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SOD1 Gene: Your Antioxidant Defense System

Key takeaways:

  • The SOD1 gene encodes an enzyme important in reducing oxidative stress and protecting your cells from damage.
  • SOD1 uses copper and zinc in neutralizing free radicals, such as superoxide radicals, turning them into less reactive molecules that the body can clear out.
  • This helps to prevent damage to DNA and other proteins in cells.
  • Genetic variants in SOD1 can change how well this antioxidant system works. These variants may increase the risk of several chronic diseases.
Members will see their genotype report below, plus additional solutions in the Lifehacks section. Join today 

SOD1: Superoxide Dismutase 1

Our body has built-in antioxidants that fight against cellular stress. The superoxide dismutase (SOD1) enzyme fights against oxidative stress in your cells, constantly battling to balance out oxidants with antioxidants.

The SOD1 gene codes for the copper-zinc superoxide dismutase enzyme. This cellular enzyme protects against oxidative stress by deactivating reactive oxygen species (ROS).

Three types of superoxide dismutases are part of our built-in antioxidant system:[ref]

  • SOD1, found in the cytosol or fluid of cells
  • SOD2, a mitochondrial antioxidant
  • SOD3, which is extracellular or outside of the cells

SOD1 binds copper and zinc ions together and destroys free radicals. It is an antioxidant that our body produces, which converts superoxide radicals into oxygen and hydrogen peroxide. Other enzymes then break down the hydrogen peroxide.

Balancing out oxidation reactions:

This is all about electrons.. Superoxide is two oxygen molecules bonded together but with one electron missing (O2). Normal oxygen that we breathe in the air is a stable combo of two oxygen molecules.

The superoxide compound, which lacks an electron, is highly reactive, wanting to bind with another molecule to balance out its charge.

SOD1 – superoxide dismutase 1 – can counteract the superoxide produced in cellular reactions. SOD1’s primary function is to convert superoxide radicals (O2) into hydrogen peroxide (H2O2) and oxygen (O2). The hydrogen peroxide produced is further converted into water by other enzymes, such as glutathione peroxidase.

While we often think of antioxidants as being good and reactive oxygen species (ROS), such as superoxide, as being ‘bad’, ROS does play a vital role in cell signaling. Our cells need to be in balance with antioxidants and pro-oxidants.[ref]

Additionally, our immune system produces pro-oxidants such as superoxide to kill invading pathogens.

Balance is key, and SOD1 helps provide that balance between ROS and oxidative stress.

Research on SOD1:

Research on the different genetic variants shows that SOD1 impacts heart disease risk, kidney disease, hearing loss, and diabetes. Oxidative stress plays a role in all of these chronic conditions, and decreased SOD1 (or too much ROS) can contribute to the development of these diseases.[ref][ref]

Oxidative stress seems to play a role in Alzheimer’s disease as well, and SOD1 variants have been studied to see if they affect the risk of Alzheimer’s. For rs2070424, the G allele offers protection against Alzheimer’s disease regardless of APOE gene status.[ref][ref]

Related article: Check your APOE genes  (only if you want to know more about your Alzheimer’s risk)

Overall, higher SOD activity has links to decreased mortality in women. Oddly, this statistic didn’t hold true for men.[ref]

SOD1 in ALS:

One of the first genetic mutations linked to the familial form of ALS was in the SOD1 gene. More recent research points to misfolded SOD1 proteins being present both in the hereditary type of ALS (about 10% of ALS patients) and in the sporadic type. While there is still a lot that researchers don’t know here, it looks like the SOD1 mutations cause a gain-of-function and altered folding in a way that causes a loss of motor neuron function.[ref]


SOD1 Genotype Report:

SOD1 genetic variants can cause either an increase or a decrease in enzyme activity. Rare mutations in SOD1 have links to several diseases, including an inherited form of ALS (Lou Gehrig’s disease).[ref] More common variants are linked with conditions such as diabetes, cardiovascular disease, kidney disease, and hearing damage.

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Lifehacks for increasing SOD1:

Dietary changes:

A recent clinical trial looked at the effect of a high-antioxidant diet on oxidative stress. The study participants on a Mediterranean diet were also supplemented with apple and bergamot juice. After two weeks, they had an increase in SOD1.[ref]

Increasing zinc was shown in a clinical trial involving multiple myeloma patients to increase SOD1 levels.[ref] The study used a low-dose supplement, but dietary sources of zinc include oysters, beef, pumpkin seeds, crab, dark-meat poultry, and dairy.

4 Natural Supplements to increase SOD1:

Acai:
Freeze-dried acai powder, in an animal model of SOD1 deficiency, shows an increase in healthy aging and reduction of oxidative damage.[ref] Freeze-dried Acai powder can be found online, and acai juice can be found in most grocery stores.

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Related Articles and Topics:

Best Supplements to Boost BDNF

Blood Glucose Levels: Genetics and Blood Sugar Regulation

Nrf2 Pathway: Increasing the Body’s Ability to Get Rid of Toxins


References:

Gualtieri, Paola, et al. “Antioxidant-Enriched Diet on Oxidative Stress and Inflammation Gene Expression: A Randomized Controlled Trial.” Genes, vol. 14, no. 1, Jan. 2023, p. 206. PubMed, https://doi.org/10.3390/genes14010206.

Jahankhani, Kasra, et al. “Adjuvant Therapy with Zinc Supplementation; Anti-Inflammatory and Anti-Oxidative Role in Multiple Myeloma Patients Receiving Autologous Hematopoietic Stem Cell Transplantation: A Randomized Controlled Clinical Trial.” Biometals: An International Journal on the Role of Metal Ions in Biology, Biochemistry, and Medicine, vol. 37, no. 6, Dec. 2024, pp. 1609–27. PubMed, https://doi.org/10.1007/s10534-024-00630-0.

Abud, Gabriela Ferreira, et al. “Taurine as a Possible Antiaging Therapy: A Controlled Clinical Trial on Taurine Antioxidant Activity in Women Ages 55 to 70.” Nutrition, vol. 101, Sept. 2022, p. 111706. ScienceDirect, https://doi.org/10.1016/j.nut.2022.111706.
Kase, Benjamin A., et al. “Association of Copper-Zinc Superoxide Dismutase (SOD1) and Manganese Superoxide Dismutase (SOD2) Genes with Non-Syndromic Myelomeningocele.” Birth Defects Research. Part A, Clinical and Molecular Teratology, vol. 94, no. 10, Oct. 2012, pp. 762–69. PubMed Central, https://doi.org/10.1002/bdra.23065.
Khan, Md Asaduzzaman, et al. “Regulatory Effects of Resveratrol on Antioxidant Enzymes: A Mechanism of Growth Inhibition and Apoptosis Induction in Cancer Cells.” Molecules and Cells, vol. 35, no. 3, Mar. 2013, pp. 219–25. PubMed, https://doi.org/10.1007/s10059-013-2259-z.
Laslo, Mara, et al. “A Botanical Containing Freeze Dried Açai Pulp Promotes Healthy Aging and Reduces Oxidative Damage in Sod1 Knockdown Flies.” Age, vol. 35, no. 4, Aug. 2013, pp. 1117–32. PubMed Central, https://doi.org/10.1007/s11357-012-9437-3.
Liu, Yi-Min, et al. “Association between Polymorphisms in SOD1 and Noise-Induced Hearing Loss in Chinese Workers.” Acta Oto-Laryngologica, vol. 130, no. 4, Apr. 2010, pp. 477–86. PubMed, https://doi.org/10.3109/00016480903253587.
Mao, Chen, et al. “Associations between Superoxide Dismutase, Malondialdehyde and All-Cause Mortality in Older Adults: A Community-Based Cohort Study.” BMC Geriatrics, vol. 19, Apr. 2019, p. 104. PubMed Central, https://doi.org/10.1186/s12877-019-1109-z.
Mohammedi, Kamel, et al. “Allelic Variations in Superoxide Dismutase-1 (SOD1) Gene Are Associated with Increased Risk of Diabetic Nephropathy in Type 1 Diabetic Subjects.” Molecular Genetics and Metabolism, vol. 104, no. 4, Dec. 2011, pp. 654–60. PubMed, https://doi.org/10.1016/j.ymgme.2011.08.033.
Montllor-Albalate, Claudia, et al. “Extra-Mitochondrial Cu/Zn Superoxide Dismutase (Sod1) Is Dispensable for Protection against Oxidative Stress but Mediates Peroxide Signaling in Saccharomyces Cerevisiae.” Redox Biology, vol. 21, Feb. 2019, p. 101064. ScienceDirect, https://doi.org/10.1016/j.redox.2018.11.022.
Morikawa, Daichi, et al. “Antioxidant Treatment with Vitamin C Attenuated Rotator Cuff Degeneration Caused by Oxidative Stress in Sod1-Deficient Mice.” JSES Open Access, vol. 2, no. 1, Mar. 2018, pp. 91–96. PubMed Central, https://doi.org/10.1016/j.jses.2017.11.003.
Neves, Ana Luísa, et al. “Allelic Variations in Superoxide Dismutase-1 (SOD1) Gene and Renal and Cardiovascular Morbidity and Mortality in Type 2 Diabetic Subjects.” Molecular Genetics and Metabolism, vol. 106, no. 3, July 2012, pp. 359–65. PubMed, https://doi.org/10.1016/j.ymgme.2012.04.023.
Otaki, Yoichiro, et al. “The Impact of Superoxide Dismutase-1 Genetic Variation on Cardiovascular and All-Cause Mortality in a Prospective Cohort Study: The Yamagata (Takahata) Study.” PLOS ONE, vol. 11, no. 10, Oct. 2016, p. e0164732. PLoS Journals, https://doi.org/10.1371/journal.pone.0164732.
Pansarasa, Orietta, et al. “SOD1 in Amyotrophic Lateral Sclerosis: ‘Ambivalent’ Behavior Connected to the Disease.” International Journal of Molecular Sciences, vol. 19, no. 5, May 2018, p. 1345. PubMed Central, https://doi.org/10.3390/ijms19051345.
“SOD1.” Wikipedia, 6 Mar. 2026. Wikipedia, https://en.wikipedia.org/w/index.php?title=SOD1&oldid=1342047310.
Spisak, Karolina, et al. “Rs2070424 of the SOD1 Gene Is Associated with Risk of Alzheimer’s Disease.” Neurologia I Neurochirurgia Polska, vol. 48, no. 5, 2014, pp. 342–45. PubMed, https://doi.org/10.1016/j.pjnns.2014.09.002.
VCV000549678.6 – ClinVar – NCBI. https://www.ncbi.nlm.nih.gov/clinvar/variation/549678/. Accessed 18 Mar. 2026.
VCV000932081.10 – ClinVar – NCBI. https://www.ncbi.nlm.nih.gov/clinvar/variation/932081/. Accessed 18 Mar. 2026.
Yin, Jiawei, et al. “Interactions between Plasma Copper Concentrations and SOD1 Gene Polymorphism for Impaired Glucose Regulation and Type 2 Diabetes.” Redox Biology, vol. 24, Mar. 2019, p. 101172. PubMed Central, https://doi.org/10.1016/j.redox.2019.101172.
———. “Interactions between Plasma Copper Concentrations and SOD1 Gene Polymorphism for Impaired Glucose Regulation and Type 2 Diabetes.” Redox Biology, vol. 24, June 2019, p. 101172. PubMed, https://doi.org/10.1016/j.redox.2019.101172.
Zheng, Yi, et al. “Resveratrol Protects Human Lens Epithelial Cells against H2O2-Induced Oxidative Stress by Increasing Catalase, SOD-1, and HO-1 Expression.” Molecular Vision, vol. 16, Aug. 2010, pp. 1467–74.

About the Author:
Debbie Moon is a biologist, engineer, author, and the founder of Genetic Lifehacks where she has helped thousands of members understand how to apply genetics to their diet, lifestyle, and health decisions. With more than 10 years of experience translating complex genetic research into practical health strategies, Debbie holds a BS in engineering from Colorado School of Mines and an MSc in biological sciences from Clemson University. She combines an engineering mindset with a biological systems approach to explain how genetic differences impact your optimal health.