ascorbic-acid and Acquired-Immunodeficiency-Syndrome

Pathogenic organism can be considered as pro-oxidant agents because they produce cell death and tissue damage. In addition organism can be eliminated by specific cell defense mechanism which utilize in part, reactive oxygen radicals formed by oxidative stress responses. The cause of the necessarily defense process results in cell damage thereby leading to development of inflammation, a characteristic oxidative stress situation. This fact shows the duality of oxidative stress in infections and inflammation: oxygen free radicals protect against microorganism attack and can produce tissue damage during this protection to trigger inflammation. Iron, a transition metal which participates generating oxygen free radicals, displays also this duality in infection. We suggest also that different infectious pathologies, such as sickle cell anemia/malaria and AIDS, may display in part this duality. In addition, it should be noted that oxidative damage observed in infectious diseases is mostly due the inflammatory response than to the oxidative potential of the pathogenic agent, this last point is exemplified in cases of respiratory distress and in glomerulonephritis. This review analyzes these controversial facts of infectious pathology in relation with oxidative stress.

Topics: Acquired Immunodeficiency Syndrome; Adult; Anemia, Sickle Cell; Animals; Antioxidants; Arachidonic Acid; Ascorbic Acid; Cells, Cultured; Child; Endotoxins; Fetus; Free Radicals; Glomerulonephritis; Humans; Infections; Inflammation; Iron; Malaria; Mice; Oxidative Stress; Phagocytosis; Rabbits; Respiratory Distress Syndrome; Sheep

Intracellular oxidative stress in CD4+ lymphocytes due to disturbed glutathione homeostasis may lead to impaired lymphocyte functions and enhanced HIV replication in patients with HIV infection, especially in those with advanced immunodeficiency. The aim of the present study was to assess whether short-term, high-dose antioxidant treatment might have effects on immunological and virological parameters in patients with HIV infection.. In this pilot study, we examined virological and immunological effects of antioxidant combination treatment for 6 days with high doses of N-acetylcysteine (NAC) and vitamin C in 8 patients with HIV infection. The following were assayed before, during and after antioxidant treatment: HIV RNA plasma levels; numbers of CD4+, CD8+, and CD14+ leukocytes in blood; plasma thiols; intracellular glutathione redox status in CD4+ lymphocytes and CD14+ monocytes; lymphocyte proliferation; lymphocyte apoptosis and plasma levels of tumour necrosis factor (TNF)alpha; soluble TNF receptors and neopterin in plasma.. No significant changes in HIV RNA plasma levels or CD4+ lymphocyte counts in blood were noted during antioxidant treatment in the patient group. However, in the 5 patients with the most advanced immunodeficiency (CD4+ lymphocyte counts < 200 x 106 L(-1)), a significant rise in CD4+ lymphocyte count, a reduction in HIV RNA plasma level of 0.8 log, an enhanced lymphocyte proliferation and an increased level of intracellular glutathione in CD4+ lymphocytes were found. No change in lymphocyte apoptosis was noted.. Short-term, high-dose combination treatment with NAC and vitamin C in patients with HIV infection and advanced immunodeficiency lead to immunological and virological effects that might be of therapeutic value.

Topics: Acetylcysteine; Acquired Immunodeficiency Syndrome; Adult; Antioxidants; Antiviral Agents; Apoptosis; Ascorbic Acid; CD4-CD8 Ratio; CD4-Positive T-Lymphocytes; Cell Division; Cysteine; Dipeptides; Drug Therapy, Combination; Glutathione; Humans; Interleukin-10; Lipopolysaccharide Receptors; Male; Middle Aged; Monocytes; Neopterin; Oxidative Stress; Pilot Projects; Receptors, Tumor Necrosis Factor; Solubility; Tumor Necrosis Factor-alpha

Past studies document decreased levels of antioxidants and selenium and increased levels of oxidative stress in people living with HIV/acquired immunodeficiency syndrome (AIDS). Cigarette smoking is another source of oxidative stress. Excessive oxidative stress can induce HIV replication, resulting in disease progression. The purpose of this study was to determine whether subjects with HIV/AIDS who smoke cigarettes have increased oxidative stress and decreased antioxidant status compared with nonsmokers with HIV/AIDS.. Thirty-one men with HIV/AIDS (adhering to highly active antiretroviral therapy for the previous 3 months) were recruited during regular visits to a Veterans Affairs Medical Center Infectious Disease Clinic in a southeastern US city. Plasma was obtained from a 1-time blood draw for this comparison study. Plasma lipid peroxide (LPO) was used as a marker of oxidative stress. Indicators of antioxidant capacity included plasma glutathione peroxidase (GPx, the functional indicator of selenium status), vitamin C, and antioxidant potential (AOP).. Fifteen smokers and 10 nonsmokers with HIV/AIDS were enrolled. Median plasma LPO level was above the normal range of 0-1.3 micromol/L in both nonsmokers (2.5 [0-23.4] micromol/L, median [range]) and smokers (4.0 [0-47.5] micromol/L), but there was no difference between groups. Plasma GPx concentration was significantly lower in smokers (169 [118-295] mumol/min/L) compared with nonsmokers (197 [149-414] micromol/min/L). Vitamin C and AOP levels were not different between groups.. This pilot study suggests that effects of smoking on oxidative stress are not additive, as no striking differences were observed in oxidative stress or antioxidant capacity between clinically stable smoking and nonsmoking men with HIV/AIDS.

Topics: Acquired Immunodeficiency Syndrome; Antioxidants; Ascorbic Acid; Biomarkers; Cohort Studies; Glutathione Peroxidase; Humans; Longitudinal Studies; Male; Middle Aged; Nutritional Status; Oxidative Stress; Pilot Projects; Smoking; Statistics, Nonparametric

Knowledge of the antioxidant profile and its relation to lipid peroxidation in tuberculosis patients with or without accompanying HIV infection is scarce, particularly in developing countries.. The objective was to further investigate the interaction between HIV, tuberculosis, and antioxidants and their relations with markers of oxidative stress in a large population of Ethiopians.. In a cross-sectional study, we evaluated antioxidants and markers of oxidative stress in Ethiopian tuberculosis patients with (n = 25) and without (n = 100) HIV infection and in Ethiopian (n = 45) and Norwegian (n = 25) healthy control subjects.. Concentrations of the antioxidant vitamins C and E and of vitamin A were significantly lower in tuberculosis patients than in healthy Ethiopians. Tuberculosis patients also had significantly lower thiol concentrations, particularly of the reduced forms. Tuberculosis patients, particularly those who were co-infected with HIV, had higher malondialdehyde concentrations than did control subjects. High malondialdehyde concentrations were associated with clinical severity as measured by the Karnofsky Performance Status Index and anthropometric scores. Ethiopian control subjects had lower concentrations of vitamin E and higher concentrations of malondialdehyde than did Norwegian control subjects.. Our findings further support a link between oxidative stress, tuberculosis, and HIV infection. However, whether antioxidant supplementation will improve tuberculosis outcome or is of importance for its prevention should be further examined in future prospective studies.

Topics: Acquired Immunodeficiency Syndrome; Adult; Antioxidants; Ascorbic Acid; Blood Donors; Case-Control Studies; Cross-Sectional Studies; Ethiopia; Female; Humans; Karnofsky Performance Status; Lipid Peroxidation; Male; Malondialdehyde; Norway; Nutritional Status; Oxidative Stress; Tuberculosis; Vitamin A; Vitamin E

VIP receptor binding in the frontal cortex, a region with substantial neuronal loss, was unaltered in individuals who had died of acquired immunodeficiency syndrome (AIDS) neurotoxicity. In contrast, ascorbic acid, which suppresses human immunodeficiency virus (HIV) replication and modulates glutamatergic neuronal activity, was reduced by nearly 60% in the same brain region. These findings indicate that while neurons containing ascorbic acid may be lost, vasoactive intestinal polypeptide (VIP) receptor bearing cells remain viable. This finding supports previous observations that VIP prevents HIV induced neuronal death. The reduced ascorbic acid levels may contribute to particular neurons being vulnerable to damage from oxidative stress and possibly clinically to the development of dementia.

Topics: Acquired Immunodeficiency Syndrome; Adult; Aged; Ascorbic Acid; Brain Chemistry; Child; Female; Frontal Lobe; Humans; Male; Middle Aged; Receptors, Vasoactive Intestinal Peptide

Topics: Acquired Immunodeficiency Syndrome; Ascorbic Acid; HIV; Humans; Virus Replication

Topics: Acquired Immunodeficiency Syndrome; Ascorbic Acid; Cytotoxicity, Immunologic; HIV; HIV Infections; Humans; In Vitro Techniques; Neoplasms; T-Lymphocytes

Recent evidence suggests that HIV infection and the clinical and laboratory manifestations of acquired immunodeficiency syndrome (AIDS) are a result of the genetic influence of the virus on cellular adrenocorticotrophic hormone (ACTH) and cortisol metabolism. Recent genetic studies substantiate this view with the observation that the HIV-1 genome is linked to glucocorticoid inducibility and to glucocorticoid receptor binding, and may explain the strong ability of cortisol to enhance HIV replication. Adrenocortical hyperactivity observed in HIV-infected individuals has been found to be independent of the hypothalamic-pituitary axis, and is apparently a result of increased ACTH production by HIV. It is proposed that the HIV-induced cortisol excess is the foundation of the immunosuppression seen in AIDS, and is the basis for alternative avenues of treatment, including the use of ascorbic acid.

Topics: Acquired Immunodeficiency Syndrome; Adrenocorticotropic Hormone; Ascorbic Acid; Genome, Viral; Glucocorticoids; HIV; HIV-1; Humans; Hydrocortisone; Lupus Erythematosus, Systemic; Models, Biological; Pituitary Hormones; Receptors, Glucocorticoid; Virus Replication

Topics: Acquired Immunodeficiency Syndrome; Aged; Animals; Ascorbic Acid; Child; Child, Preschool; Guinea Pigs; Humans; Immunity, Maternally-Acquired; Infant; Milk, Human; Nutritional Status; Pyridoxine; Smoking; Tuberculosis; Zinc

The amount of oral ascorbic acid that a patient can tolerate without diarrhea, increases somewhat proportionately to the "toxicity" of his disease. Clinically, in a disease ameliorated by ascorbate, there is a suppression of symptoms only with very high doses and approximately to that extent which a nonrate-limited, antioxidant free radical scavenger, might be expected to affect that disease process if all harmful free radicals and highly reactive oxidizing substances were quenched. In most pathologic processes, the rate at which free radicals and highly reactive oxidants are produced, exceeds the rate at which the ordinary rate-limited antioxidant free radical scavenging mechanisms can quench those free radicals and oxidants. When ascorbate acts as a scavenger, dehydroascorbate is formed; but if the ascorbate/dehydroascorbate (AA/DHA) ratio is kept high (the redox potential kept reducing) until the unstable dehydroascorbate undergoes hydrolysis or can be reduced back to ascorbate, the dehydroascorbate will do no harm. Since even at very high doses, ascorbate is virtually nontoxic, it may be given in the enormous doses necessary to quench almost all unwanted free radicals and oxidants. The wide spectrum of infectious diseases ameliorated by massive doses of ascorbate indicates some common pathologic processes in these diseases.

Topics: Acquired Immunodeficiency Syndrome; Antioxidants; Ascorbic Acid; Ascorbic Acid Deficiency; Diarrhea; Dose-Response Relationship, Drug; Free Radicals; Glucosephosphate Dehydrogenase Deficiency; Humans; Infant; Kidney Calculi; Kinetics; Oxidation-Reduction; Scurvy; Sudden Infant Death

My previous experience with the utilization of ascorbic acid in the treatment of viral diseases led me to hypothesize that ascorbate would be of value in the treatment of AIDS (acquired immune deficiency syndrome). Preliminary clinical evidence is that massive doses of ascorbate (50-200 grams per 24 hours) can suppress the symptoms of the disease and can markedly reduce the tendency for secondary infections. In combination with usual treatments for the secondary infections, large doses of ascorbate will often produce a clinical remission which shows every evidence of being prolonged if treatment is continued. This clinical remission is achieved despite continuing laboratory evidence of helper T-cell suppression. There may be a complete or partial destruction of the helper T-cells during an initial infection that does not necessitate a continuing toxicity from some source to maintain a permanent or prolonged helper T-cell suppression. However, it is possible ascorbate may prevent that destruction if used adequately during that prodrome period. Emphasis is put upon the recognition and treatment of the frequent intestinal parasites. Food and chemical sensitivities occur frequently in the AID syndrome and may aggravate symptoms considered to be part of the AID syndrome. A topical C-paste has been found very effective in the treatment of herpes simplex and, to a lesser extent, in the treatment of some Kaposi's lesions. Increasingly, clinical research on other methods of treating AIDS is being "contaminated" by patients taking ascorbate.

Topics: Acquired Immunodeficiency Syndrome; Administration, Oral; Administration, Topical; Ascorbic Acid; Candida albicans; Free Radicals; Homosexuality; Humans; Intestines; Leukocyte Count; Male; Self Medication; T-Lymphocytes, Helper-Inducer