Saturated, unsaturated, and trans-fatty acids modulate oxidative burst induced by high dextrose in human umbilical vein endothelial cells

ObjectiveWe determined whether hyperglycemia-induced oxidative burst is augmented in the presence of saturated, unsaturated, and trans-fatty acids (FAs).MethodsThe time course of superoxide (O2−) production in human umbilical vein endothelial cells treated with 5.5 mM (D100) or 27.5 mM (D500) of dextrose and select FAs were measured using the hydroethidene fluorescence method.ResultsThe rate of O2− production in cells treated with D500 was significantly higher (55% to125% increase) than the rate observed in control cells treated with D100 (P < 0.001). The rate of O2− production (mean ± standard deviation, in arbitrary units) was increased when cells were treated with 250, 500, and 1000 μM of myristic acid (C14; 0.189 ± 0.04, 0.240 ± 0.04, 0.234 ± 0.02, respectively; P > 0.1, P < 0.05, P < 0.05, respectively), palmitate (C16; 0.151 ± 0.03, 0.218 ± 0.01, 0.289 ± 0.07; P > 0.1, P < 0.05, P < 0.01), and stearic acid (C18; 0.321 ± 0.03, 0.259 ± 0.02, 0.341 ± 0.03; P < 0.01 for all comparisons) compared with control cells treated with D100 only (0.184 ± 0.01). In the presence of D500, myristic acid did not significantly augment O2− production, whereas stearic acid caused a significant further increase in O2− production. The cis unsaturated FA (oleic, C18:1; linoleic, C18:2; or linolenic acid, C18:3) stimulated O2− production significantly more than did saturated FA or trans-unsaturated FA such as elaidic, linolelaidic, or linolenelaidic acid.ConclusionsFatty acids have the ability to modulate oxidative load in hyperglycemia and this effect may be related to the length, saturation, and possibly cis/trans orientation of the FA.