Over the last few years, a relative decline of the morbidity and mortality of human immunodeficiency virus (HIV) infection in industrialised countries has been observed due to the use of a potent combined therapy known as high active antiretroviral therapies (HAARTs). It has led to a decrease of viral load and a quantitative and qualitative improvement of immune function in patients, especially CD4(+) T-lymphocyte count, having as a consequence a decrease of infectious complications and a global clinical improvement. Besides the positive effects of HAARTs on immune and metabolic alterations during HIV infection, it has been reported that the commonly used drugs AZT, ddI, and ddC are toxic to hepatocytes. Recent reports continue to point to the mitochondria as targets for toxicity. The prevalence of these symptoms is continued during acquired immunodeficiency syndrome ( AIDS). The effects of oxidative stress occurring as a consequence of mitochondrial toxicity may amplify some of the pathophysiological and phenotypic events during infection. Mitochondrial stabilisation and antioxidative strategies are possible new therapeutic aims since the antiretroviral treatment is prolonged with increased longevity from AIDS, which has become a more manageable chronic illness. The aim of the present review article is to summarize the current knowledge about mitochondrial dysfunction during HAART and its consequence for patients with chronic treatment. Oxidative stress may serve as one pathway for cellular damage in AIDS and its treatment. One important future goal is to prevent or attenuate the side effects of HAART so that improved disease management can be achieved.

The Publisher regrets that this article is an accidental duplication of an article that has already been published, http://dx.doi.org/10.1016/j.biomag.2010.09.001. The duplicate article has therefore been withdrawn.

The Publisher regrets that this article is an accidental duplication of an article that has already been published, http://dx.doi.org/10.1016/j.bionut.2010.09.005. The duplicate article has therefore been withdrawn.

Abstract Over the last few years, a relative decline of the morbidity and mortality of human immunodeficiency virus (HIV) infection in industrialised countries has been observed due to the use of a potent combined therapy known as high active antiretroviral therapies (HAARTs). It has led to a decrease of viral load and a quantitative and qualitative improvement of immune function in patients, especially CD4+ T-lymphocyte count, having as a consequence a decrease of infectious complications and a global clinical improvement. Besides the positive effects of HAARTs on immune and metabolic alterations during HIV infection, it has been reported that the commonly used drugs AZT, ddI, and ddC are toxic to hepatocytes. Recent reports continue to point to the mitochondria as targets for toxicity. The prevalence of these symptoms is continued during acquired immunodeficiency syndrome (AIDS). The effects of oxidative stress occurring as a consequence of mitochondrial toxicity may amplify some of the pathophysiological and phenotypic events during infection. Mitochondrial stabilisation and antioxidative strategies are possible new therapeutic aims since the antiretroviral treatment is prolonged with increased longevity from AIDS, which has become a more manageable chronic illness. The aim of the present review article is to summarize the current knowledge about mitochondrial dysfunction during HAART and its consequence for patients with chronic treatment. Oxidative stress may serve as one pathway for cellular damage in AIDS and its treatment. One important future goal is to prevent or attenuate the side effects of HAART so that improved disease management can be achieved.

Diabetes mellitus is a complex metabolic disorder characterized by a disturbance in glucose metabolism. Recent evidences suggest that increased oxidative damage as well as deficits in antioxidants defence systems could be related to the complications in Diabetes patients' type I. The aim of this study was to investigate an extensive array of redox status indices: glutathione (GSH), malondialdehyde (MDA), peroxidation potential, superoxide dismutase (SOD), catalase (CAT), total hydroperoxide (TH) and advanced oxidation protein products (AOPP) in relation to blood glucose and glucose indicators control such as glycosylated haemoglobin (HbA1c) and fructosamine by spectophotometric techniques. Forty Diabetes Mellitus patients' type I and 40 healthy subjects were recruited. Both a reduction of GSH levels and an increase in MDA and TH levels were observed in the serum of patients. These patients also showed an increase of AOPP and PP levels as well as an increase of both CAT and SOD activity. Relatively to the control group, patients had significant differences in global indices of oxidant/antioxidant status and indicators of glycaemia control. These results contribute both to the evidences that substantial oxidative stress occurs during Diabetes Mellitus type I without early complications and to an integral overview of the oxidant/antioxidant balance in these patients.

Several recent studies in human immunodeficiency virus (HIV) patients have identified micronutrient deficiencies as affecting progression to acquired immunodeficiency syndrome (AIDS) and death. Although the mechanisms are not known, micronutrient deficiencies may exacerbate the oxidative stress induced by HIV. In addition, infection and its evolution likely lead to an increased requirement for nutritional micronutrients, especially antioxidants. To evaluate this, 40 relatively healthy, institutionalized HIV-infected individuals were recruited for assessment before or three months after fresh fruit and vegetable supply were increased due to seasonal supply. Seven-day dietary records were recorded at the beginning (December) and end of the three-month study period (March). Oxidative stress indices and CD4+, CD38+/CD8+, and CD95+ T-lymphocyte subsets were also measured at these times. No significant differences were found in calorie or protein intake across the study period, but vitamin A, C, and E intakes all increased. A number of redox indicators were modified (increase: total antioxidant status, glutathione peroxidase, and glutathione; and decrease: superoxide dismutase) during the study period. However, no change in malondialdehyde, hydroperoxides, or DNA damage was noted but a significant reduction in CD38+/CD8+ relative count was seen. Within the context and limitations of this study, the increase of dietary fruits and vegetables intake for three months had some beneficial effects on nutrition, systemic redox balance, and immune parameters in HIV-infected persons.

An association between viral diseases and increased oxidative stress has been suggested. The time course of serum levels of total antioxidant status (TAS), peroxidation potential (PP), glutathione (GSH), lipid peroxidation measured as hydroperoxides, and malondyaldehyde and 4-hydroxyalkenals (MDA + 4-HDA), as well as antioxidant enzymatic activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx), were measured in 22 serologically confirmed dengue patients. Most of the patients had dengue fever and three of them had dengue hemorrhagic fever. The redox parameters were compared with those of age- and sex- matched controls. No significant difference was observed for levels of GSH and TAS between patients and controls. Levels of PP, MDA + 4-HDA, and SOD were significantly higher. Levels of GPx and total hydroperoxides were significantly lower in patients in comparison with controls. These findings suggest that the alteration in redox status could result of increased oxidative stress and it may play a role in the pathogenesis of the disease.

SUMMARY. Infection by human immunodeficiency virus (HIV) continues to increase worldwide. The progression of the disease in children may be rapid. Oxidative stress is well documented in adult HIV/AIDS patients. Viral Tat protein plays a role in the intracellular generation of reactive oxygen species thus increasing apoptotic index, and depleting CD4 + T lymphocytes. The aim of this study was to investigate 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) and DNA fragmentation in AIDS pediatrics patients compared to healthy subjects. Blood samples from 11 pediatric patients and 22 healthy subjects were tested by spectrophotometric techniques in order to measure oxidative stress indices. Both a reduction of GSH levels and an increase in MDA and TH levels were detected in the plasma of AIDS patients. These patients also showed an increase of DNA fragmentation in lymphocytes as well as a reduction of GPx and an increase in SOD activity in erythrocytes. Relatively to the control group, AIDS patients had differences in global indices of total antioxidant status. These results contribute to the evidences that substantial oxidative stress occurs during AIDS pediatric infection. RESUMEN. “ Evaluacio n del Estre s Oxidativo en Pacientes Pediatricos con SIDA” . La infeccio n por el virus de la inmunodeficiencia humana (VIH) continua aumentando a nivel mundial. La progresio n de la infeccio n en ninos es rapida. El proceso de estre s oxidativo asociado a la infecci o n en adultos esta bien documentado. La proteina viral Tat juega un papel reconocido en la generaci o n intracelular de especies reactivas de ox igeno, evento este que repercute en el incremento del indice de apoptosis y en la disminuci o n de los linfocitos T CD4 + . El objetivo del presente trabajo fue evaluar un extenso grupo de marcadores del estado redox tales como: glutati o n (GSH), malonildialdehido (MDA), potencial de peroxidacio n (PP), estado antioxidante total (TAS), glutati o n peroxidasa (GPx), supero xido dismutasa (SOD), hidropero xidos totales (TH) y % de fragmentacio n del ADN, en pacientes pediatricos comparados estadisticamente con individuos sanos. Muestras de sangre de 11 pacientes SIDA pedi atricos y de 22 individuos sanos fueron utilizadas para realizar las mediciones de los marcadores del estado redox por te cnicas espectro fotome tricas. En el plasma de los pacientes SIDA pedi atricos se detecto un nivel bajo de GSH, asi como niveles altos de MDA y TH. Ademas se observo un mayor porcentaje de fragmentacio n del ADN en linfocitos, actividad enzim atica de GPx disminuida y actividad mayor de SOD en eritrocitos en comparaci o n con el grupo de individuos sanos. Se observaron diferencias significativas en cuanto a los indices del estado antioxidante global. Estos resultados corroboran las evidencias que el estado de estr e s oxidativo se manifiesta durante la infeccio n SIDA en pacientes pediatricos.

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.

Human T cell lymphotrophic virus I (HTLV-I) is a retrovirus that causes adult cell leukemia and the neurological disorder known as tropical spastic paraparesis. Pathology apparently results from the expression of viral and cellular genes which might lead to cell transformation, immortalization and disease. The aim of the present study is to compare levels of lipid peroxidation, peroxidation potential and sulfhydryl content measured as oxidative stress indicators in 9 asymptomatic HTLV-I seropositive (HTLV-I+) and 10 healthy individuals (HTLV-I -). These parameters are related to changes in the levels of CD3, CD4, CD8 and CD25 T cell subsets. Spectrophotometric techniques were assayed for evaluation of oxidative stress indicators and flow cytometry for determination of T cell subsets. Significant differences were found (p < 0,05) between HTLV-I+ and HTLV-Isubjects regarding to stress indicators, except the concentration of total sulfhydryl group. The CD4+ T lymphocytes count stays inside the normal intervals whereas the CD8+ T lymphocytes count was slightly increased. Relative values of CD25 also showed significant differences between HTLV-I+ and HTLV-Isubjects. These results reveal both the presence of a pro-oxidant state with the activation of the cytotoxic cellular response and the activation of cellular gene expression. These determinations may be of interest for knowledge of physiopathology of the infection and for possible preventive therapeutic interventions.