Читать книгу Bioprospecting of Microorganism-Based Industrial Molecules - Группа авторов - Страница 61

Photoaging refers to an accelerated skin aging process due to overexposure with the UV component of sunlight [34]. For an individual with light skin, prolonged exposure to the sun will have histological, biochemical, and genetic consequences. UV‐exposed skin display thickened epidermis with an increased quantity of melanocytes and abnormal elastic fibers [35]. Conversely, the dermis layer reduces in density with a decrease in the number of fibroblasts, keratinocytes, and reduced levels of extracellular matrix collagen [10]. Sustained UV exposure to skin is also known to induce higher expression of MMPs, leading to the degradation of elastin and collagen, causing fibroblast senescence [36]. In the normal state, tissue inhibitor of metalloproteinase (TIMP) keeps a check on the levels of MMPs, thereby maintaining the homeostasis. However, during photoaging, expression of TIMP reduces reinforcing the MMPs‐mediated collagen and elastin degradation [15]. Solar UV component is thoroughly studied for causing direct DNA damage and indirect cellular damage by producing ROS. Trans‐urocanic acid is a subcutaneous chromophore known to absorb the UV‐A radiation. Upon excitation, it generates many ROSs causing oxidative stress and senescence in fibroblasts and associated cells. Dermal collagen also contains significant composition UV‐B absorbing amino acids such as cysteine, histidine, tyrosine, tryptophan, and phenylalanine. They collectively contribute to the generation of ROS beyond a certain threshold [37]. UV‐induced ROS can also damage nuclear and mitochondrial DNA causing an alteration in gene expression, dysfunctional mitochondria, oncogenesis, and senescence.