Total plasma antioxidant capacity in cystic fibrosis.

Abstract

Several studies have demonstrated ongoing oxidative stress in cystic fibrosis (CF). With the complexity of the antioxidant network, measurement of individual antioxidants does not necessarily assess how they work in combination. One measure that has been proposed as a gauge of total plasma antioxidant capacity is the Trolox-equivalent antioxidant capacity (TEAC) of plasma. We decided to look at plasma TEAC levels in children with CF, and relate this measure to their nutritional status, lung function, and blood measurements of several known antioxidants. We hypothesized that values in general would be lower than healthy control values, especially during acute pulmonary exacerbations. Twenty-nine children were evaluated, five of whom were during an acute pulmonary exacerbation. Height and weight, expiratory spirometry, and lung volumes were assessed, as were serum concentrations of vitamins A and E, uric acid, albumin, and lymphocyte glutathione (GSH) concentrations. TEAC values for nonhospitalized patients (1.40 +/- 0. 20 mmol/L) were not different from laboratory control values (1.35 +/- 0.11 mmol/L), but greater than values for hospitalized patients (1.09 +/- 0.17 mmol/L). TEAC correlated with anthropometric values (height: r = 0.39, P < 0.03; weight: r = 0.50, P < 0.01; body mass index: r = 0.47, P < 0.01), and pulmonary function (forced expiratory volume in 1 sec: r = 0.43, P < 0.02; residual volume/total lung capacity: r = -0.42, P < 0.03), but not with age. Univariate correlation with blood measurements demonstrated a significant correlation of TEAC with uric acid (r = 0.49, P < 0.02), but not with albumin, vitamins A or E, or lymphocyte GSH. Multiple regression analysis demonstrated a correlation between TEAC and uric acid, albumin, and lymphocyte GSH in the non-hospitalized group (r(2) = 0.38, P < 0.03). We conclude that TEAC appears to represent a mixed antioxidant response, rather than response to a single antioxidant. While being responsive to oxidative stress, the mechanism of the response may differ between clinical situations, such that the clinical significance of changes in plasma TEAC remains to be defined.