Oxidative Stress, DNA Damage and DNA Repair in Female Patients with Diabetes Mellitus Type 2

Autor: Helmut Brath, Bianca Guggenberger, Annemarie Grindel, Anela Tosevska, David Briskey, Christina Pöppelmeyer, Lukas Eichberger, Michaela Gschaider, Karl-Heinz Wagner, George Mare
Rok vydání: 2016
Předmět:
0301 basic medicine
Physiology
lcsh:Medicine
Blood Pressure
Xenopus Proteins
medicine.disease_cause
Biochemistry
Antioxidants
Body Mass Index
DNA Ligase ATP
chemistry.chemical_compound
XRCC1
Endocrinology
Diabetes mellitus
0302 clinical medicine
Malondialdehyde
DNA-(Apurinic or Apyrimidinic Site) Lyase
Diabetes diagnosis and management
Poly-ADP-Ribose Binding Proteins
lcsh:Science
Aged
80 and over

chemistry.chemical_classification
F2-Isoprostanes
Multidisciplinary
Glutathione peroxidase
Hematology
Middle Aged
Catalase
Glutathione
Body Fluids
DNA-Binding Proteins
Lipoproteins
LDL

Nucleic acids
Blood
030220 oncology & carcinogenesis
Female
Anatomy
Research Article
Adult
medicine.medical_specialty
HbA1c
DNA Ligases
Endocrine Disorders
DNA repair
DNA damage
Biology
03 medical and health sciences
Internal medicine
Genetics
medicine
Humans
Hypoglycemic Agents
Hemoglobin
Triglycerides
Aged
Glycated Hemoglobin
Medicine and health sciences
Glutathione Peroxidase
Biology and life sciences
Superoxide Dismutase
Cholesterol
HDL

lcsh:R
Proteins
Cholesterol
LDL

DNA
Cell Biology
APEX1
Diagnostic medicine
Cross-Sectional Studies
X-ray Repair Cross Complementing Protein 1
030104 developmental biology
Diabetes Mellitus
Type 2

Gene Expression Regulation
chemistry
Oxidative stress
Metabolic Disorders
Leukocytes
Mononuclear

lcsh:Q
Gene expression
Glycated hemoglobin
Zdroj: PLoS ONE, Vol 11, Iss 9, p e0162082 (2016)
PLoS ONE
ISSN: 1932-6203
Popis: Background Diabetes mellitus type 2 (T2DM) is associated with oxidative stress which in turn can lead to DNA damage. The aim of the present study was to analyze oxidative stress, DNA damage and DNA repair in regard to hyperglycemic state and diabetes duration. Methods Female T2DM patients (n = 146) were enrolled in the MIKRODIAB study and allocated in two groups regarding their glycated hemoglobin (HbA1c) level (HbA1c≤7.5%, n = 74; HbA1c>7.5%, n = 72). In addition, tertiles according to diabetes duration (DD) were created (DDI = 6.94±3.1 y, n = 49; DDII = 13.35±1.1 y, n = 48; DDIII = 22.90±7.3 y, n = 49). Oxidative stress parameters, including ferric reducing ability potential, malondialdehyde, oxidized and reduced glutathione, reduced thiols, oxidized LDL and F2-Isoprostane as well as the activity of antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase were measured. Damage to DNA was analyzed in peripheral blood mononuclear cells and whole blood with single cell gel electrophoresis. DNA base excision repair capacity was tested with the modified comet repair assay. Additionally, mRNA expressions of nine genes related to base excision repair were analyzed in a subset of 46 matched individuals. Results No significant differences in oxidative stress parameters, antioxidant enzyme activities, damage to DNA and base excision repair capacity, neither between a HbA1c cut off />7.5%, nor between diabetes duration was found. A significant up-regulation in mRNA expression was found for APEX1, LIG3 and XRCC1 in patients with >7.5% HbA1c. Additionally, we observed higher total cholesterol, LDL-cholesterol, LDL/HDL-cholesterol, triglycerides, Framingham risk score, systolic blood pressure, BMI and lower HDL-cholesterol in the hyperglycemic group. Conclusion BMI, blood pressure and blood lipid status were worse in hyperglycemic individuals. However, no major disparities regarding oxidative stress, damage to DNA and DNA repair were present which might be due to good medical treatment with regular health checks in T2DM patients in Austria.
Databáze: OpenAIRE