NADPH-oxidase activity and lipid peroxidation in neutrophils from rats fed fat-rich diets.
In order to investigate the effect of fat-rich diets on neutrophil functions, 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 control diet supplied with coconut oil (15 per cent final fat content). Glycogen-elicited peritoneal neutrophils from rats fed soybean and coconut oil-enriched diets presented a reduction in spontaneous and PMA-stimulated H2O2 generation relative to neutrophils from rats fed the control diet. The activity of superoxide dismutase, glutathione peroxidase and catalase did not change in animals fed fat-rich diets. In addition, the capacity to generate O2-, spontaneously or in response to PMA, did not change in neutrophils from animals fed fat-rich diets. Values attained matched those observed in animals fed the control diet, regardless of the method used to measure O2-, the superoxide dismutase-inhibitable reduction of cytochrome c or the lucigenin-dependent chemiluminescence. However, the initial rate of O2- generation both in resting neutrophils and in PMA-stimulated cells was significantly 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-phosphate dehydrogenase. The concentration of thiobarbituric acid reactive substances, an index of lipid peroxidation, was increased in animals fed both fat-rich diets. This was accompanied by an increase in arachidonic acid content in these cells. Results presented suggest that lipid peroxidation in neutrophils from animals fed fat-rich diets may be associated with a consumption of H2O2 yielding more reactive oxygen-derived species such as the hydroxyl radical.
Lopes
L R
LR
Department of Physiology and Biophysics, University of São Paulo, Brazil.
Laurindo
F R
FR
Mancini-Filho
J
J
Curi
R
R
Sannomiya
P
P
D000818:Animals; D002273:Carcinogens / Q000494:pharmacology; D002374:Catalase / Q000378:metabolism; D000074263:Coconut Oil; D004032:Diet; D005227:Fatty Acids / Q000032:analysis; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006593:Hexokinase / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D015227:Lipid Peroxidation / Q000502:physiology*; D008297:Male; D019255:NADPH Oxidases / Q000378:metabolism*; D009504:Neutrophils / Q000737:chemistry / Q000187:drug effects / Q000201:enzymology*; D016877:Oxidants / Q000378:metabolism; D010938:Plant Oils / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013024:Soybean Oil / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
D002273:Carcinogens; D005227:Fatty Acids; D016877:Oxidants; D010938:Plant Oils; D017392:Thiobarbituric Acid Reactive Substances; D013481:Superoxides; D013024:Soybean Oil; D006861:Hydrogen Peroxide; D005954:Glucosephosphate Dehydrogenase; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D019255:NADPH Oxidases; D006593:Hexokinase; D013755:Tetradecanoylphorbol Acetate; D000074263:Coconut Oil