029 for MDA, buy Erastin P<0.003 for vitamin A, P<0.012 for zinc and P<0.05 for vitamin E (Table 4). There were no differences, however, in glutathione peroxidase levels (779±79 vs. 788±94 IU/L in the coinfected and monoinfected groups, respectively; P=0.710); plasma selenium levels for all participants were adequate (selenium >0.085 mg/dL) with no significant differences (0.12±0.02 vs. 0.12±0.01 mg/dL in the coinfected and monoinfected groups, respectively;
P=0.901) between the two groups. Glutathione peroxidase, an enzymatic antioxidant, was significantly increased in liver disease, as measured by APRI (β=0.00118, P=0.0082) and FIB-4 (β=0.0029, P=0.0177) or FIB-4>1.45 (β=0.00178, P=0.0287), regardless of HCV status. Vitamin A significantly decreased (β=−0.00581, P=0.0417) as APRI increased. As shown in Table 5, all antioxidants showed a tendency to decrease as the indexes of liver disease increased, and was significantly lower for those identified
by FIB-4 (>1.45) with liver disease. Both HIV Dabrafenib solubility dmso and HCV monoinfections have been recognized as conditions that elevate oxidative stress, which in turn contributes to liver fibrosis, and may be one of the mechanisms involved in the pathogenesis of HCV. There is limited information in the literature, however, on oxidative stress and antioxidant status in HIV/HCV coinfection. Our study shows that the HIV/HCV-coinfected participants had evidence of liver damage as substantiated by significantly increased transaminases, significantly lower levels of plasma albumin,
and elevated APRI and FIB-4 indexes. The HIV/HCV-coinfected participants had significantly higher levels of oxidative stress, demonstrated by elevated plasma levels of MDA, a marker of oxidative stress, and significantly lower levels of plasma antioxidants (vitamins A and E, and zinc), than the HIV-monoinfected group. These relationships remained after adjusting for age, gender, CD4 cell count, HIV RNA viral load and race, and were not related to ART. In addition, glutathione peroxidase levels significantly increased as the markers of liver disease, APRI and FIB-4, increased, Uroporphyrinogen III synthase and were significantly higher in those with FIB-4>1.45. HIV infection increases oxidative stress [11,27,28], which is accompanied by decreased levels of plasma antioxidant micronutrients, including vitamins A and E, zinc and selenium [29,30]. It is also well documented that HCV produces oxidative stress that is more severe than that observed in other inflammatory liver diseases [10,31–33] and is accompanied by reduced hepatic and plasma levels of antioxidants . Increased levels of oxidative stress have been demonstrated in patients monoinfected with HCV [10,31,33,35]. Moreover, oxidative stress in the form of increased MDA levels has been shown to correlate with severity of HCV infection [14,36,37].