History of HIV infection and hepatitis A, B or C was obtained from the interview and confirmed serologically and using medical charts. Serological proof of coinfection with HCV and HIV was obtained using the Procleix HIV-1/HCV nucleic acid testing kit (Gen-Probe, San Diego, CA, USA) [23]. Plasma MDA was tested as the marker of oxidative stress using the TBAR kit (ZeptoMetrix, Buffalo, NY, USA). In this test, thiobarbituric acid was reacted with MDA, and the concentration of MDA in plasma determined by fluorimetry at an excitation wavelength of 530 nm and emission of 550 nm. Plasma glutathione peroxidase activity was determined using the Total Glutathione Peroxidase assay kit (ZeptoMetrix).

Plasma levels of zinc and selenium were determined by flame atomic absorption spectrophotometry. Plasma vitamin A and vitamin E levels were determined by BVD-523 molecular weight high-performance liquid chromatography (HPLC). Weight and height were obtained in participants wearing light clothing and no shoes utilizing a standard scale calibrated prior to each measurement. Height was measured with the participant’s heels touching the base of the vertical board of the stadiometer. The moveable headboard was brought to the most superior point on the head with sufficient pressure to compress the hair. Body mass index (BMI) was calculated using the standard formula that divides weight in kilograms by the square of height in

metres (kg/m2). To estimate liver disease stage, we calculated the aminotransferase to platelet ratio index (APRI) and fibrosis index (FIB-4) indexes, Sorafenib molecular weight which include routine tests to predict liver fibrosis in patients with HIV/HCV coinfection [24]. The objectives were (1) to determine whether there was a significant difference in the proportion and degree of liver damage between the HIV/HCV-coinfected and HIV-monoinfected groups and (2) to determine whether there was a relationship between the stage of

liver disease and oxidative stress and plasma antioxidants, regardless of the aetiology of liver damage and HCV status. The APRI was calculated according to the formula: [AST (× upper limit of normal range) × 100]/platelet count (109 cells/L). The upper limit of normal for the present study was 0.45. The FIB-4 formula uses age and the relatively inexpensive test of transaminases (AST and ALT) and platelet counts Lonafarnib mouse (PLT): [age (years) × AST (U/L)]/[PLT (109 cells/L) × ALT1/2 (U/L)]. At a cut-off of <1.45, the negative predictive value to exclude advanced fibrosis (stages 4–6 of the Ishak scale) was 90% with a sensitivity of 70%. A cut-off of >3.25 had a positive predictive value of 65% and a specificity of 97% to predict advanced disease [24]. Animal and human studies have associated obesity, type 2 diabetes and hypertriglyceridaemia with increased oxidative stress and nonalcoholic liver disease [25,26]. For this reason, only the values for participants without diabetes, whose BMI was <28 kg/m2, and who had plasma triglycerides <150 mg/dL were used in the final analysis.