SUPEROXIDE PRODUCTION AND LDL OXIDATION BY DIABETIC NEUTROPHILS

The mechanism(s) resulting in the premature atherosclerosis of diabete s is unknown. Increased phagocyte release of reactive oxygen species s uch as superoxide anion (O-2(-)), resulting in low-density lipoprotein (LDL) oxidation, could be one possible cause. The purpose of the pres ent study was to compare the abilities of polymorphonuclear leukocytes (PMN) from 12 non-insulin-dependent diabetes mellitus (NIDDM) subject s free of vascular disease to produce O-2(-) anion and oxidize LDL wit h PMN from age- and gender-matched normoglycemic controls. PMN were ac tivated with phorbol 12-myristate 13-acetate (PIMA) to measure O-2(-) production. In addition, the PMN were activated with PMA and opsonized zymosan (OZ) to assess LDL oxidation over 5 hours. LDL oxidation was measured by conjugated diene formation and apolipoprotein B (ape B) fl uorescence. PMN superoxide production stimulated by PMA was similar be tween groups. LDL oxidation by PMN was also not different between the NIDDM and control groups. The results of this study indicate that PMN O-2(-) production and LDL oxidation are not enhanced in NIDDM subjects without vascular disease. Other factors, such as reduced antioxidant concentrations and non-enzymatic glycation of LDL, may play a greater role in the premature atherosclerosis of diabetes.