| Abstract [eng] |
Oxidative stress is an important factor in the pathogenesis and progression of allergic dermatitis. It is characterised by the generation of oxidants in the body‘s cells and the impairment of their accumulation and neutralisation. The most common oxidants in oxidative stress are reactive oxygen species, which are usually the product of the reduction of a single oxygen electron. The aim of this work is to investigate all scientific data of the influence of oxidative stress on the course of allergic dermatitis, with special attention to atopic dermatitis. Allergic contact dermatitis is a type IV hypersensitivity immune response to a molecule on the sensitised skin, while atopic dermatitis is the most common chronic inflammatory skin disease in which immune cells are activated to induce increased production of immunoglobulin E, exacerbating symptoms of inflammation and itching. Oxidative stress is influenced by both endogenous and exogenous factors. Endogenous factors include a high glutathione/glutathione disulphate ratio, levels of urinary 8-hydroxydeoxyguanosine, malondialdehyde, lipid hydroperoxides and damaged epidermal keratinocytes. Exogenous factors include ultraviolet radiation, air pollutants, psychological stress and Staphylococcus aureus colonisation. All these factors, through different pathophysiological pathways, accentuate the course of allergic dermatitis. The direct effects of reactive oxygen species can be assessed by measuring biomarkers such as urinary 8-hydroxydeoxyguanosine, malondialdehyde, glutathione, glutathione disulphate. These markers directly correlate with the severity of allergic contact dermatitis and atopic dermatitis. |
