Cj. Fuller et al., SUPEROXIDE PRODUCTION AND LDL OXIDATION BY DIABETIC NEUTROPHILS, Journal of diabetes and its complications, 10(4), 1996, pp. 206-210
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.