In the body, dangerous naturally occurring substances called free radicals pose a risk of harm to many tissues. The body deploys an “antioxidant defense system” to hold them in check. Superoxide dismutase (SOD) is one of the most important elements of this system. It controls levels of a chemical named “superoxide.” The body manufactures superoxide to kill bacteria and for other uses, but excess levels of superoxide can injure healthy cells. SOD converts superoxide to hydrogen peroxide. Then another enzyme, catalase, neutralizes hydrogen peroxide.
Nutrients such as vitamin C and vitamin E also help neutralize free radicals. In the 1990s, such 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 supplement. Unfortunately, the results of several large studies tended to dash these hopes. Compared to ordinary antioxidants, SOD suffers from the additional disadvantages of being expensive and poorly absorbed when taken by mouth.
When taken orally, little to no SOD is absorbed.1,2 Some manufacturers advertise a sublingual (under the tongue) form of SOD to get around this problem. However, there does not appear to be any meaningful evidence that SOD can be absorbed any better this way.
Weak evidence hints that a form of SOD in which the substance is encapsulated in structures called liposomes may be absorbable.1,3 The optimum dose, if any, is not known.
Various websites promote SOD for a wide variety of health problems, from preventing aging to enhancing sports performance. However, as noted above, oral SOD supplements may be ineffective due to poor absorption.
SOD applied directly to wounds may enhance wound healing, according to experiments in animals.9
Inhaled SOD appears to be useful for premature infants, helping to prevent a condition called respiratory distress syndrome.14-16
However, the only evidence for benefits with any oral form of SOD is a study in animals involving the special liposome form of the supplement mentioned above. It found possible anti-inflammatory effects.3
Oral SOD is presumably quite safe, since it is apparently not absorbable. The safety of other forms of SOD (including the possibly absorbable encapsulated form) has not been established.
1. Regnault C, Soursac M, Roch-Arveiller M, Postaire E, Hazebroucq G. Pharmacokinetics of superoxide dismutase in rats after oral administration. Biopharm Drug Dispos. 1996;17:165–74.
2. Giri SN, Misra HP. Fate of superoxide dismutase in mice following oral route of administration. Med Biol. 1984;62:285–9.
3. Regnault C, Roch-Arveiller M, Tissot M, et al. Effect of encapsulation on the anti-inflammatory properties of superoxide dismutase after oral administration. Clin Chim Acta. 1995;240:117–27.
4. Delanian S, Martin M, Bravard A, Luccioni C, Lefaix JL. Cu/Zn superoxide dismutase modulates phenotypic changes in cultured fibroblasts from human skin with chronic radiotherapy damage. Radiother Oncol. 2001;58:325–31.
5. Delanian S, Baillet F, Huart J, Lefaix JL, Maulard C, Housset M. Successful treatment of radiation-induced fibrosis using liposomal Cu/Zn superoxide dismutase: clinical trial. Radiother Oncol. 1994;32:12–20.
6. Housset M, Baillet F, Michelson AM, Puget K. Action of liposomal superoxide dismutase on measurable radiation-induced fibrosis. Ann Med Interne (Paris). 1989;140:365–7.
7. Lefaix JL, Delanian S, Leplat JJ, et al. Radiation-induced cutaneo-muscular fibrosis (III): major therapeutic efficacy of liposomal Cu/Zn superoxide dismutase [in French]. Bull Cancer. 1993;80:799–807.
8. Ratcheva I, Stefanova Z, Vesselinova A, Nikolova S, Kujumdjieva A, Neychev H. Treatment of adjuvant arthritis in mice with yeast superoxide dismutase. Pharmazie. 2000;55:533–7.
9. Vorauer-Uhl K, Furnschlief E, Wagner A, et al. Reepithelialization of experimental scalds effected by topically applied superoxide dismutase: controlled animal studies. Wound Repair Regen. 2002;10:366–71.
10. Flanagan SW, Anderson RD, Ross MA, Oberley LW. Overexpression of manganese superoxide dismutase attenuates neuronal death in human cells expressing mutant (G37R) Cu/Zn-superoxide dismutase. J Neurochem. 2002;81:170–7.
11. Gallagher IM, Jenner P, Glover V, Clow A. CuZn-superoxide dismutase transgenic mice: no effect on longevity, locomotor activity and 3H-mazindol and 3H-spiperone binding over 19 months. Neurosci Lett. 2000;289:221–3.
12. Huang TT, Carlson EJ, Gillespie AM, Shi Y, Epstein CJ. Ubiquitous overexpression of CuZn superoxide dismutase does not extend life span in mice. J Gerontol A Biol Sci Med Sci. 2000;55:B5–9.
13. Parkes TL, Elia AJ, Dickinson D, Hilliker AJ, Phillips JP, Boulianne GL. OMIM extension of Drosophila lifespan by overexpression of human SOD1 in motorneurons. Nat Genet. 1998;19:171–4.
14. Davis JM, Rosenfeld WN, Richter SE, et al. The effects of multiple doses of recombinant human CuZn superoxide dismutase (rhSOD) in premature infants with respiratory distress syndrome (RDS). Pediatr Res. 1999;45:193A (Abstract no.1129).
15. Davis JM, Richter SE, Biswas S, et al. Long-term follow-up of premature infants treated with prophylactic, intratracheal recombinant human CuZn superoxide dismutase. J Perinatol. 2000;4:213–216.
16. Rosenfeld WN, Davis JM, Parton L, et al. Safety and pharmacokinetics of recombinant human superoxide dismutase administered intratracheally to premature neonates with respiratory distress syndrome. Pediatrics. 1996;97:811–817.
Last reviewed December 2015 by EBSCO CAM Review Board Last Updated: 12/15/2015