DNA damage and apoptosis in mononuclear cells from glucose-6-phosphate dehydrogenase-deficient patients (G6PD Aachen variant) after UV irradiation
Autor: | Rainhardt Osieka, Ursula Fabry, Thomas Efferth |
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Rok vydání: | 2001 |
Předmět: |
Adult
Male Heterozygote Adolescent Ultraviolet Rays DNA damage Immunology Apoptosis Glucosephosphate Dehydrogenase Biology Polymerase Chain Reaction Peripheral blood mononuclear cell law.invention chemistry.chemical_compound law Humans Immunology and Allergy Glucose-6-phosphate dehydrogenase Polymerase chain reaction Aged chemistry.chemical_classification Reactive oxygen species Genetic Variation Heterozygote advantage DNA Cell Biology Glutathione Middle Aged Molecular biology Glucosephosphate Dehydrogenase Deficiency chemistry Leukocytes Mononuclear Female DNA Damage Genes T-Cell Receptor delta |
Zdroj: | Scopus-Elsevier |
ISSN: | 1938-3673 0741-5400 |
DOI: | 10.1189/jlb.69.3.340 |
Popis: | Patients affected with X chromosome-linked, hereditary glucose-6-phosphate dehydrogenase (G6PD) deficiency suffer from life-threatening hemolytic crises after intake of certain drugs or foods. G6PD deficiency is associated with low levels of reduced glutathione. We analyzed mononuclear white blood cells (MNC) of three males suffering from the German G6PD Aachen variant, four heterozygote females of this family, one G6PD-deficient male from another family coming from Iran, and six healthy male volunteers with respect to their DNA damage in two different genes (G6PD and T-cell receptor-δ) and their propensity to enter apoptosis after UV illumination (0.08–5.28 J/cm2). As determined by PCR stop assays, there was more UV-induced DNA damage in MNC of G6PD-deficient male patients than in those of healthy subjects. MNC of G6PD-deficient patients showed a higher rate of apoptosis after UV irradiation than MNC of healthy donors. MNC of heterozygote females showed intermediate rates of DNA damage and apoptosis. It is concluded that increased DNA damage may be a result of deficient detoxification of reactive oxygen species by glutathione and may ultimately account for the higher rate of apoptosis in G6PD-deficient MNC. |
Databáze: | OpenAIRE |
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