title: Contribution to characterization of oxidative stress in HIV/AIDS patients.
abstract: Infection by human immunodeficiency virus (HIV) causes persistent chronic inflammation. Viral Tat protein plays a role in the intracellular increase of reactive oxygen species (ROS) thus increasing apoptotic index, mostly the one mediated by FAS/CD95, and depleting CD4+ T lymphocytes. The aim of this study was to investigate whether there is a relationship between an extensive array of redox status indices (glutathione (GSH), malondialdehyde (MDA), peroxidation potential, total antioxidant status, glutathione peroxidase (GPx), superoxide dismutase (SOD), total hydroperoxide (TH), DNA fragmentation) and relative CD4, CD95, CD38/CD8 T lymphocyte counts in HIV/AIDS patients compared to healthy subjects. Blood samples from 85 HIV/AIDS patients and 40 healthy subjects were tested by spectrophotometric techniques in order to measure oxidative stress indices, and by flow cytometry to quantify T cell subsets. Patients were divided in two groups according to CDC 1993 guidelines. CD95 and CD38 increase paralleled the severity of HIV infection. Both a reduction of GSH levels and an increase in MDA and TH levels were detected in the plasma of HIV+ patients. These patients also showed an increase of DNA fragmentation in lymphocytes as well as a significant (P<0.05) reduction of GPx and an increase in SOD activity in erythrocytes. Relatively to the control group, HIV-infected patients had significantly differences in global indices of total antioxidant status. These results corroborate that substantial oxidative stress occurs during HIV infection. To our knowledge this study is the first relating oxidative stress indices with both CD38/CD8 and CD95 lymphocytes subsets.
authors.affiliation: Department of Clinical Pharmacology, Institute of Tropical Medicine Pedro Kouri (IPK), P.O. Box 601, Marianao 13, Ciudad de La Habana, Havana, Cuba. lgil@ipk.sld.cu
authors.forename: Lizette
authors.initials: L
authors.lastname: Gil
authors.forename: Gregorio
authors.initials: G
authors.lastname: Martínez
authors.forename: Ivón
authors.initials: I
authors.lastname: González
authors.forename: Alicia
authors.initials: A
authors.lastname: Tarinas
authors.forename: Alejandro
authors.initials: A
authors.lastname: Alvarez
authors.forename: A
authors.initials: A
authors.lastname: Giuliani
authors.forename: Randelis
authors.initials: R
authors.lastname: Molina
authors.forename: Rolando
authors.initials: R
authors.lastname: Tápanes
authors.forename: Jorge
authors.initials: J
authors.lastname: Pérez
authors.forename: Olga Sonia
authors.initials: OS
authors.lastname: León
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D053938:DNA Fragmentation; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D005978:Glutathione / Q000097:blood; D005979:Glutathione Peroxidase / Q000097:blood; D015658:HIV Infections / Q000097:blood* / Q000276:immunology; D006801:Humans; D006861:Hydrogen Peroxide / Q000097:blood; D015227:Lipid Peroxidation / Q000502:physiology; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology*; D012016:Reference Values; D013482:Superoxide Dismutase / Q000097:blood; D016176:T-Lymphocyte Subsets
chemical_list: D015415:Biomarkers; D008315:Malondialdehyde; D006861:Hydrogen Peroxide; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione