Effects of a New Human Recombinant MnSOD in the Treatment of Photoaging and Actinic Keratosis


Physiological processes, as aerobic metabolism and inflammatory response, generate reactive oxygen species (ROS) that may induce cellular injury when their amount is increased and antioxidant defense mechanisms are overwhelmed. Also, ROS are generated following UV skin irradiation able to deplete the natural antioxidant defenses in the skin. The increase in exposure to UV may lead to photoaging and precancerous skin lesions (actinic keratosis). New antioxidant strategies in the prevention and therapy of skin lesions are urgently needed. In this study, we evaluated the antioxidant efficacy of a recombinant form of human manganese superoxide dismutase able to inhibit reactive oxygen species production in some patients affected by severe photoaging and actinic keratosis.

Share and Cite:

M. Ruggiero, M. Pollio, A. Schiattarella, A. Borrelli, A. Mancini, A. Pica and P. Forgione, "Effects of a New Human Recombinant MnSOD in the Treatment of Photoaging and Actinic Keratosis," Journal of Cancer Therapy, Vol. 4 No. 6A, 2013, pp. 56-59. doi: 10.4236/jct.2013.46A1009.

Conflicts of Interest

The authors declare no conflicts of interest.


[1] C.-H. Lee, S.-B. Wu, C.-H. Hong, H.-S. Yu and Y.-H. Wei, “Molecular Mechanism of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy,” International Journal of Molecular Sciences, Vol. 14, No. 3, 2013, pp. 6414-6435. doi:10.3390/ijms14036414
[2] P. Santoianni and M. Nino, “ Sunlight and Cancer Risk,” Italian Journal of Dermatology and Venereology, Luce Solare e Rischio Oncologico, Giornale Italiano di Dermatologia e Venereologia, Vol. 138. No. 6, 2003, pp. 455-464.
[3] F. Debacq-Chainiaux, C. Leduc, A. Verbeke and O. Toussaint, “UV, Stress and Aging,” Dermato-Endocrinology, Vol. 4, No. 3, 2012, pp. 236-240. doi:10.4161/derm.23652
[4] H. Masaki, “Role of Antioxidants in the Skin: Anti-Aging Effects,” Journal of Dermatological Science, Vol. 58, No. 2, 2010, pp. 85-90. doi:10.1016/j.jdermsci.2010.03.003
[5] A. Borrelli, A. Schiattarella, R. Mancini, B. Morrica, V. Cerciello, M. Mormile, V. D’Alesio, L. Bottalico, F. Morelli, M. D’Armiento, F. P. D’Armiento and A. Mancini, “A Recombinant MnSOD Is Radioprotective for Normal Cells and Radiosensitizing for Tumor Cells,” Free Radical Biology and Medicine, Vol. 46, No. 1, 2009, pp. 110-116. doi:10.1016/j.freeradbiomed.2008.10.030
[6] M. W. Epperly, J. E. Gretton, C. A Sikora, M. Jefferson, M. Bernarding, S. Nie and J. S. Greenberger, “Mitochondrial Localization of Superoxide Dismutase Is Required for Decreasing Radiation-Induced Cellular Damage,” Radiation Research, Vol. 160, No. 5, 2003, pp. 568-578. doi:10.1667/RR3081
[7] D. Robbins and Z. Yunfeng, “The Role of Manganese Superoxide Dismutase in Skin Cancer,” Enzyme Research, Vol. 2011, No. 2011, 2011, Article ID: 409295. doi:10.4061/2011/409295
[8] A. Mancini, A. Borrelli, A. Schiattarella, S. Fasano, A. Occhiello, A. Pica, P. Sher, M. Tommasino, J. P. F. Nüesch and J. Rommelaere, “Tumor Suppressive Activity of a Variant Isoform of Manganese Superoxide Dismutase Released by a Human Liposarcoma Cell Line,” International Journal of Cancer, Vol. 119, No. 4, 2006, pp. 932-943.
[9] A. Occhiello, F. Bentivegna, A. Borrelli, A. Schiattarella, A. Mancini and A. Pica, “Skin Necrosis in Sea Turtle Cold Stunning: Regeneration Following rMnSOD Topic Treatment in a Specimen of Caretta caretta,” Comparative Clinical Pathology, Vol. 18, No. 4, 2009, pp. 365-369. doi:10.1007/s00580-009-0816-9
[10] A. Mancini, A. Borrelli, M. T. Masucci, A. Schiattarella, S. Filice, J. Rashan and T. Maggino, “A Conditioned Medium from a Human Liposarcoma-Derived Cell Line Induces p53-Dependent Apoptosis in Several Tumor Cell Lines,” Oncology Reports, Vol. 7, No. 3, 2000, pp. 629-637.

Copyright © 2021 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.