Total antioxidant capacity – a novel early bio-chemical marker of oxidative stress in HIV infected individuals

Total antioxidant capacity (TAC) and lipid peroxidation were evaluated in 50 HIV-1 seropositive patients (including HIV-1 symptomatics and asymptomatics). Controls included 50 age and sex matched and apparently healthy HIV-1 seronegative subjects. Serum malondialdehyde (MDA), Total antioxidant capacity [TAC] (by ferric reducing antioxidant power assay), vitamin E, vitamin C and superoxide dismutase (SOD) enzyme activity were estimated among controls and cases. Statistical comparisons and correlations at 5% level of significance were determined.The mean MDA concentrations were significantly elevated in both HIV-1 asymptomatic (CD4+ count > 500 cells/microliter) and HIV-1 symptomatic (CD4+ count <500 cells/microliter) groups (Mean ± S.D values were 2.2 +/- 0.7 nmol/ml and 2.8 +/- 0.8 nmol/ml respectively) when compared with the control group (Mean ± S.D value was 0.9 +/- 0.2 nmol/ml) (p < 0.01). The mean TAC of HIV- 1 asymptomatic and HIV-1 symptomatic (Mean ± S.D values were 754.6 ± 135.6 μmol/L and 676.6 ± 154.1 μmol/L respectively) patients were significantly reduced compared with the control group (Mean ± S.D value was 1018.7 ± 125.6 μmol/L) (p < 0.01). Also, there were significantly decreased levels of vitamin E, vitamin C and SOD among HIV-1 seropositive patients(controls > asymptomatic > symptomatic) compared to controls (p < 0.01). TAC showed significant negative correlation with MDA among HIV-1 infected patients (p < 0.01).Our results clearly show that severe oxidative stress occurs in the HIV-1 seropositive patients in comparison with controls, and increases significantly with the progression of disease, i.e. HIV-1 symptomatics > asymptomatics > controls. TAC can be used as a novel early bio-chemical marker of oxidative stress in HIV-1 infected patients which may result in reduced tissue damage by free radicals and help to monitor and optimize antioxidant therapy in such patients.HIV infection is characterized by numerical and functional decline in CD4 cells