrf2 Release
Modified KEAP1 can no longer hand NRF2 to the ubiquitin machinery, so newly made NRF2 escapes degradation and enters the nucleus (PMID 29717933).
ARE Binding
NRF2 binds antioxidant response elements, principally as a heterodimer with a small MAF protein, and initiates transcription (PMID 29717933).
Enzymatic Defense
Transcription of the NRF2 gene battery rises, including HMOX1, NQO1 and the glutathione synthesis enzymes GCLC and GCLM (PMID 24647116).
Stimulating Endogenous Antioxidants
These act on antioxidant signaling by different routes: some as mild stressors that induce the NRF2 programme, others by supplying substrate or scavenging oxidants directly. The two are not equivalent, and the second can blunt the first.
Sulforaphane (Cruciferous Sprouts)
Highly studied natural activator of Nrf2. Interacts with Keap1 to trigger robust upregulation of glutathione synthesis and detoxification genes.
N-Acetylcysteine (NAC) & Selenium
Dietary supplementNAC supplies cysteine for glutathione synthesis. Selenium is not a cofactor: it is built into glutathione peroxidases as selenocysteine while the protein is being translated, so it is a constituent amino acid of the enzyme (PMID 24987004).
High-Intensity Physical Conditioning
Creates transient oxidative spikes associated with higher SOD2 expression. That induction runs through PGC-1α and FOXO3 rather than the KEAP1-NRF2 axis described above (PMID 17055439).
Astaxanthin & Polyphenols
Dietary supplementAstaxanthin scavenges free radicals directly. Because NRF2 activation depends on oxidant modification of KEAP1, direct scavenging and NRF2 induction can work against each other rather than together.
Therapies That Act on These Pathways
These therapies act on genes this panel reports. Biomeme does not prescribe, supply, recommend or evaluate any of them, and listing one here is not a claim that it works. Several are available only by prescription; some are not approved for any use. Where the published evidence is thin or points the other way, the card says so.
Scientific Citations (5)
- [1] Kops GJ, Dansen TB, Polderman PE, et al. Forkhead transcription factor FOXO3a protects quiescent cells from oxidative stress. Nature. 2002;419(6904):316-321.
- [2] St-Pierre J, Drori S, Uldry M, et al. Suppression of reactive oxygen species and neurodegeneration by the PGC-1 transcriptional coactivators. Cell. 2006;127(2):397-408.
- [3] Hayes JD, Dinkova-Kostova AT. The Nrf2 regulatory network provides an interface between redox and intermediary metabolism. Trends Biochem Sci. 2014;39(4):199-218.
- [4] Labunskyy VM, Hatfield DL, Gladyshev VN. Selenoproteins: molecular pathways and physiological roles. Physiol Rev. 2014;94(3):739-777.
- [5] Yamamoto M, Kensler TW, Motohashi H. The KEAP1-NRF2 System: a Thiol-Based Sensor-Effector Apparatus for Maintaining Redox Homeostasis. Physiol Rev. 2018;98(3):1169-1203.
The Biomeme Molecular Ecosystem
From deep whole-transcriptome sequencing in the laboratory to rapid point-of-care instrumentation in the field.
High-Depth RNA Sequencing
Processed at One Health Labs, Biomeme's CLIA-certified laboratory, using Illumina NovaSeq high-depth paired-end RNA sequencing. Samples are collected in venous PAXgene blood RNA tubes to stabilize cellular transcription at the moment of draw.
Biomeme/5 Handheld Platform
Beyond central-lab genomics, Biomeme engineers patented, battery-powered real-time PCR instruments. Our deployable hardware brings decentralized molecular detection directly to the field and clinical points of care.
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ABOUT THESE PANELS
Biomeme's wellness transcriptomic panels are general wellness products. They report gene activity to support a healthy lifestyle. They are not intended to diagnose, treat, cure, mitigate or prevent any disease or condition, and they are not a substitute for evaluation by a licensed healthcare professional. Results describe the state of the measured transcripts at the moment the sample was taken.