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Page 6 of 16                                               Burke. Plast Aesthet Res 2020;7:59  I  http://dx.doi.org/10.20517/2347-9264.2020.154










































               Figure 3. Mechanisms of solar-induced photoaging and carcinogenesis of the skin. Solar ultraviolet B (UVB) directly mutates cellular
               DNA to cause photoaging and to initiate carcinogenesis. Ultraviolet A (UVA) interacts synergistically with pollutants to form DNA-
               adducts, initiating carcinogenesis. Both UVA and UVB generate ROS that oxidize DNA to form 8-OHdG, leading directly to photoaging
               and tumor initiation. ROSs further activate signal transduction of inflammatory cytokines and matrix-destructive enzymes, which
               exacerbate photoaging and cellular proliferation to promote carcinogenesis. Exposure to solar (and technological) VL and IR heat
               also induces photoaging of the skin. (Modified from Saladi et al. [18]  with consent of authors.). ROS: reactive oxygen species; 8-OHdG:
               8-hydroxy deoxyguanosine; VL: visible light; IR: infrared light

                                                                                           [16]
               in contrast, only minimal concentrations were measured when exposed to UVB after BaP . Cells exposed
               to UVA after having been incubated with BaP increased 8-OHdG by a factor of 17, while exposure to
                                                           [1]
               UVB resulted in only an increase by a factor of 3 . Another experiment exposed human keratinocytes
               to UVA after incubation with BαP: H O  production increased 6-fold compared to only a factor of 1.2
                                                   2
                                                 2
                                   [1]
               after exposure to UVB . In the skin, all of this oxidative damage manifests clinically as photoaging and
               proclivity to carcinogenesis.
               With exposure to UV, BaP forms diol epoxide (BPDE) which combines covalently to DNA to form BPDE-
                                                           [17]
               DNA adducts that directly initiate carcinogenesis . Exposure to UVA generates more than double the
                                                 [18]
               number generated by exposure to UVB . These adducts directly produce ROS. Furthermore, the BaP is
               recycled within cells, a reaction enhanced by UVA exposure, making even small amounts of BaP extremely
               damaging. This sequence of reactions leading to photoaging of the epidermis and dermis as well as to
               initiation and promotion of skin cancer is shown in Figure 3.

               OZONE
               In the stratosphere (10-30 miles above the earth’s surface), O  protects us by blocking dangerous solar UVC
                                                                  3
               and dangerous high-energy UVB. On the other hand, low level tropospheric O  causes significant oxidative
                                                                                  3
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