Page 56 - Read Online

Page 4 of 6 González et al. Plast Aesthet Res 2022;9:32 https://dx.doi.org/10.20517/2347-9264.2022.04

collagen integrity and content in the ECM, which lead to disruption of structure and metabolism of this
protein and consequently to photo-aging, characterized by scaling, dryness, and hyperpigmentation of skin.
The neutralization of free radicals through administration of antioxidants could prevent this damage,
protecting cells and contributing to restore cutaneous homeostasis. Moreover, there are several targeted
intervention strategies intended to stimulate the production of collagen or inhibit its degradation, such as
surgical aesthetic treatments, topical treatments, or the use of oral supplements. This latter strategy, which is
referred as nutricosmeceuticals, involves the administration of hydrolysed bioactive collagen peptides that
are easily absorbed into bloodstream. Examples of these supplements containing collagen peptides are Pure
Gold Collagen® and Gold Collagen® Forte, which have been shown to contribute to restoration of the levels
of collagen and elastin in ECM leading to an increase in skin elasticity and a reduction of the visible signs of
aging. It should be also noted the importance of vitamin C because of its role as a co-factor to several
enzymes in the production of collagen and as an antioxidant against oxidative damage. Since fibroblasts are
the main responsible of collagen production, there is a growing interest in the development of new
strategies based on counteracting the replicative senescence of fibroblasts and the shortening of its telomere.

[5]
Environmental aging of the skin: new insights. Burke . Protection of skin is essential for healthspan, even
more when our lifestyle means we are increasingly exposed to environmental stressors, such as radiations
(e.g., ultraviolet, visible, and infrared) or airborne pollution (e.g., ozone, polycyclic aromatic hydrocarbons,
volatile organic compounds, and particulate matter), that cause consequences from premature aging to skin
cancer. Exposure to solar UV radiation leads to an immediate pigmentary darkening and the
overproduction of melanin, with the consequent generation of ROS and damaging DNA photoproducts.
UVB induces persistent “fingerprint mutations” (intra-strand pyrimidine dimers) that give rise to pre-
cancerous conditions (e.g., actinic keratoses) and skin cancers (e.g., basal cell carcinoma, squamous cell
carcinoma, and melanoma). UVA doses to which we are usually exposed do not initiate skin cancer but
inhibit the normal immune response. Individuals with pale or fair skin (phototypes I and II), are
particularly sensitive to UV because of their low melanin content and their few dermal papillae. Exposure to
visible light also leads to oxidative stress and inflammatory cascades that contribute to dermal matrix
destruction and photoaging. Clinical cutaneous manifestations after infrared (IR) exposure (and concretely
IRA) are similar than after UV, but IRA induces genes regulating apoptosis, extracellular matrix or calcium
metabolism and leads to a marked elastosis. Polycyclic aromatic hydrocarbons, such as benzo[a]pyrene,
present in urban environments are metabolized to quinones which generate ROS. In addition, the
synergistic interaction between polycyclic aromatic hydrocarbons and UVA induce the formation of DNA
adducts that also produce oxidative damage. Volatile organic compounds (e.g., nitrogen oxides, methane,
carbon monoxide or sulfuric compounds) pollution in the indoor and outdoor environment, increase the
ozone levels on the earth’s surface, which oxidizes lipids on the skin, triggering inflammatory cascades that
disrupt dermal cells and extracellular matrix and accelerate extrinsic aging. Particulate matter emitted by
factories, power plants, diesel engines or traffic, also cause skin disorders through oxidation of surface lipids
with the subsequent generation of ROS and inflammation process. Cigarette smoke is one of the main
indoor pollutants, contains thousands of chemicals (including both particulate matter and volatile organic
compounds), and can accelerate extrinsic aging through skin barrier disruption. The aryl hydrocarbon
receptor present in skin cells is the main natural mechanism of binding and clearing xenobiotic pollutants
and plays a crucial role in maintenance of epidermal barrier function, regulation of keratinocyte
differentiation and proliferation, melanogenesis, immunity and skin inflammation. For that reason, in
addition to the active study of antioxidant compounds, research on protection of skin against extrinsic
damage is also focused on understanding at a cellular level aryl hydrocarbon receptor mechanism in order
to find methods to modulate it.