Jaroslav Sýkora | Akateeminen Kirjakauppa

Formation of reactive oxygen species (ROS) is a natural process during oxidative metabolism. ROS play an important role not only in pathological processes of human organism as usually presented but less attention is paid to their proper important role in cell signalling, biosynthesis or non-specific anti-infectious defence. Overproduction of ROS during numerous pathological situations in presence of insufficient antioxidant protection leads to substantial oxidative changes of lipids, proteins, sugars, and also DNA. Protection against ROS is assured by different extracellular or intracellular antioxidant mechanisms as studied during last decades. Antioxidant enzymes rectifying the oxidative damage are studied with regard to their different activities and usefulness in body protection. Their genetic polymorphisms are certainly involved in different response to oxidative stress. Special attention should be devoted to the topic of oxidative nuclear and mitochondrial DNA damage and its restoring via DNA repair process, especially base excision repair (BER). A large scale of antioxidant enzymes is involved in correction of DNA oxidative damage. Natural trend of worsened DNA repair is usually associated with aging. Other pathologies related with deficient DNA repair are susceptibility to carcinogenesis (lack of apoptosis control) or degenerative diseases. Oxidative stress is involved in the pathophysiology of diabetes mellitus (DM -- oxidative stress of mainly metabolic origin) and inflammatory bowel diseases (IBD -- oxidative stress of mainly inflammatory origin). In spite of confirmed OS in DM or IBD, the substantial information about the intensity of DNA repair and its possible relationship to the disease course and development of chronic complications is missing. The author pilot studies completed both in adult and paediatric patients with DM or IBD confirmed an increased oxidative stress as well as oxidative DNA damage examined with comet assay. The surprising findings were ascertained in intensity of DNA repair (analysed with modified comet assay).