Supplementation with commercial mixtures of conjugated linoleic acid in association with vitamin E and the process of lipid autoxidation in rats.
CLA has been studied for its beneficial effects on health. However, the possibility of adverse effects, such as increased oxidative stress, must also be considered. The present work aims to assess the effect of CLA supplementation on the process of lipid autoxidation, both in the presence and in absence of an antioxidant. The investigation consisted in a biological assay with 60 rats divided into six groups: C (control), CE (control + vitamin E), AE (AdvantEdgeCLA), AEE (AdvantEdgeCLA + Vitamin E), CO (CLA One) and COE (CLA One)+ vitamin E). The CLA amount was 2% of feed consumption. Animals were supplemented for 42 days. As indicators of lipid autoxidation, peroxide (IP), malondialdehyde (MDA), 8-iso-PGF2(alpha) isoprostane and catalase were determined. Hepatic IP results indicated that CLA increased oxidation: values for CLA-supplemented groups, particularly group CO (84.38 +/- 10.97 mequiv/kg), were higher than those of the control group (54.75 +/- 9.70 mequiv/kg). In contrast, serum MDA results showed that CLA reduces oxidation both for group AE (1.8 +/- 0.67 mg of MDA/l) and for group CO (2.43 +/- 0.61 mg of MDA/l) as compared to the control group (3.85 +/- 0.24 mg of MDA/l). Serum catalase indicated a reduction of oxidation: groups AE and CO displayed 4734.23 +/- 1078.93 kU/l and 5916.06 +/- 2490.71 kU/l, respectively. These values are significantly lower than those of the control group. An increase in 8-iso-PGF2(alpha) in urine was observed, particularly in group AE (95.13 +/- 20.26 pg/ml) as compared to the control group (69.46 +/- 16.65 pg/ml). It was concluded that the influence of CLA on lipid autoxidation is dependent on supplement type, supplement dosage and chosen indicator, including its tissue and determination methodology.
Santos-Zago
Lilia Ferreira
LF
Laboratory of Lipids, Department of Food and Nutrition, College of Food Engineering, State University of Campinas, P.O. Box 6121, Campinas, SP, 13083-862, Brazil. lzago@fea.unicamp.br
Botelho
Adriana Prais
AP
de Oliveira
Admar Costa
AC
D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology*; D019587:Dietary Supplements; D015237:Dinoprost / Q000031:analogs & derivatives / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D044243:Linoleic Acids, Conjugated / Q000008:administration & dosage / Q000494:pharmacology*; D050356:Lipid Metabolism / Q000187:drug effects*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D010084:Oxidation-Reduction / Q000187:drug effects; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014810:Vitamin E / Q000008:administration & dosage / Q000494:pharmacology*
D000975:Antioxidants; D044243:Linoleic Acids, Conjugated; D014810:Vitamin E; C075750:8-epi-prostaglandin F2alpha; D008315:Malondialdehyde; D015237:Dinoprost