Short Communication: Oxidative Stress in HIV-Infected Individuals: A Cross-Sectional Study

Abstract

HIV infection increases the oxidative stress process, and antiretroviral combination therapy increases protein oxidation and preexistent oxidative stress. The latter induces production of reactive oxygen species. Lipid peroxidation (LPO) is a means of determining oxidative stress. There is also a deficiency of glutathione in HIV infection. Persistent oxidative load leads to an accelerated rate of consumption of glutathione (GSH). This study measured LPO and GSH levels in plasma of HIV-infected individuals with or without therapy and compared these with healthy controls. One hundred HIV-infected individuals and 30 healthy controls were included in the study. LPO and GSH levels were measured in plasma according to previously described methods. The mean level of LPO in HIV-infected individuals was 0.7 +/- 0.1 micromol/ml (range, 0.5-0.9 micromol/ml), whereas the mean LPO level in controls was 0.3 +/- 0.1 micromol/ml (range, 0.2-0.4 micromol/ml). The mean LPO levels were significantly higher in HIV-infected individuals as compared to healthy controls (p value <0.0001). The mean GSH level in HIV-infected individuals was 0.06 +/- 0.01 micromol/ml (range, 0.03-0.08). The mean GSH level in healthy controls was 0.09 +/- 0.01 micromol/ml (range, 0.05-0.1). The mean glutathione level in HIV-infected individuals was significantly lower in compared to healthy controls (p value < 0.0001). There was a significant positive correlation between absolute CD4 cells and GSH levels (rho = 0.182, p = 0.045). There is increased oxidative stress in HIV-infected patients. Whether supplementation with antioxidants will reduce this oxidative stress is still unknown.

Multivariate discriminant analysis of redox and progression indexes in Cuban AIDS patients with Kaposis sarcoma

“…It has been previously shown that the HIV-infected populations have significantly lower antioxidant concentrations than non-HIV individuals [9,10,13]. Lower non-enzymatic antioxidant concentrations occurred also in HIV patients with diverse neoplastic manifestation [41,42].…”

“…Consistent changes in redox responsive cascades and in the expressions of corresponding target genes may have a similar or even greater impact on senescence as the direct radical inflicted damage of cellular constituents [9,16].…”

“…Diverse authors have been contributed to the observation that oxidative stress in HIV could drive disulfide CD4 modification, necessary for HIV entry on host, CD4 T lymphocyte depletion and also viral replication increase influencing both aspects on the HIV immunodeficiency condition with unfavorable evolution [9][10][11][12][13][14]. Furthermore, antiretroviral therapy could influence on oxidative stress in HIV infection [15].…”

Altered Redox Regulation as Cofactor in Comorbidities and Accelerated Aging in HIV Infection Evolution and Antiretroviral Treatment

“…The study and enhancement of surrogate markers of HIV disease progression, including OS indexes, continues to be an important area of research particularly with the advent of therapies that claim to halt or slow the process of immunological decline [68][69][70][71][72]. Additional markers and combinatorial analysis that add value to T-CD4+ lymphocyte subset would therefore be useful i.e.…”

The Role of Human Immunodeficiency Virus Type 1 (HIV-1) Proteins and Antiretroviral Drug Therapy in HIV-1-Induced Oxidative Stress

“…In addition, there was a significant positive correlation between absolute CD4 + T cells and GSH levels. However, there was no significant difference in the levels of LPO and GSH among HIV-1 infected individuals receiving antiretroviral therapy (ART) and those without ART (Wanchu et al, 2009). Jordão Júnior et al (1998) evaluated 28 serologically positive HIV-1 patients, 16 patients with AIDS (with < 200/mm 3 CD4 + T lymphocytes) and 12 HIV-1 infected and asymptomatic patients (with 200-500/mm 3 CD4 + T lymphocytes).…”