title: Antioxidant enzymes and atherosclerosis in Japanese quail: heritability and genetic correlation estimates.
abstract: OBJECTIVE
  To estimate, in male quail susceptible to atherosclerotic plaque formation (SUS) fed a regular diet and an atherogenic diet, the genetic and phenotypic parameters associated with antioxidant enzymes and atherogenesis.
  
  
  METHODS
  Genetic parameters were estimated from variance components of the analysis of variance on 70 males from 13 full-sib families.
  
  
  RESULTS
  Under the regular diet, seven of 35 males developed mild atherosclerosis. Heritability was zero for atherosclerotic plaque score and plasma cholesterol level. Plaque score was highly correlated to plasma triglyceride level (rp = 0.96) and liver fattiness (rp = 0.97), but only moderately to plasma cholesterol level (rp = 0.39). With the high cholesterol diet, plasma cholesterol level increased sixfold and became heritable (h2 = 0.4). Many males developed severe atherosclerosis. Plaque score became associated more with plasma and aortic cholesterol levels (rp = 0.56) and 0.76, respectively) than with plasma triglyceride level (rp = 0.54). Aortic glutathione reductase activity was negatively correlated with plaque score (rp = -0.42; rg = -0.51) and aortic cholesterol level (rp = -0.39; rg = -0.62).
  
  
  CONCLUSIONS
  Plasma triglyceride level was an important factor affecting the development of fatty streaks and the early progression of atherosclerotic plaques. Without high levels of dietary cholesterol in the plasma and aorta, any early atherosclerotic plaques that developed did not progress further within the time-frame of the experiment. Aortic cholesterol concentration and glutathione reductase activity were important factors in the advancement of severe plaque formation. Heritability of plaque score was high in the SUS line, and further selective breeding should increase the susceptibility of these quail to cholesterol-induced atherosclerosis.
authors.affiliation: Department of Animal Science, University of British Columbia, Vancouver. kmtc@unixg.ubc.ca
authors.forename: K M
authors.initials: KM
authors.lastname: Cheng
authors.forename: S E
authors.initials: SE
authors.lastname: Aggrey
authors.forename: C R
authors.initials: CR
authors.lastname: Nichols
authors.forename: M E
authors.initials: ME
authors.lastname: Garnett
authors.forename: D V
authors.initials: DV
authors.lastname: Godin
mesh_terms: D000818:Animals; D001011:Aorta / Q000201:enzymology / Q000473:pathology; D001161:Arteriosclerosis / Q000150:complications / Q000235:genetics* / Q000473:pathology; D002784:Cholesterol / Q000097:blood / Q000235:genetics*; D002791:Cholesterol, Dietary / Q000008:administration & dosage; D003370:Coturnix; D004036:Diet, Atherogenic; D004195:Disease Models, Animal; D005234:Fatty Liver / Q000150:complications / Q000235:genetics; D005979:Glutathione Peroxidase / Q000097:blood / Q000235:genetics / Q000378:metabolism; D005980:Glutathione Reductase / Q000235:genetics* / Q000378:metabolism; D008297:Male; D010641:Phenotype; D014280:Triglycerides / Q000097:blood*
chemical_list: D002791:Cholesterol, Dietary; D014280:Triglycerides; D002784:Cholesterol; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase