Successfully protecting the skin from sun damage

 Its natural ageing process can be prematurely accelerated by photoageing, which describes the superposition of environmental effects on chronological skin changes that comprise: increased proteolytic activation, decreased collagen content and abnormal extracellular matrix (ECM) turnover. Although sun rays are the main source of vitamin D, induce happiness and motivation, promote cell function and energy in the short term, and regulate our natural biorhythm cycles, they are among the most damaging environmental aggressions responsible for acute and chronic skin negative effects. Sun exposure can cause higher degradation of the dermal collagen and elastic fibres, more alterations of the skin conditions and properties, and finally visible effects like spots, wrinkles, uneven pigmentation and loss of elasticity, if it is not properly controlled. Representing 95% of UV radiation, UVA rays (320 nm-400 nm) can penetrate the epidermis and indirectly alter DNA due to reactive oxygen species (ROS) production, single-strand breaks in DNA and in DNA–protein cross-links, dermal damages and matrix remodelling that imply abnormal elastin fibres and increased collagen degradation and cross-linking.1,2 UVB radiation (290 nm-320 nm) is more cytotoxic and mutagenic so, although it is mostly absorbed by the epidermis, it is able to directly induce DNA alterations.3,4 Internal reactions are also important to consider as they can generate highly reactive species, like free radicals, that induce premature skin ageing and accelerate photoageing. ROS are the most well-known free radical species able to modify biological macromolecules such as DNA, carbohydrates, lipids, proteins and polyunsaturated fatty acids.5,6,7 Although the skin presents extremely efficient antioxidant properties to protect from such ROS-related damages and repair them, due to its constant and daily exposure to pro-oxidant agents, this endogenous capacity diminishes over time and also due to photoageing. This fact results in higher levels of ROS and oxidative stress, which is the usual term to describe the steady state level of oxidative damage caused by reactive species. Additionally, ROS can directly oxidise proteins, yielding highly reactive carbonyl species (RCS), which are potent mediators of cellular carbonyl stress that may result from other endogenous processes.8,9 Intracellular RCS seem to play a significant role in oxidative stress-related mutagenesis because they appear to cause DNA alterations and inhibit the DNA repairing mechanisms, being trans-4-hydroxy-2- nonenal (4-HNE) among the most abundant and cytotoxic RCS due to its capacity to bind proteins, impair their function and inhibit the DNA repairing capacity in human cells.10,11 Moreover, reactive nitrogen species (RNS) are also able to cause extensive cell damage by altering proteins and DNA, inhibiting enzymatic activity and interfering regulatory functions. Among these radicalnitrogen- based molecules which facilitate nitrosylation reactions, peroxynitrite is one of the most powerful compounds being linked to the degradation of hyaluronan (component of the ECM) and tyrosinebased nitration towards 3-nitrotyrosine. This tyrosine residue’s nitration is an irreversible process compromising the cyclic interconversion between tyrosine forms that activate and deactivate enzymes and receptors.12 After any stress exposure, the natural protective response implies a fundamental change in the pattern of protein synthesis which involves a protein synthesis reduction followed by specific transcription of the genes encoding for heat shock proteins (HSP) or stress proteins, with the consequent marked increase in HSPs’ synthesis.13,14 The HSP group is a set of highly conserved proteins intracellularly expressed in all cells and organisms from prokaryotes to humans. They participate in protein folding and transport, and they are thought to represent a response mechanism to cellular stress, in order to protect intracellular proteins.13 Hsp72 (also named Hsp70) is the inducible form of the HSP70 family and the major protecting HSP in human skin. Hsp72 expression is enhanced under stressing conditions but it has a basal expression that gets impaired with ageing.14 Bearing in mind all these potential damaging factors, a preventive approach that protects the skin from sun rays and enhances its antioxidant mechanisms becomes essential to minimise future damages and maintain a radiant and young aspect every day. Lipotec offers an efficient molecular protection from premature ageing, free radicals and the consequences of daily stressors consisting of three active ingredients: Lipochroman, Preventhelia and Thermostressine. Lipochroman (INCI name: Dimethylmethoxy Chromanol) is a powerful antioxidant active ingredient that protects from oxidative stress due to its notable ROS and RNS scavenging properties. Preventhelia (INCI name: Diaminopropionoyl Tripeptide-33) offers a significant photoprotective effect, preventing from UVA-induced DNA damage and promoting its repairing system, at the same time as it quenches 4-HNE, inhibiting the formation of carbonylated proteins. Thermostressine (INCI name: Acetyl Tetrapeptide-22) is a tetrapeptide that boosts HSP70 expression, a family of skin proteins that protects from stressing situations such as UVB radiation, heat, cold and dehydration.

Materials and methods

Blockage of 3-nitrotyrosine formation