Prevention of Infrared-A Radiation Mediated Detrimental Effects in Human Skin

P. Schroeder, PhD; C. Calles, Dipl.-Biol (MSc); J. Krutmann, MD


Institut fuer Umweltmedizinische Forschung (IUF) at the University of Duesseldorf, Duesseldorf, Germany

ABSTRACT

Photoaging and skin damage that is caused by solar radiation is well known. We have recently learned that within the solar spectrum this damage not only results from ultraviolet (UV) radiation, but also from longer wavelengths, in particular near infrared radiation. Accordingly, infrared radiation (IR) has been shown to alter the collagen equilibrium of the dermal extracellular matrix in at least 2 ways: (1) by leading to an increased expression of the collagen degrading enzyme matrixmetalloproteinase-1 while (2) decreasing the de novo synthesis of the collagen itself. Infrared-A (IRA) radiation exposure, therefore, induces similar biological effects to UV, but the underlying mechanisms are substantially different. IRA acts via the mitochondria and therefore protection from IR requires alternative strategies.

Key Words:
infrared, photoaging, skin aging, solar radiation

Physics of Infrared (IR) Radiation

Solar radiation in wavelengths of 290nm to 4000nm reaches the earth’s surface after atmospheric filtering. This part of the electromagnetic spectrum is divided into 3 major bands:

ultraviolet (UV) radiation (290-400nm)
visible light (400-760nm)
IR radiation (760-4000nm)

IR is further divided into IRA (760-1440nm), IRB (1440-3000nm), and IRC (3000nm-1mm). Of the total amount of solar energy reaching the human skin, 54% is IR, while only 7% is UV.¹ Roughly 30% of the total solar energy is IRA, which penetrates deeply into the human skin.¹ Most of the IRA radiation load on human skin is of solar origin, but in recent years artificial IRA sources are used increasingly. In addition to therapeutic approaches, the use of IRA for wellness and lifestyle purposes is steadily rising.

Detrimental Effects of IRA and Underlying Molecular Mechanisms

More than 20 years ago, Kligman reported that IR in guinea pigs causes actinic skin damage that resembled skin damage caused by UV.² This observation has since been confirmed in another animal model.³ Moreover, IRA was reported to interfere with apoptotic pathways, thus preventing UV-damaged cells from executing programmed cell death, which indicates a co-carcinogenic potential for IRA.^4,5 Until now in vivo carcinogenesis studies for IRA alone and in combination with other noxae like UV have not been published. For IRC, the occurrence of a skin lesion described as erythema ab igne, which may progress to squamous cell carcinoma, has been reported.⁶ However, interference with apoptotic pathways,⁴ involvement in the repair of damaged DNA,⁵ stimulation of proliferation and accelerated woundhealing⁷ underline the necessity to further investigate the role of IRA in photocarcinogenesis.

The molecular basis of IRA induced photoaging of the skin was assessed by Schieke et al,⁸ who were the first to show that physiological doses of IRA lead to a disturbance of the dermal extracellular matrix by upregulation of the expression of the collagen degrading enzyme matrixmetalloproteinase-1 (MMP1). This finding was confirmed in independent in vivo and in vitro studies by different laboratories.^9,10 In addition, IRA exposure was recently shown to lead to a downregulation of collagen de novo synthesis.¹¹ The IRA-induced upregulation of MMP1 was found to be different from that induced by UV at the mechanistic level, since it involves the formation of mitochondrial reactive oxygen species (ROS) and the subsequent initiation of a retrograde signaling response (i.e., from the mitochondria to the nucleus) in human skin.^12,13 The omnipresence of IRA, its biophysical properties, and the fact that it acts differently from UV points to the necessity of including specific IRA-directed strategies in modern sunscreens.

Protection Strategies Against IRA

Complete photoprotection of human skin must include protection against IRA. Currently there are no specific chemical or physical filters directed against IRA that are available, or at least the available compounds need to be tested for their IRA-filtering capacity. While it is unlikely, that UV-specific filters work against IRA, physical filters might provide protection in addition to their potential against UV. Controlled studies determining the effectiveness of UV filters in IRA protection are currently not available.

An alternative approach for photoprotection against IRA is the use of antioxidants, especially mitochondrially-targeted antioxidants, e.g., epigallocatechin gallate (found in grape seed extracts and tea extracts), and mitoquinone (MitoQ™, Antipodean Pharmaceuticals), which is a coenzyme Q derivative. Accordingly, topically applying such antioxidants on human skin in vivo prior to IRA treatment has shown that it significantly abrogates the IRA-induced detrimental shift in dermal gene expression.¹⁰

Conclusion

Recent data clearly indicate that in addition to UV, protection against IRA must be taken into account when it comes to modern sun protection. IRA photoprotection requires specific strategies because existing UV protective measures miss the problem. A feasible and effective approach is the topical application of mitochondrially-targeted antioxidants. In addition, unnecessary exposure to IRA radiation from artificial irradiation devices should be avoided.

References

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