title: Ubiquinol reduces gamma glutamyltransferase as a marker of oxidative stress in humans.
abstract: BACKGROUND
  The reduced form of Coenzyme Q10 (CoQ10), ubiquinol (Q10H2), serves as a potent antioxidant in mitochondria and lipid membranes. There is evidence that Q10H2 protects against oxidative events in lipids, proteins and DNA. Serum gamma-glutamyltransferase (GGT) activity is associated with cardiovascular diseases. In a physiological range, activity of GGT is a potential early and sensitive marker of inflammation and oxidative stress.In this study, we first examined the relationship between CoQ10 status and serum GGT activity in 416 healthy participants between 19 and 62 years of age in a cross-sectional study (cohort I). In the second step, 53 healthy males (21-48 years of age; cohort II) underwent a 14-day Q10H2 supplementation (150 mg/d) to evaluate the effect of Q10H2 supplementation on serum GGT activity and GGT1 gene expression.
  
  
  RESULTS
  There was a strong positive association between CoQ10 status and serum GGT activity in cohort I. However, a gender-specific examination revealed differences between male and female volunteers regarding the association between CoQ10 status and serum GGT activity. Q10H2 supplementation (cohort II) caused a significant decrease in serum GGT activity from T0 to T14 (p < 0.001). GGT1 mRNA levels declined 1.49-fold after Q10H2 supplementation. Of note, other liver enzymes (i.e., aspartate aminotransferase, AST) were not affected by Q10H2 supplementation.
  
  
  CONCLUSIONS
  CoQ10 level is positively associated with serum GGT activity. Supplementation with Q10H2 reduces serum GGT activity. This effect might be caused by gene expression. Overall, we provide preliminary evidence that higher Q10H2 levels improve oxidative stress via reduction of serum GGT activity in humans.
  
  
  BACKGROUND
  Current Controlled Trials ISRCTN26780329.
authors.forename: Simone
authors.initials: S
authors.lastname: Onur
authors.forename: Petra
authors.initials: P
authors.lastname: Niklowitz
authors.forename: Gunnar
authors.initials: G
authors.lastname: Jacobs
authors.forename: Ute
authors.initials: U
authors.lastname: Nöthlings
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Lieb
authors.forename: Thomas
authors.initials: T
authors.lastname: Menke
authors.affiliation: Institute of Human Nutrition and Food Science, Division of Molecular Prevention, Christian Albrechts University Kiel, Heinrich-Hecht-Platz 10, 24118 Kiel, Germany. sek@molprev.uni-kiel.de.
authors.forename: Frank
authors.initials: F
authors.lastname: Döring
mesh_terms: D000328:Adult; D000975:Antioxidants / Q000008:administration & dosage / Q000378:metabolism*; D015415:Biomarkers / Q000097:blood; D019587:Dietary Supplements; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D018384:Oxidative Stress; D012307:Risk Factors; D014451:Ubiquinone / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000097:blood; D005723:gamma-Glutamyltransferase / Q000097:blood*
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D014451:Ubiquinone; D005723:gamma-Glutamyltransferase; C024989:coenzyme Q10; C003741:ubiquinol