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Scientists hail anti-aging impact of TPF 50 sunscreen

By Andrew McDougall+

11-Mar-2014
Last updated on 11-Mar-2014 at 17:53 GMT

Scientists hail anti-aging impact of TPF 50 sunscreen

A new clinical study has highlighted the efficacy of Triple Protection Factor broad spectrum sunscreen in preventing sun damage and aging on the skin.

In their head-to-head comparison study, the researchers found that TPF50 was more effective than both the main DNA repair and AO existing products.

Released in the Journal of Drugs in Dermatology (JDD), the researchers - Enzo Emanuele MD, PhD, from Italy, James M. Spencer MD, MS from New York, and Martin Braun MD from Vancouver - also found that TPF 50 helps to prevent Non-Melanoma Skin Cancer (NMSC).

‘Significant advance’

Continued exposure to ultraviolet radiation (UVR) is one of the major risk factors for photo-aging and the development of non-melanoma skin cancer (NMSC).

According to JDD, mainstream sunscreens cannot ensure a complete protection against all molecular lesions associated with UVR exposure, making the emergence of TPF 50 a significant advance in preventive science.

"JDD offers one of the fastest routes for disseminating dermatologic information. The JDD is pleased to publish this relevant, timely breakthrough research for dermatologists,” says the publication’s editor-in-chief and Professor Emeritus of Dermatology at New York University School of Medicine.

“This new information is important, very beneficial and is another treatment in the dermatologist's armamentarium in preventing skin cancers.”

Study

Non-melanoma skin cancers are the most common human neoplasms and continue to represent an important public health issue with greater than one million cases diagnosed each year.

The primary factor contributing to the molecular pathogenesis of NMSC is unprotected skin exposure to UV radiation; both UVA and UVB.

Skin carcinogenesis by DNA damage is the current predominant model of UV toxicity, which may be caused by direct damaging effects of energy deposited by photons, or indirect oxidative action of short-lived reactive oxygen species (ROS) formed from water that reacts with biomacromolecules.

UV rays are capable to induce direct DNA damage and growing evidence suggests that the efficiency of DNA repair after exposure to UV radiation is crucially dependent on the levels of oxidative protein damage, including but not limited to DNA repair proteins.

JDD says that the identification of key DNA and protein signatures of photodamage may represent a therapeutic target for translational studies of innovative therapeutic and preventive approaches for reducing both skin aging and the morbidity and mortality associated with NMSC.

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