Uvinduced Photodamage And Photoprotection

UVR is the main etiological agent for most of the skin cancer incidence and a key factor responsible for photoaging and photodamage (Gonzalez et al., 2008). UV spectrum reaching earth's surface has been classified as UVB (290-320 nm) and UVA (320-400 nm). UVB causes acute sunburn, DNA mutation, or even cancer by its absorbance in the epidermis, whereas the longer wavelengths of UVA region can penetrate much deeper into the skin.

Continuous exposure to UV irradiation (both UVA and UVB) leads to skin cancer and other photoaging complications, which are typically mediated by the reactive oxygen species (ROS), generated in the oxidative pathways (Dummermuth et al., 2003; Pallela et al., 2010). Normal skin cells generate ROS such as superoxide anion (O2 ) and hydrogen peroxide (H2O2) as a result of normal metabolism in minute concentrations. Both O2- and H2O2 may be converted to the highly reactive hydroxyl radical (OH-) by iron (Fe +)-catalyzed Haber-Weiss and Fenton reactions. Similarly, reactive nitrogen species (RNS) are generated as a result of sequential reactions that begin with nitric oxide synthase (NOS)-mediated conversion of arginine to citrulline. In this reaction, NO is generated, which reacts with O2- to produce peroxynitrite (ONOO-). Similarly, ROS and RNS can be formed as a result of exposure to environmental agents including chemicals (xenobiotics) and solar UVA and UVB. Many xenobiotics are converted to toxic quinones by the family of functionally related enzymes known as cytochrome P450 (CYP). These quinones are redox-sensitive agents and are reversibly reduced to semihydroquinones/hydroquinones, which generate O2-. Both UVA and UVB produce similar free radicals and/or singlet oxygen (XO2) either directly following interaction with cellular components or in the presence of chemical agents known as photosensitizers. These photoactive chemicals while in their lowest energy or ground state absorb incident radiation (including UVA/UVB), within their absorption spectrum. The energy of the absorbed photon creates an excited state molecule, which is highly unstable under ambient conditions. In returning to the ground state, excited species transfer energy to adjacent intracellular chemical moieties particularly molecular oxygen (O2) and thereby convert it into ROS. These ROS interact with lipid-rich plasma membranes and initiate a reaction known as lipid peroxidation. Numerous intracellular enzymes serve to degrade these reactive species. Some of these enzymes are specific such as SODs, which dismute O2- to H2O2, whereas others have overlapping substrate affinities such as catalase and glutathione peroxidases, both of which can degrade H2O2 to water and O2 but glutathione peroxidases also degrade organic peroxides to relatively nontoxic alcoholic species. These enzymes also require GSH during the course of peroxide degradation and convert GSH into its oxidized form, which is recycled by the enzyme gluta-thione reductase. Similarly, toxic quinones are converted to relatively less toxic hydroquinones by quinone reductases (QR).

As a result of UVA/UVB-mediated ROS generation during the patho-genesis of various skin diseases, a number of signaling pathways are activated. ROS drive activation of MAPKs, the most important of which are ERK, JNK, and p38 kinases. ERK and JNK are important in recruiting c-Fos and c-Jun to the nucleus where they activate the transcription factor AP-1, whereas activation of p38 and inhibitory kappa kinases (IKK) is important in the transcriptional activation of NF-kB. Both of these factors are important in regulating the diverse array of genes, which play key roles in the pathogenesis of inflammation (such as iNOS, COX-2) and in regulation of cell cycle, proliferation, and apoptosis (cyclin D1, Bcl2, Bclx, IAP, p21, p53, etc.).

Hence, photoprotection is a critical and crucial concern to avoid these undesired effects. The increase in solar UVR on the earth's surface due to the deterioration in the stratospheric ozone layer has increased the interest for searching natural, photoprotective compounds from various sources (Rastogi et al., 2010). Stratospheric ozone depletion leads to an increase in the short wavelengths of UVR and in consequence to an increase in H2O2 formation in surface waters. In such cases, algae undergo oxidative stress, where UVR induces the formation of H2O2 by photoacti-vation of dissolved organic material (DOM), photochemical degradation, and liberation of exited electrons, which initiate reduction of molecular oxygen (Dummermuth et al., 2003). Hence, photoprotective processes prevent or minimize generation of oxidizing molecules, scavenge ROS efficiently, and repair damage that inevitably occurs (Niyogi, 1999). Micronutrients such as carotenoids, tocopherols, ascorbates, flavonoids, or ffl-3 fatty acids can act as UV absorbers or antioxidants, or can modulate signaling pathways elicited upon UV exposure. In addition, protection depends on the topical applications as well as the algal consumption, which constitute many of the UV absorbers as mentioned above. Hence, algae are the richest source for these photoprotecting constituents and can be recommended as highly nutritional supplements, which can bring resilience to human body.

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