DNA DSB can occur via a variety of routes including exposure to exogenous ionising radiation during clinical anticancer radiotherapy (2), exposure to certain classes of anticancer chemotherapeutic drugs (3), and as a result of endogenously derived reactive oxygen species as a consequence of normal cellular metabolism (1).
Skin is an organ subjected to a high degree of oxidative stress from both endogenous (metabolism, inflammation) and exogenous sources (radiation, smoking, chemical air pollutants, wind, etc), the most important being ultraviolet (UV) radiation.
In mammalian, ROS can be of endogenous or exogenous origin (radiation, pollution, drugs, medication, smoking).
Several etiological hypotheses related to intrinsic (sociodemographic, anthropometric, hormonal, immunological, genetic) and exogenous (ionizing radiation, electromagnetic fields, diet, infections, pesticides, drugs) risk factors have led to analytical epidemiological studies to establish relationships with CNS tumors.
or the action of exogenous agents (radiation, naturally occurring radioisotopes, chemical mutagens such as heavy metals, etc).
DNA lesions can be caused by either endogenous (reactive oxygen species (ROS) resulting from metabolic processes) or exogenous (ionizing radiation (IR), UV) agents.
This ROS increase originates from several sources, both exogenous (ultraviolet radiations, trauma, stress, infections, malignancies, certain drugs) and endogenous.
Of the known exogenous factors, ionizing radiation, such as X-rays [ 44] or UV radiation [ 39– 41] are the most prominent causes of DSBs.
These include alcohol consumption, exogenous estrogen, ionizing radiation and in postmenopausal women, obesity.
