Dismutase

Other Names

Cambialistic superoxide dismutaseCopper-zinc superoxide dismutaseCu,Zn-SODCu/Zn superoxide dismutaseCupreinCuZnSODCytocupreinEC-SODErythrocupreinExtracellular superoxide dismutaseFe-SODFerrisuperoxide dismutaseHemocupreinHepatocupreinIndophenol oxidaseIron superoxide dismutaseManganese superoxide dismutaseMn-SODMnSODOrgoteinSODSOD-1SOD-2SOD-3Super Dioxide DismutaseSuperoxidase dismutaseSuperoxide dismutaseSuperoxide dismutase 1Superoxide dismutase ISuperoxide dismutase IISuperoxide oxidoreductaseSuperóxido Dismutasa

Synopsis

Superoxide Dismutase (SOD): A Comprehensive Reference

1. Identity: Names, Chemical Nature, and Common Forms

Superoxide dismutase (SOD) is the principal enzymatic ingredient sold under the common name "dismutase" in the dietary supplement market. It is a metalloenzyme that catalyzes the dismutation of superoxide anion radicals (O₂⁻) into molecular oxygen (O₂) and hydrogen peroxide (H₂O₂), functioning as the first line of defense against reactive oxygen species (ROS) in nearly all aerobic organisms. This enzymatic reaction protects cellular components such as DNA, proteins, and lipids from oxidative damage caused by superoxide, a byproduct of aerobic respiration and other metabolic processes.

Synonyms and trade names used in the literature and in commerce include Orgotein (the bovine-derived parenteral drug form), GliSODin (a melon-derived SOD bound to wheat gliadin), SOD B Extramel (a melon pulp concentrate), and Palosein. Other names in use include "Super Dioxide Dismutase," "Superóxido Dismutasa," and "Superoxyde Dismutase."

1.1 Isoforms and Metal Cofactors

In mammals, three primary isoforms exist, distinguished by their metal cofactors and subcellular localization: SOD1 (Cu/Zn-SOD), a homodimeric enzyme predominant in the cytosol and nucleus; SOD2 (Mn-SOD), a homotetrameric form located in the mitochondrial matrix; and SOD3, the extracellular copper-zinc form.

SOD1 (Cu/Zn-SOD): SOD1 is a 32 kDa homodimeric protein, with each subunit containing one copper and one zinc ion. It is predominantly localized in the cytosol, with additional presence in the mitochondrial intermembrane space. The copper ion is responsible for the catalytic activity, while the zinc ion provides structural stability to the enzyme.
SOD2 (Mn-SOD): SOD2, located in the mitochondria, relies on manganese to neutralize superoxide radicals generated during mitochondrial respiration, thereby protecting mitochondrial DNA and proteins.
SOD3 (Extracellular SOD): SOD3, an extracellular enzyme, also utilizes copper and zinc to protect against oxidative damage in the extracellular matrix and plasma. In contrast to the ubiquitous expression of SOD1 and SOD2, levels of SOD3 expression vary greatly between organs; under physiological conditions, SOD3 mRNA levels are highest in the heart, lung, and pancreas, but low in brain tissue.

Beyond the three mammalian isoforms, other classes exist in other kingdoms of life. Four classes have been identified depending on selective binding of metals, namely Cu,Zn-SOD, Fe-SOD, Mn-SOD, and Ni-SOD. The relatively newer type, Ni-SOD, binds nickel and is observed in bacteria, including the genus Streptomyces. Fe-SOD and Mn-SOD are also present in bacteria.

1.2 Natural Sources

Superoxide dismutase is present in virtually all living organisms, including plants. Some of the richest natural sources are green vegetables such as broccoli, Brussels sprouts, cabbage, spinach, and wheatgrass, as well as certain melons. Some cereals such as wheat or barley, vegetables like peas or broccoli, and fruits such as melon or certain types of berries contain relatively high levels of SOD; however, recent research has shown that one of the main natural sources of SOD is found in certain types of marine algae or phytoplankton.

Melon (Cucumis melo L.) — rare varieties, such as a cantaloupe melon from southern France, are exceptionally concentrated in SOD and used for extracting standardized, supplement-grade forms. Superoxide dismutase requires a bond to zinc and copper (Cu-Zn-SOD), manganese or iron. As such, it is no surprise that the richest dietary sources are also rich in one or more of these essential minerals.

1.3 Common Preparations and Supplement Forms

Some superoxide dismutase products are made from cows (bovine-derived). Others are made from melons or created in a lab. SOD was initially biochemically extracted from the serum and liver of animals, as well as from plant sources. Commercial preparations previously relied on bovine-derived SOD (orgotein and palosein), with patents also filed for yeast- and marine-derived SOD.

The principal commercial forms encountered in the dietary supplement market include:

GliSODin®: A trade name for SOD extracted from cantaloupe melon and combined with wheat gliadin. Clinical research and scientific evidence demonstrates that gliadin protects SOD during passage through the stomach, thus allowing absorption of the SOD enzyme once inside the intestine.
SOD B Extramel®: A supplement which uses melon pulp concentrate. It is made by the French company Bionov, who use non-GMO cantaloupe.
Plant-based / vegetable-culture extracts: Products derived from specially grown vegetable cultures containing naturally associated phytochemicals and polyphenolic compounds alongside SOD and catalase, dehydrated at low temperature.
Injectable (parenteral) forms: As a shot, superoxide dismutase has been used for treating pain and swelling caused by osteoarthritis, sports injuries, and rheumatoid arthritis; a kidney condition called interstitial cystitis; gout; poisoning caused by a weed-killer called paraquat; cancer; and lung problems in newborns. SOD is also given as a shot for improving tolerance to radiation therapy, improving rejection rates in kidney transplantation, and minimizing heart damage caused by heart attacks.
Topical / ophthalmic preparations: A sterile solution containing superoxide dismutase is sometimes applied directly to the eyes for treating ulcers on the cornea.
Recombinant SOD: Recombinant SOD, produced in systems such as E. coli or Pichia pastoris, delivers high-purity, customizable isoforms with superior stability, making it ideal for research, therapeutic, and cosmetic applications. Recombinant production allows precise control over enzyme properties, activity, and consistency.
SOD mimetics: Synthetic small-molecule compounds that replicate SOD's catalytic action, such as avasopasem manganese (GC4419), which are under active pharmaceutical development distinct from the conventional dietary supplement category.

2. Historical and Traditional Use

Superoxide dismutase does not have a traditional herbal or ethnomedical history in the same sense as botanical medicines; rather, its history is one of modern biochemical discovery and subsequent pharmaceutical and nutraceutical development.

2.1 Scientific Discovery

With the discovery of the superoxide dismutases by McCord and Fridovich in 1968–1969, the concomitant discovery that superoxide can be produced by enzymes, and the finding that free radicals can be substrates for an enzyme, the thinking on the role of free radicals in biology was completely revolutionized. Using bovine erythrocytes obtained from a gallon of blood from a slaughterhouse, Fridovich and McCord purified the enzyme that catalyzed the dismutation of superoxide radicals, superoxide dismutase (SOD).

Originally considered to be a Cu storage protein, its crucial role as an intracellular antioxidant was discovered in 1969, when McCord and Fridovich recognised that redox cycling of Cu⁺ bound within the two active sites of the SOD1 homodimer enabled it to effectively convert O₂•⁻ to O₂ and H₂O₂ by oxidation and reduction, respectively. Fridovich's and McCord's superoxide dismutase paper, published in the Journal of Biological Chemistry in November 1969, has been cited more than 9,300 times by other scientists and opened an entirely new field of medicine and biology devoted to oxygen free radicals.

2.2 Early Pharmaceutical and Clinical Use

In 1975, Marberger et al. described a new drug with anti-inflammatory properties. Orgotein was a bovine-derived Cu/Zn SOD, and within a year, the radioprotective potential of the drug was suggested by studies in patients receiving pelvic radiation who were at risk for treatment-associated cystitis. By the end of 1977, a series of patents had been filed by Huber et al. with the US Patent Office for Orgotein and its use to protect against radiation therapy toxicities.

In the 1990s, antioxidant supplements were widely promoted for preventing a variety of diseases, including cancer and heart disease. During this period, oral SOD became popular as a supplemental antioxidant. The results of several large studies tended to dash these hopes — primarily because simple oral SOD tablets were found to be degraded in the gastrointestinal tract before absorption could occur.

The parenteral formulation, Orgotein, is classified by the FDA as an orphan drug, not as a dietary supplement, for the treatment of familial amyotrophic lateral sclerosis.

3. Biochemistry: Active Enzyme, Mechanism of Action, and Cofactors

3.1 The Dismutation Reaction

Superoxide dismutases (SODs) are a group of metalloenzymes that protect against cellular damage by reactive oxygen species (ROS). SOD catalyzes the dismutation of superoxide anion free radical (O₂⁻) into molecular oxygen and hydrogen peroxide (H₂O₂). ROS in cells can damage nucleic acids, proteins and lipids, leading to decreased cellular function and possible apoptosis. The ability to convert ROS into harmless molecules is crucial for protecting cellular function and overall health.

SOD works in tandem with two other internally created antioxidant enzymes — glutathione and catalase. Their job is to convert the byproduct of superoxide radicals, hydrogen peroxide, to harmless water and oxygen.

Superoxide dismutase is the only known enzyme to directly scavenge a free radical. Specifically, SOD dismutes superoxide to oxygen and hydrogen peroxide with high specificity and efficiency. Since its discovery in 1969 by Dr. Irwin Fridovich, SOD has been shown to be present in every living organism on Earth and, thus, essential for life.

3.2 Role in Redox Signaling

In the late 1970s it was observed that cancer cells that have low activity of the mitochondrial form of SOD (MnSOD) grow faster than those with higher activities of MnSOD. These observations indicated that SOD, superoxide, and hydrogen peroxide affected the basic biology of cells and tissues, not just via damaging oxidation reactions. It is now realized that superoxide and hydrogen peroxide are essential for normal cellular and organism function. MnSOD appears to be a central player in the redox biology of cells and tissues.

3.3 Physiological Importance: Knockout Model Evidence

The physiological importance of SODs is illustrated by the severe pathologies evident in mice genetically engineered to lack these enzymes. Mice lacking SOD2 die several days after birth, amid massive oxidative stress. Mice lacking SOD1 develop a wide range of pathologies, including hepatocellular carcinoma, an acceleration of age-related muscle mass loss, an earlier incidence of cataracts, and a reduced lifespan. Mice lacking SOD3 do not show any obvious defects and exhibit a normal lifespan, though they are more sensitive to hyperoxic injury.

3.4 Age-Related Decline

While almost all organisms naturally produce some type of SOD, the levels of SOD produced in cells fall as the subject ages or when the subject is afflicted with certain health disorders.

4. Bioavailability: The Central Challenge

A defining constraint in the clinical and supplemental use of exogenous SOD is poor oral bioavailability.

SOD is a large, complex protein molecule that is susceptible to degradation and denaturation under physiological conditions. Moreover, SOD has poor oral bioavailability and limited tissue penetration, further complicating its formulation and delivery. It is available in the form of supplements, but these are not absorbed following oral administration.

The poor bioavailability of exogenous SODs has been criticized. However, improvements in SOD formulation may overcome this limitation and boost interest in its therapeutic properties.

Several delivery strategies have been explored to address this limitation:

Gliadin encapsulation: The GliSODin® approach combines SOD extracted from cantaloupe melon with wheat gliadin. Clinical research and scientific evidence demonstrates that gliadin protects SOD during passage through the stomach, thus allowing absorption of the SOD enzyme once inside the intestine.
Nanoparticle and liposomal carriers: Encapsulation in liposomes, nanoparticles, and other delivery vehicles has been explored. These formulations can protect SOD from enzymatic degradation and enhance its pharmacokinetic profile, thereby improving its therapeutic efficacy and tissue distribution.
Enteric coating and microencapsulation: Plant-derived SOD extracts, particularly from melon and barley, are frequently used, though their oral bioavailability can be limited due to digestion in the gastrointestinal tract. Advanced delivery methods, such as microencapsulation, enteric coating, liposomal carriers, and mineral-bound complexes, help protect SOD during digestion and improve absorption.
Soluble dietary fiber encapsulation: Underutilized plants could serve as sources of SOD and soluble dietary fiber. Soluble dietary fiber has the potential to be used as an encapsulating agent for SOD.

5. Scientific Evidence by Area of Use

5.1 Osteoarthritis and Joint Inflammation

This is one of the most clinically studied areas for SOD supplementation, primarily using injectable bovine SOD (Orgotein).

The clinical trials performed with bovine superoxide dismutase (SOD) have been reviewed in the peer-reviewed literature. SOD, applied intraarticularly at a dosage of 2–16 mg, proved to be effective in osteoarthritis of the knee joint in three placebo-controlled and one steroid-controlled double-blind trials. Its efficacy in other inflammatory joint disorders is documented by uncontrolled trials. Similarly, some controlled and many open studies support the efficacy of locally injected SOD in periarticular inflammation. Systemic treatment of rheumatoid arthritis by SOD at the dosages indicated yielded disappointing results.

One clinical trial supports the use of superoxide dismutase injections into the knee for osteoarthritis, but more research is needed. The long-term effectiveness and safety of such injections is not known.

A more recent intervention used the oral gliadin-encapsulated melon SOD form. This double-blind, randomized study investigated the effects of superoxide dismutase (SOD)-rich melon extract (Melon GliSODin®) on locomotive syndrome. For 6 months, oral Melon GliSODin® (500.4 mg/day) or a placebo was administered to 24 and 22 women, respectively (aged 50–80 years), with knee or lower back discomfort or pain. Downregulation of superoxide dismutase (SOD) in human knee OA cartilage and Sod2 loss in chondrocytes has been shown to accelerate cartilage degeneration in a murine surgical OA model.

Evidence strength: Intra-articular injectable SOD has controlled trial evidence for knee osteoarthritis, though this delivery route is not available as a dietary supplement. Oral encapsulated SOD for joint outcomes has preliminary positive signals but very limited controlled human trial data and small sample sizes.

5.2 Stress, Mental Fatigue, and Quality of Life

A randomized, double-blind, placebo-controlled trial investigated effects of SOD-melon concentrate supplementation on psychological stress, physical and mental fatigue in healthy people. The trial was performed on 61 people divided in two groups: active supplement (n=32) and placebo (n=29) for 12 weeks. Volunteers were given one small hard capsule per day containing 10 mg of SOD-melon concentrate (140 U of SOD) and starch for the active supplement, and starch only for the placebo. The supplementation with SOD-melon concentrate significantly decreased perceived stress, compared to placebo. Moreover, quality of life was improved and physical and mental fatigue were reduced with SOD-melon concentrate supplementation. SOD-melon concentrate supplementation appears to be an effective and natural way to reduce stress and fatigue.

Evidence strength: A single small randomized controlled trial (n=61, 12 weeks) with positive results on stress and fatigue psychometric scales. The authors of this study were affiliated with the manufacturing company (Bionov), which represents a significant limitation. Replication by independent groups is lacking.

5.3 Radiation Therapy Support and Cystitis

Well-documented, though open uncontrolled, studies demonstrated beneficial effects of locally administered SOD in radiation cystitis, interstitial cystitis and Peyronie's disease. Tolerance is good, but allergic reactions at low incidence have to be anticipated.

Studies of possible effects of Orgotein in treating radiation-induced cystitis have yielded mixed results. A topical SOD formulation did not significantly improve postradiation fibrosis.

A few studies support the use of superoxide dismutase injections to prevent cystitis. More research is needed. No studies support the use of oral superoxide dismutase supplements for this use.

Evidence strength: Mixed and primarily from open, uncontrolled studies. Several randomized studies exist for orgotein in radiation-induced cystitis but results are inconsistent. Not established as effective for the oral supplement form.

5.4 Radiation-Induced Oral Mucositis (SOD Mimetics)

The most robust modern clinical evidence involving dismutase-type activity relates not to natural SOD supplements but to synthetic SOD mimetics — notably avasopasem manganese (GC4419).

Avasopasem manganese (avasopasem) is a highly-selective, small molecule (MW 483) mimetic of naturally occurring superoxide dismutase (SOD) enzyme, which, like native SOD, converts superoxide to hydrogen peroxide and molecular oxygen specifically and selectively, at an enzymatic rate comparable to that of the native SOD.

A phase 1b/2a trial provided promising results regarding the effectiveness and safety of a cyclic polyamine SOD mimetic, avasopasem Mn or GC4419, at reducing the severe oral mucositis that is induced by radiation-concurrent cisplatin in oral-cavity and oropharyngeal cancer. Patients (n=46) with oral-cavity or oropharyngeal cancer, stages III–IVb, received intensity-modulated radiation therapy with concurrent cisplatin. GC4419 doses of 30 and 90 mg/day, administered throughout the chemoradiotherapy period, were the most effective and showed no particular safety concerns.

Additionally, the results of the Phase 2b trial suggest that, in addition to its radioprotective impact on oral mucositis, avasopasem also reduced the incidence and severity of cisplatin-related nephrotoxicity.

The Food and Drug Administration granted Breakthrough Therapy and Fast Track designations to GC4419 for the reduction of the severity and incidence of radiation and chemotherapy-induced oral mucositis.

Evidence strength: Phase 1b through Phase 2b randomized controlled trials with an FDA Breakthrough Therapy Designation and an ongoing Phase 3 trial (ROMAN). This is the strongest available clinical evidence for any dismutase-activity agent in humans, but GC4419 is a pharmaceutical-class synthetic compound, not a dietary supplement.

5.5 Locomotor Dysfunction and Musculoskeletal Aging

Downregulation of SOD in human knee OA cartilage has been described, and Sod2 loss in chondrocytes has been shown to accelerate cartilage degeneration. Further, Sod2 deficiency in osteocytes induces bone loss, and Sod2 deficiency in skeletal muscle induces muscle fatigue. These findings suggest a close association between locomotive syndrome and oxidative stress, and that controlling oxidative stress may be an important interventional approach.

SOD-rich melon extract (Melon GliSODin®) is an oral supplement in which SOD extracted from melon is combined with wheat gliadin. The 6-month randomized controlled trial described above (500.4 mg/day in women aged 50–80) examined musculoskeletal outcomes including the Japanese Knee Osteoarthritis Measure, Locomo 25, Roland–Morris Disability questionnaire, and the Chalder Fatigue Scale alongside oxidative, inflammatory, and bone metabolism markers.

Evidence strength: Preliminary. A single small double-blind, randomized controlled trial; industry-affiliated; more independent replication required.

5.6 Cardiovascular Disease and Oxidative Stress

Protective effects have been observed against irradiation, carcinogenesis, apoptosis and neurodegeneration. SOD administration has also been reported to alleviate inflammatory, infectious, respiratory, metabolic and cardiovascular diseases and genitourinary and fertility disorders.

A 2021 review in Molecules noted that the generic antioxidant effects of SODs are beneficial under all tested conditions, from ocular and cardiovascular diseases to neurodegenerative disorders and metabolic diseases, including diabetes and its complications and obesity. However, it must be underlined that clinical evidence for its efficacy is limited and consequently, this efficacy is currently far from being demonstrated.

Evidence strength: Largely preclinical and mechanistic. Human clinical evidence for cardiovascular endpoints specifically attributable to SOD supplementation is insufficient to draw firm conclusions.

5.7 Neonatal Lung Disease

Healthcare providers give superoxide dismutase as a shot for certain bladder infections (interstitial cystitis), osteoarthritis, rheumatoid arthritis (RA), and lung damage that sometimes develops in premature infants who have been given oxygen to help them survive. Studies of intratracheal recombinant human CuZn-SOD in premature infants have been conducted, though longer-term outcomes remain under investigation.

Evidence strength: Small investigational studies; this is a medical application administered parenterally under clinical supervision and not a dietary supplement context.

5.8 Neurodegenerative Disease Associations

Since oxidative stress is a pathological hallmark of neurodegeneration, SOD dysfunction is implicated in diseases characterized by neuronal loss. Mutations in SOD1 contribute to the development of familial amyotrophic lateral sclerosis (ALS), and multiple studies suggest that reduced SOD2 activity may be associated with Alzheimer's and Parkinson's diseases.

Human studies have confirmed that SOD1 levels are significantly decreased in AD patients, while mitochondrial SOD (SOD2) and extracellular SOD (SOD3) levels remain unchanged. These findings suggest that enhancing SOD1 activity could be a therapeutic strategy to inhibit AD progression by reducing oxidative stress.

Evidence strength: Associative and largely preclinical. There are no established clinical trials demonstrating that exogenous SOD supplementation modifies the course of neurodegenerative diseases in humans.

5.9 Sports and Exercise Recovery

One study investigated the effect of plant superoxide dismutase extract (GliSODin) supplementation on the balance of oxidants and antioxidants in the serum and erythrocytes of competitive rowers. The double-blinded study included 19 members of the Polish rowing team who were participating in a preparatory camp. Subjects were randomly assigned to the supplemented group (n=10), who received 2 capsules (500 mg) of GliSODin extract once daily for 6 weeks, or the placebo group (n=9). At the beginning and end of the study, subjects performed a 2,000-m maximum-effort test on a rowing ergometer.

Evidence strength: Very preliminary. Single small study in 19 athletes; insufficient to draw conclusions about efficacy for sports recovery.

5.10 Overall Summary of Clinical Evidence

Overall analysis of peer-reviewed published data suggests that intake of SOD-gliadin might have advantageous health effects. These conclusions are dependent on the condition or pathology under consideration. In general, the authors who analyzed SOD-gliadin supplementation support the use of SOD-gliadin supplementation as a complementary treatment rather than a therapeutic treatment. To further clarify the importance of dietary SOD-gliadin administration, additional large-scale clinical trials are recommended.

Despite the promising preclinical evidence supporting the therapeutic potential of SOD, the clinical translation of SOD-based therapies faces numerous challenges that have hindered their widespread adoption in clinical practice.

6. Body Systems and Health Areas Associated with SOD

Musculoskeletal system: Osteoarthritis, rheumatoid arthritis, periarticular inflammation, locomotive syndrome (osteoarthritis, osteoporosis, sarcopenia), sports injuries.
Urogenital system: Interstitial cystitis, radiation-induced cystitis, Peyronie's disease, fertility disorders.
Oncology / radiation support: Radiation-induced mucositis, radiation cystitis, radioprotection of normal tissues.
Neurological system: Associations with ALS, Alzheimer's disease, Parkinson's disease (via SOD deficiency research).
Cardiovascular system: Ischemia-reperfusion injury, atherosclerosis, hypertension (preclinical and observational data).
Pulmonary system: Bronchopulmonary dysplasia in neonates, general respiratory oxidative stress.
Skin / dermatology: Anti-aging topical applications, UV protection, wound healing, scar tissue reduction.
Metabolic health: Diabetes complications, obesity-associated oxidative stress (evidence largely preclinical).
Psychological / fatigue: Stress reduction and reduction of physical and mental fatigue (one small RCT).

7. Dosage Forms and Doses Reported in Studies

The following dosages are drawn directly from published study reports:

Oral (encapsulated melon SOD, GliSODin-type):
- One capsule per day containing 10 mg of SOD-melon concentrate (140 U of SOD) for 12 weeks, in a randomized controlled trial on stress and fatigue.
- Superoxide dismutase has most often been used by adults in doses of 140 IU by mouth daily for up to 4 months.
- Two capsules (500 mg) of GliSODin extract once daily for 6 weeks, in a study of competitive rowers.
- Oral Melon GliSODin® at 500.4 mg/day for 6 months, in women aged 50–80 with joint discomfort.
Intra-articular injection (bovine SOD / Orgotein):
- Intraarticularly at a dosage of 2–16 mg, proving effective in osteoarthritis of the knee joint in placebo-controlled and steroid-controlled double-blind trials.
SOD Mimetic GC4419 (avasopasem manganese, IV):
- GC4419 doses of 30 and 90 mg/day, administered throughout the chemoradiotherapy period, were the most effective in clinical trials for radiation-induced mucositis.

No standardized or officially recommended dosage exists for oral SOD dietary supplements. The efficacy of oral SOD supplements is debated due to poor absorption, leading to limited clinical validation.

8. Safety Considerations and Interactions

8.1 General Safety Profile

Information from large clinical studies is lacking; however, adverse effects appear to be limited. Pain and irritation at injection sites have been reported. SOD is regarded as nontoxic, based on data from earlier studies.

Injectable (shot) forms of superoxide dismutase that have been used in research studies appear to be safe.

8.2 Allergic Reactions

Tolerance is good, but allergic reactions at low incidence have to be anticipated. A case report documented anaphylactic shock caused by impurities in orgotein (bovine SOD) preparations. Prior techniques involving recovery from bovine or other animal cells have serious limitations and the orgotein so obtained may produce allergic reactions in humans because of its non-human origin.

8.3 Gliadin/Gluten Content

Commercially available wheat gliadin encapsulated melon SOD has been proven to enhance mammalian health, but gluten/gliadin intolerance in certain animals and humans may limit its marketability. Individuals with celiac disease or non-celiac gluten sensitivity should note that GliSODin® and related products contain wheat gliadin as a carrier.

8.4 SOD Mimetic (GC4419) Side Effects

Safety was comparable across all three arms of the Phase 1b/2a trial, and GC4419 side effects (i.e., hypotension and oral/facial paresthesia) were mild and transient, usually resolving within 1 hour of infusion completion.

8.5 Theoretical Drug Interactions

While confirmed drug interactions are limited, theoretical concerns include antioxidants potentially interfering with certain chemotherapy or radiation therapies, and altered inflammatory signaling when combined with immune-modulating medications. This concern arises from the theoretical possibility that adding exogenous antioxidant activity during oxidative-stress-dependent cancer treatments could reduce therapeutic efficacy, though this has not been definitively demonstrated for oral SOD supplements.

8.6 Bovine-Derived Products and BSE Risk

The FDA has issued guidance regarding public health and safety concerns related to dietary supplements containing specific bovine tissues, given concerns about bovine spongiform encephalopathy (BSE). This is specifically relevant to orgotein and other bovine-derived SOD preparations.

8.7 Populations with Insufficient Safety Data

Safety data in pregnant or breastfeeding women, children, and individuals with severe renal or hepatic impairment have not been well established in controlled clinical trials for any form of exogenous SOD supplementation.

References

Health Conditions

Health conditions that Dismutase may help support.

No conditions available.

Body Systems

Body systems that Dismutase may help support.

No body systems available.