As we explained, infra-red (IR) radiation makes up 54.3 % of the sun’s rays that reach the earth and is classified into types A, B and C depending on its wavelength and penetration into the skin’s layers.

While traditional physical and chemical filters protect against UV radiation, they do not protect against the harmful effects of IR radiation. This means that simply using sunscreen will not protect you from extreme sun exposure as IR radiation will continue to work on the skin.

IR radiation creates an imbalance in mitochondrial electron transport, triggering decreased energy production and increased reactive oxygen species (ROS) formation.

A strategy for the development of more robust sunscreens able to prevent sun damage caused by IR radiation involves using antioxidants or compounds which prevent redox imbalance and maintain cellular homeostasis.

In addition to quantifying redox homeostasis enzymes, extracellular matrix proteins and connective tissue proteases, measuring advanced glycation end products (AGEs) markers, cellular senescence and mitochondrial enzymes are treatment strategies for evaluating protection against IR radiation.

One mechanism that has been used is that of mitochondrial protection. Mitochondria are the major cell source of ROS. During respiration, 1% of the oxygen consumed by this organelle becomes ROS and is constantly removed by cellular antioxidants and antioxidant defense enzymes.

The pathological effects of the final AGEs products are related to these compounds’ ability to modify the chemical and functional properties of diverse biological structures that range from free radical generation to the formation of cross-protein connections or cell receptors’ interactions. In the skin, the main target of glycation is the extracellular matrix proteins, resulting in the loss of firmness and elasticity.

Oxidative stress and glycation of fundamental skin structures culminate in cellular senescence, where the cell loses its ability to reproduce and apoptosis begins. This process prevents the abnormal proliferation of transformed cells, preventing the development of neoplasia.

Experimental models for evaluating IR-induced sun damage include cultured human fibroblasts and cultured human skin obtained from elective cosmetic surgery. These models allow evaluation, using various laboratory techniques, of the damage caused by a specific IR simulator and the photoprotective effects of an active test.

A more reliable alternative for assessing the biological effects of a sunscreen is to use biopsies from human volunteers exposed to IR radiation. These biopsies are an option for evaluating the actual use of a product.

The search for substances that may retard or reverse the skin aging process is a constant goal of research and development in the cosmetics and dermatology field. Several cellular protection mechanisms against oxidative stress are now known, and there are various experimental models for assessing the effects of IR radiation of a cosmetic product in the fight against the signs of skin aging.

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