Topical Therapy Reduces Radiation-Induced Skin Damage
By MedImaging International staff writers Posted on 11 Nov 2016 |
A newly developed topical therapy applied before or after radiation exposure prevents potential skin damage due to oxidative stress, according to a new study.
Developed by researchers at the University of Pittsburgh (Pitt; PA, USA), the synthetic molecule, named JP4-039, is a mitochondrial targeted antioxidant designed to prevent accumulation of reactive oxygen species (ROS), thereby limiting oxidative damage and preserving mitochondrial function. According to the researchers, this is important as mitochondria are particularly susceptible to oxidative stress, and mitochondrial dependent apoptosis plays a major role in radiation induced tissue damage.
The researchers found that in both mouse and human skin models, topical application of JP4-039 prevented and mitigated radiation-induced skin damage, as characterized by clinical dermatitis, loss of barrier function, inflammation, and fibrosis. The damage mitigation also reduced apoptosis, helped preserve the skin’s antioxidant capacity, and reduced the irreversible DNA and protein oxidation associated with oxidative stress. The study was published on September 23, 2016, in the Journal of Investigative Dermatology.
“During the course of radiation therapy, patients can develop irritating and painful skin burns that can lead to dangerous infections and diminished quality of life. Sometimes the burns are so severe that patients must stop their treatment regimen,” said corresponding author Louis Falo, MD. “Our results show that topical treatment with this therapeutic agent prevents skin damage at the source.”
Radiation-induced skin damage ranges from photoaging and carcinogenesis due to ultraviolet (UV) exposure, to treatment-limiting radiation dermatitis associated with radiation therapy (RT), and to cutaneous radiation syndrome, a frequently fatal consequence of exposures from nuclear accidents. The skin radiation leads to a complex pattern of direct tissue injury involving damage to cells of the epidermis and endothelial cells within the walls of blood vessels, as well as the inflammatory cell recruitment.
Related Links:
University of Pittsburgh
Developed by researchers at the University of Pittsburgh (Pitt; PA, USA), the synthetic molecule, named JP4-039, is a mitochondrial targeted antioxidant designed to prevent accumulation of reactive oxygen species (ROS), thereby limiting oxidative damage and preserving mitochondrial function. According to the researchers, this is important as mitochondria are particularly susceptible to oxidative stress, and mitochondrial dependent apoptosis plays a major role in radiation induced tissue damage.
The researchers found that in both mouse and human skin models, topical application of JP4-039 prevented and mitigated radiation-induced skin damage, as characterized by clinical dermatitis, loss of barrier function, inflammation, and fibrosis. The damage mitigation also reduced apoptosis, helped preserve the skin’s antioxidant capacity, and reduced the irreversible DNA and protein oxidation associated with oxidative stress. The study was published on September 23, 2016, in the Journal of Investigative Dermatology.
“During the course of radiation therapy, patients can develop irritating and painful skin burns that can lead to dangerous infections and diminished quality of life. Sometimes the burns are so severe that patients must stop their treatment regimen,” said corresponding author Louis Falo, MD. “Our results show that topical treatment with this therapeutic agent prevents skin damage at the source.”
Radiation-induced skin damage ranges from photoaging and carcinogenesis due to ultraviolet (UV) exposure, to treatment-limiting radiation dermatitis associated with radiation therapy (RT), and to cutaneous radiation syndrome, a frequently fatal consequence of exposures from nuclear accidents. The skin radiation leads to a complex pattern of direct tissue injury involving damage to cells of the epidermis and endothelial cells within the walls of blood vessels, as well as the inflammatory cell recruitment.
Related Links:
University of Pittsburgh
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