title: Dietary supplementation with 11trans- and 12trans-18:1 and oxidative stress in humans.
abstract: BACKGROUND
  High consumption of trans fat has been associated with high oxidative stress in humans, which could increase the risk of the development or acceleration of several diseases, such as atherosclerosis, cancer, and type 2 diabetes.
  
  
  OBJECTIVE
  Several urinary and blood biomarkers of oxidative stress [8-iso-prostaglandin-F(2alpha) (PGF(2alpha)), 15-keto-dihydro-PGF(2alpha), and 7,8-dihydro-8-oxo-2'-deoxy-guanosine in urine and alpha-,beta-,gamma-,delta-tocopherol, and retinol in plasma] were monitored to evaluate the oxidative stress induced by dietary supplementation of 11trans- and 12trans-18:1 isomers in humans during a 6-wk intervention.
  
  
  METHODS
  After a 14-d adaptation period free of trans fatty acid supplementation (baseline), the test group (n = 12) received 3.0 g 11trans-18:1/d and 3.0 g 12trans-18:1/d (Sigma 6.0 g/d), and the control group (n = 12) consumed a control oil free of trans fatty acids and conjugated linoleic acids for 6 wk.
  
  
  RESULTS
  The postintervention concentration of urinary 8-iso-PGF(2alpha) (free radical-induced lipid peroxidation) in the test group was significantly higher than baseline and significantly higher than that observed in the control group. The concentrations of 15-keto-dihydro-PGF(2alpha) (cyclooxygenase-mediated inflammatory response indicator) and 7,8-dihydro-8-oxo-2'-deoxy-guanosine (oxidative DNA damage) were not affected by the 11trans- and 12trans-18:1 supplementation.
  
  
  CONCLUSIONS
  Although an increase in urinary 8-iso-PGF(2alpha) was observed and the effects of prolonged high (ie, >5.0 g/d) consumption of trans fat could be relevant to the development of disease, the mean intakes of 11trans- and 12trans-18:1 in Europeans are estimated to be significantly below the amounts administered in this study (ie, 6.0 g/d); such low intakes could minimize the possible risk of detrimental effects on human health.
authors.affiliation: Institute of Nutrition, Friedrich Schiller University, Jena, Germany.
authors.forename: Katrin
authors.initials: K
authors.lastname: Kuhnt
authors.forename: Andreas
authors.initials: A
authors.lastname: Wagner
authors.forename: Jana
authors.initials: J
authors.lastname: Kraft
authors.forename: Samar
authors.initials: S
authors.lastname: Basu
authors.forename: Gerhard
authors.initials: G
authors.lastname: Jahreis
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000284:Administration, Oral; D000328:Adult; D000975:Antioxidants / Q000378:metabolism; D015415:Biomarkers / Q000097:blood / Q000652:urine; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000652:urine; D019587:Dietary Supplements; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D013237:Stereoisomerism; D024505:Tocopherols / Q000097:blood; D044242:Trans Fatty Acids / Q000008:administration & dosage*; D014801:Vitamin A / Q000097:blood
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D044242:Trans Fatty Acids; D014801:Vitamin A; C008228:15-keto-13,14-dihydroprostaglandin F2alpha; C075750:8-epi-prostaglandin F2alpha; D000080242:8-Hydroxy-2'-Deoxyguanosine; D015237:Dinoprost; D003849:Deoxyguanosine; D024505:Tocopherols