Genetics of Antioxidant Defence

Antioxidant defence systems protect cells from oxidative damage by neutralising reactive oxygen and nitrogen species. Genetic variants in NRF2, superoxide dismutase, glutathione peroxidase, and catalase influence individual antioxidant capacity.

This page is for educational and informational purposes only. Not a diagnostic tool. Always consult a qualified healthcare provider.

What is Antioxidant Defence?

Cells continuously produce reactive oxygen species (ROS) as byproducts of metabolism and immune activity. Antioxidant defence systems neutralise these reactive molecules through enzymatic (SOD, GPX, catalase) and non-enzymatic (glutathione, vitamin C, vitamin E) mechanisms. NRF2 (NFE2L2) is the master transcription factor coordinating antioxidant gene expression. Genetic variants reducing antioxidant enzyme activity or NRF2 function increase cellular vulnerability to oxidative damage — relevant to Long COVID, where elevated oxidative stress markers have been consistently reported.

Biological pathways commonly discussed in relation to Antioxidant Defence

Research into Antioxidant Defence and Free Radical Protection has highlighted several biological pathways that may be relevant. Genetic variants within these pathways may influence individual susceptibility, symptom severity, or the trajectory of the condition.

Nrf2 Antioxidant

NRF2 (NFE2L2) activates antioxidant response element (ARE) genes including SOD2, GPX1, NQO1, HMOX1, and GCLC. Variants affecting NRF2 activation or KEAP1 repression alter the magnitude of antioxidant gene induction.

Superoxide Dismutase

SOD1 (cytoplasmic) and SOD2 (mitochondrial) convert superoxide radicals to hydrogen peroxide. SOD2 Val16Ala (rs4880) is the most studied antioxidant variant, affecting mitochondrial SOD2 import and activity.

Glutathione Peroxidase

GPX1-4 reduce peroxides using glutathione. GPX1 Pro198Leu (rs1050450) reduces enzyme activity. GPX4 specifically protects against lipid peroxidation and ferroptosis.

Catalase Peroxiredoxin

Catalase (CAT) and peroxiredoxins (PRDX1-6) provide additional hydrogen peroxide neutralisation. Variants in CAT and PRDX genes affect overall antioxidant capacity.

Key genes studied in relation to Antioxidant Defence

The following genes have been studied in relation to Antioxidant Defence and Free Radical Protection. These genes span the biological pathways most commonly discussed in this area of research.

Genetic variants commonly discussed

The following genetic variants (SNPs) are found in genes that have been studied in relation to Antioxidant Defence. Each variant represents a position in the genome where individuals may carry different alleles.

9 variants total across genes studied in relation to Antioxidant Defence.

How personal DNA data may provide educational insights

Consumer DNA files from 23andMe, AncestryDNA, and MyHeritage contain raw SNP data. When you upload your file to ChronicDNA, the analysis engine checks your genotype against a curated panel of 80+ genes selected for their relevance to Long COVID, ME/CFS, and connected biological pathways - some of which may relate to areas such as Antioxidant Defence.

This is not a diagnostic service. Genetic variants do not determine whether you have Antioxidant Defence, nor do they predict your clinical outcomes. The report is educational - it explains which variants you carry, what the research says about them, and how they fit into the biological pathways most relevant to chronic illness. All results should be discussed with a qualified healthcare provider.

Related conditions and pathways

Antioxidant Defence shares biological pathways and genetic associations with the following related conditions and areas of research.

Frequently asked questions

What is the NRF2 pathway and why is it relevant to chronic illness?

NRF2 is the master regulator of antioxidant defence, activating expression of dozens of protective genes in response to oxidative stress. In chronic illness contexts including Long COVID, impaired NRF2 activation may leave cells vulnerable to the oxidative damage documented in these conditions.

What is the SOD2 Val16Ala variant?

SOD2 Val16Ala (rs4880) affects the mitochondrial targeting sequence of superoxide dismutase 2. The Ala allele is associated with reduced mitochondrial SOD2 import efficiency, potentially increasing mitochondrial superoxide levels. It has been studied in relation to oxidative stress-related conditions.

How does glutathione relate to antioxidant defence?

Glutathione (GSH) is the most abundant intracellular antioxidant, acting both directly (neutralising ROS) and as substrate for glutathione peroxidases. Its synthesis requires NRF2 activation of GCLC and GCLM. Reduced glutathione levels have been documented in ME/CFS and Long COVID patients.

Which antioxidant genes are included in consumer DNA data?

Commonly included variants are SOD2 rs4880, GPX1 rs1050450, GSTM1 and GSTT1 null genotypes, NQO1 rs1800566, and NFE2L2 variants. ChronicDNA analyses these in the context of cellular antioxidant biology.

Explore DNA insights

If you already have DNA data from 23andMe, AncestryDNA, or MyHeritage, upload your raw file to ChronicDNA and receive a personalised educational report covering genes studied in relation to Antioxidant Defence and connected biological pathways.

Get Your Personalised DNA Report

Informational and educational only · Not a diagnostic tool · GDPR compliant

8 genes · 9 variants analysed in relation to Antioxidant Defence