In order to investigate the effect of fat-rich diets on neutrophil function
s, 21 day-aged rats were fed for 6 weeks with a control diet consisting of
a regular laboratory rodent chow (4 per cent final fat content), a control
diet supplied with soybean oil (15 per cent final fat content), or a contro
l diet supplied with coconut oil (15 per cent final fat content). Glycogen-
elicited peritoneal neutrophils from rats fed soybean and coconut oil-enric
hed diets presented a reduction in spontaneous and PMA-stimulated H2O2 gene
ration relative to neutrophils from rats fed the control diet. The activity
of superoxide dismutase, glutathione peroxidase and catalase did not chang
e in animals fed fat-rich diets. In addition, the capacity to generate O-2(
.-), spontaneously or in response to PMA, did not change in neutrophils fro
m animals fed fat-rich diets. Values attained matched those observed in ani
mals fed the control diet, regardless of the method used to measure O-2(.-)
, the superoxide dismutase-inhibitable reduction of cytochrome c or the luc
igenin-dependent chemiluminescence. However, the initial rate of O-2(.-) ge
neration both in resting neutrophils and in PMA-stimulated cells was signif
icantly reduced when animals were fed with coconut or soybean oil-enriched
diets due, at least in part, to a reduction in the activity of glucose-6-ph
osphate dehydrogenase. The concentration of thiobarbituric acid reactive su
bstances, an index of lipid peroxidation, was increased in animals fed both
fat-rich diets. This was accompanied by an increase in arachidonic acid co
ntent in these cells. Results presented suggest that lipid peroxidation in
neutrophils from animals fed fat-rich diets may be associated with a consum
ption of H2O2 yielding more reactive oxygen-derived species such as the hyd
roxyl radical. Copyright (C) 1999 John Wiley & Sons, Ltd.