radiations between 400 nm and 500 nm. In vitro results also showed thymine-thymine (T-T) dimer formation in response to visible light (>395 nm) radiations,53 as well as the accumulation of epidermal p53 wild-type and mutant forms.54 The reported increase on Ki67 and cyclin A expression suggest a role of visible
light at promoting keratinocytes proliferation.55
One interesting hypothesis suggests a role of visible light on skin pigmentary changes.28 Three decades ago, Kollias and Baquer56 showed that pigmentary changes could occur in response
to near-IR light in the absence of ultraviolet radiation (UVR). Porges et al57 demonstrated that exposure to visible light (385 nm - 690 nm) triggered acute and fading erythema on skin types II and III, which later resulted in darkening of the skin that remained for the duration of the experimental protocol (10 days). More recently, Mahmoud et al50 showed that melanocompetent
skin types (types IV-VI) respond to visible light with pigment formation that differs from the UVA1–induced darkening.
Interestingly, these authors showed migration of melanin from basal cells into the upper layers of the epidermis in response
to visible light. Though further investigation is required to assess the role of melanin in visible light–induced pigmentation,
it is important to remark that this pigment has the capacity to absorb visible light, generating heat that can lead to deep dermal vessels dilation, erythema, and inflammation, further aggravating potential pigmentary changes. In agreement, Chiarelli-
Neto et al58 showed that UVB–induced melanin can act as a visible light photo-sensitizer, leading to singlet oxygen (1O2) formation, which can interact with proteins, nucleic acid, and membranes to trigger cell damage.59
Antioxidant Protection and Repair
Antioxidants are widely used in the cosmetic industry due to their capacity to prevent or minimize the oxidation of molecules.
60 Though oxidation of molecules is common and essential for the cellular functioning, it can also result in damage
to key structures.61 Aside from oxidation of DNA, lipids, and proteins, overproduction of RMS modulates cellular regulatory mechanisms and signal transduction pathways, metabolism, inflammation, immune system activation, and apoptosis.62 To prevent cellular or structural damage due to unwanted or uncontrolled
oxidations, all living organisms maintain complex systems of multiple types of antioxidant, which are the natural defense against free radicals or RMS.63 Antioxidants perform their function by becoming oxidized themselves, and they act also as pro-oxidants under certain circumstances.60 This capacity of antioxidants to play “in favor of or against†our skin health and integrity needs to be taken into consideration when designing
cosmetic products to provide the maximum benefits in the absence of potentially harmful effects.
In the skin, an increase in oxidative stress, which is characterized
by enhanced production of RMS, is the main cause
