title: Aspects of oxidative stress in children with type 1 diabetes mellitus.
abstract: Diabetes mellitus is considered to be one of a rank of free radical diseases. The existence of hyperglycemia produces increased oxidative stress (OS) via non-enzymatic glycation, glucose autoxidation, and alterations in polyol pathway activity with subsequent influences on the whole organism. In childhood, Type 1 diabetes prevails and is characterized by its autoimmune character with progressive destruction of beta cells and lack of insulin in genetically predisposed patients. Our study focused on diabetic children and their 1st degree relatives and confirmed increased oxidative stress in diabetic children as well as a similar tendency in their siblings. Following this, we carried out a one-year study comprising diabetic children supplemented with vitamins E and C. The vitamin treatment improved diabetes control and reduced markers of oxidative stress substantially when compared with non-supplemented diabetic children. As oxidative stress impairs not only lipids and proteins, but also DNA, we attempted to examine the level of DNA strand breaks as well as DNA repair processes using comet assay modifications. Though children with Type 1 diabetes demonstrated increased oxidative stress (lower SOD and GSH when compared with healthy children), their oxidative DNA damage (measured as DNA strand breaks) were not substantially altered compared with normals. On the other hand, their DNA repair capacity was significantly increased. This demonstrates a stimulated DNA repair process that is most certainly a response to the permanently elevated state of oxidative stress. Owing to the presented results, it is appropriate to ponder the increased influence of oxidative stress on children with Type 1 diabetes and to take into account this fact when considering their treatment.
authors.affiliation: Department of Pediatrics, Charles University Hospital-Plzen, Alej Svobody 80, 304-60 Plzen, Czech Republic. varvarovska@fnplzen.cz
authors.forename: Jana
authors.initials: J
authors.lastname: Varvarovská
authors.forename: Jaroslav
authors.initials: J
authors.lastname: Racek
authors.forename: Rudolf
authors.initials: R
authors.lastname: Stetina
authors.forename: Josef
authors.initials: J
authors.lastname: Sýkora
authors.forename: Renata
authors.initials: R
authors.lastname: Pomahacová
authors.forename: Zdenek
authors.initials: Z
authors.lastname: Rusavý
authors.forename: Silvie
authors.initials: S
authors.lastname: Lacigová
authors.forename: Ladislav
authors.initials: L
authors.lastname: Trefil
authors.forename: Konrad
authors.initials: K
authors.lastname: Siala
authors.forename: Frantisek
authors.initials: F
authors.lastname: Stozický
mesh_terms: D000293:Adolescent; D000328:Adult; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000494:pharmacology / Q000627:therapeutic use; D002648:Child; D004249:DNA Damage / Q000187:drug effects / Q000502:physiology; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy / Q000378:metabolism*; D005260:Female; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D013482:Superoxide Dismutase / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D000975:Antioxidants; D014810:Vitamin E; D013482:Superoxide Dismutase; D005978:Glutathione; D001205:Ascorbic Acid