What you carry at this position in your DNA and what research says about it.
Oxidative Stress Defense: 7/10 evidence, 31 publications.
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Sample genotype (not yours): G/G
Typical Antioxidant Defense and Lower Vascular Risk
Two copies of the G allele encode the fully functional proline-containing enzyme. This genotype provides optimal baseline protection against cellular oxidative stress.
What this genotype means: Optimal baseline antioxidant enzyme activity; Lower susceptibility to oxidative cellular damage; Typical risk of degenerative joint issues.
Sample genotype (not yours): A/A
Reduced Antioxidant Defense and Elevated Vascular Risk
Two copies of the A allele result in a significantly less stable glutathione peroxidase 1 enzyme. This genotype is linked to higher oxidative stress and elevated joint and vascular risks.
What this genotype means: Significantly reduced glutathione peroxidase activity; Higher susceptibility to oxidative cellular damage; Elevated risk of degenerative joint and vascular issues.
Sample genotype (not yours): G/A
Slightly Reduced Antioxidant Defense and Elevated Vascular Risk
One copy of the A allele reduces the overall efficiency of the glutathione peroxidase 1 enzyme. This can lead to a mild increase in cellular vulnerability to oxidative stress.
What this genotype means: Moderately reduced glutathione peroxidase activity; Increased vulnerability to oxidative stress; Slightly elevated risk of joint and vascular complications.
Gene function and biological role
Gene Function: The GPX1 gene encodes glutathione peroxidase 1, a vital selenium-dependent enzyme that acts as a primary cellular shield against oxidative damage [1]. It specifically catalyzes the reduction of hydrogen peroxide and organic hydroperoxides into harmless water and alcohols, utilizing glutathione as a cofactor [2]. This enzymatic activity is crucial for protecting vascular endothelial cells, red blood cells, and cartilage from reactive oxygen species [3]. Because selenium is a key component of the enzyme's active site, the functional efficiency of this gene is highly dependent on dietary selenium intake [4].
Variant Impact: The rs1050450 variant represents a missense mutation in the GPX1 gene that substitutes the amino acid proline with leucine at position 200 of the protein chain [1]. This structural alteration, often referred to as Pro198Leu or Pro197Leu in scientific literature, significantly reduces the stability and overall activity of the glutathione peroxidase 1 enzyme [2]. Studies indicate that the leucine-encoding variant (the A allele) leads to an approximate 40 percent reduction in enzyme activity [5]. Consequently, cells expressing this variant are less efficient at neutralizing hydrogen peroxide, leaving tissues more vulnerable to oxidative stress and cellular damage [3].
Read on the Selenium Enzyme Activity page
Key Insight: The enzyme produced by this gene relies on selenium to function, meaning that the oxidative risks associated with the variant are significantly amplified in individuals with low dietary selenium intake. Additionally, this variant is linked to an increased risk of blood vessel re-narrowing after stent procedures.
Location: GPX1. Chromosome 3 · 3p21.31 · 49.4 Mb
Estimated prevalence by population
Global 50.0%; European 48.1%; African 50.1%; East Asian 88.7%; South Asian 59.8%; Americas 60.9%; Ashkenazi 29.1%; Finnish 27.9%; Middle Eastern 45.4%; Amish 64.2%.
Estimated GG genotype frequency.
Global 40.6%; European 42.5%; African 41.4%; East Asian 10.9%; South Asian 35.0%; Americas 34.3%; Ashkenazi 49.7%; Finnish 49.8%; Middle Eastern 44.0%; Amish 31.8%.
Estimated GA genotype frequency.
Global 9.4%; European 9.4%; African 8.5%; East Asian 0.3%; South Asian 5.1%; Americas 4.8%; Ashkenazi 21.2%; Finnish 22.2%; Middle Eastern 10.7%; Amish 3.9%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Nutrition & Metabolism
Blood Chemistry & Metabolites
Oxidative Stress Defense. Evidence: 3/10. Source: PMID 23073788. Typical Defense.
Organ Systems
Bone, Joint & Connective Tissue Health
Joint Health. Evidence: 3/10. Source: PMID 20178852. Typical Risk.
Cardiovascular & Metabolic
Heart Disease
Cardiovascular Health. Evidence: 5/10. Source: PMID 25009565. Typical Risk.
Blood Cell & Iron Traits
Hemoglobin Levels. Evidence: 7/10. Source: PMID 32327693. Higher Levels.
Showing effects for A/A genotype
Oxidative Stress Defense. Evidence: 3/10. Source: PMID 23073788. Reduced Defense.
Joint Health. Evidence: 3/10. Source: PMID 20178852. Elevated Joint Risk.
Cardiovascular Health. Evidence: 5/10. Source: PMID 25009565. Elevated Risk.
Hemoglobin Levels. Evidence: 7/10. Source: PMID 32327693. Typical Levels.
Showing effects for G/A genotype
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Cellular defense mechanisms operate at full capacity with this genotype, as the proline residue at position 200 maintains optimal enzyme stability [1]. Glutathione peroxidase 1 efficiently neutralizes hydrogen peroxide, preventing it from accumulating and causing damage to lipids, proteins, and DNA [2]. Clinical studies show that this robust antioxidant defense is associated with a lower risk of degenerative joint conditions, particularly in regions where selenium levels are low [3]. Furthermore, vascular tissues are better protected against inflammatory changes, resulting in a lower baseline risk of coronary artery calcification and cardiovascular events [4]. Individuals with this genotype also tend to maintain slightly higher hemoglobin levels, supporting efficient oxygen transport [5].
Optimal baseline antioxidant enzyme activity; Lower susceptibility to oxidative cellular damage; Typical risk of degenerative joint issues.
Sample genotype: AA (Homozygous)
Antioxidant defenses are significantly altered because both copies of the gene produce the less stable leucine-containing enzyme [1]. Research indicates that this change leads to an approximate 40 percent reduction in glutathione peroxidase 1 activity, limiting the body's ability to neutralize harmful hydrogen peroxide [2]. This accumulation of reactive oxygen species is linked to increased cellular damage in various tissues, including blood vessels and cartilage [3]. Clinical data show a nearly twofold increase in the risk of Kashin-Beck degenerative joint disease, particularly when dietary selenium is lacking [4]. Additionally, there is an elevated risk of coronary artery calcification and a higher likelihood of stent re-narrowing following cardiovascular procedures [5].
Significantly reduced glutathione peroxidase activity; Higher susceptibility to oxidative cellular damage; Elevated risk of degenerative joint and vascular issues.
Sample genotype: GA (Heterozygous)
Enzymatic clearance of hydrogen peroxide is partially compromised due to the presence of one leucine-encoding allele, which reduces overall enzyme stability [1]. This reduction in antioxidant capacity makes cells more susceptible to oxidative damage, especially during periods of physiological stress or poor nutrition [2]. In selenium-deficient environments, this genotype is associated with an increased risk of Kashin-Beck disease, a degenerative joint disorder [3]. Cardiovascular studies also indicate a higher susceptibility to coronary artery calcification and a higher rate of blood vessel re-narrowing after stent placement [4]. Maintaining adequate dietary selenium and antioxidant intake may help support enzyme function and mitigate these risks [5].
Moderately reduced glutathione peroxidase activity; Increased vulnerability to oxidative stress; Slightly elevated risk of joint and vascular complications.
Variants with shared genetic architecture
rs854560 · PON1 Gene · Chr 7 · Cardiovascular Health
rs713041 · GPX4 Gene · Chr 19 · Antioxidant and Cancer Risk
rs7493 · PON2 Gene · Chr 7 · Cardiovascular Risk
GPX1 gene Pro200Leu polymorphism, erythrocyte GPX activity, and cancer risk.
Predicted loss and gain of function mutations in ACO1 are associated with erythropoiesis.
Content updated August 2026.
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