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Ionizing radiation produces fast moving particles which have the ability to damage DNA, and produce highly reactive free radicals known as reactive oxygen species (ROS). The production of ROS in cells radiated by LDIR (Low-Dose Ionizing Radiation) occur in two ways, by the radiolysis of water molecules or the promotion of nitric oxide synthesis ...
This is an accepted version of this page This is the latest accepted revision, reviewed on 2 March 2025. "Skin pigmentation" redirects here. For animal skin pigmentation, see Biological pigment. Extended Coloured family from South Africa showing some spectrum of human skin coloration Human skin color ranges from the darkest brown to the lightest hues. Differences in skin color among ...
Overexposure to ultraviolet radiation is known to cause skin cancer, [19] make skin age and wrinkle faster, [20] mutate DNA, [21] and impair the immune system. [22] Frequent tanning bed use triples the risk of developing melanoma, the deadliest form of skin cancer, according to a 2010 study.
Eumelanin is the dominant form of melanin found in human skin. Eumelanin protects tissues and DNA from radiation damage by UV light. Melanin is produced in specialized cells called melanocytes, which are found in the lowest level of the epidermis. [84] Melanin is produced inside small membrane-bound packages called melanosomes.
These mutations arise due to chemical changes within skin cells. These mutations may be clinically related to specific signs of photoaging such as wrinkling. [5] [6] DNA UV mutation. Melanocytes and basal cells are embedded in the epidermal layer. Upon exposure to UVB rays, melanocytes will produce more melanin, a pigment
Radiolysis of intracellular water by ionizing radiation creates peroxides, which are relatively stable precursors to hydroxyl radicals. 60%–70% of cellular DNA damage is caused by hydroxyl radicals, [3] yet hydroxyl radicals are so reactive that they can only diffuse one or two molecular diameters before reacting with cellular components.
The two subpathways differ in how they recognize DNA damage but they share the same process for lesion incision, repair, and ligation. The importance of NER is evidenced by the severe human diseases that result from in-born genetic mutations of NER proteins. Xeroderma pigmentosum and Cockayne's syndrome are two examples of NER associated diseases.
The location of a transversion mutation on a gene coding for a protein correlates with the extent of the mutation. If the mutation occurs at a site that is not involved with the shape of a protein or the structure of an enzyme or its active site, the mutation will not have a significant effect on the cell or the enzymatic activity of its proteins.