title: Enhanced oxidative damage induced by total body irradiation in mice fed a low protein diet.
abstract: OBJECTIVE
  To examine the influence of the level of dietary protein on oxidative damage to lipid and protein in the liver and on chromosomal damage in the bone marrow after total body irradiation (TBI).
  
  
  METHODS
  Male mice were fed a low (7%), basal (20%) or high (33%) protein diet for 3 weeks, and then received TBI at a dose of 0, 0.5 or 1 Gy. Chromosomal damage in the bone marrow was evaluated by determining the proportion of micronucleated reticulocytes in peripheral blood. Oxidative damage in the liver and plasma, and chromosomal damage in the bone marrow were evaluated on day 2 after TBI.
  
  
  RESULTS
  The levels of lipid peroxides and protein carbonyls in the liver, lipid peroxides in the plasma, and chromosomal damage in the bone marrow, did not differ among the groups that did not receive TBI. However, the oxidative damage to lipid and protein in the liver, and the level of lipid peroxides in the plasma were increased by TBI only in the low protein group. Chromosomal damage in the bone marrow was increased by TBI in a dose-dependent manner, and the damage was consistently higher in the low protein group than in the basal and high protein groups. In the low protein group, a greater decrease of the relative spleen weight by TBI was also observed. The concentrations of antioxidants (vitamin C, E and GSH) in the liver were lower, and the concentration of non-heme iron in the liver was higher in the low protein group than in the basal and high protein groups. The TBI-induced increase in the level of plasma iron was greater in the low protein group.
  
  
  CONCLUSIONS
  Mice fed a low protein diet became susceptible to TBI-induced oxidative damage, and a decrease in antioxidants and an increase in iron are involved in the mechanism of this susceptibility.
authors.affiliation: Department of Food Science Research for Health, National Institute of Health and Nutrition, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8636, Japan.
authors.forename: S J
authors.initials: SJ
authors.lastname: Shin
authors.forename: K
authors.initials: K
authors.lastname: Yamada
authors.forename: A
authors.initials: A
authors.lastname: Sugisawa
authors.forename: K
authors.initials: K
authors.lastname: Saito
authors.forename: T
authors.initials: T
authors.lastname: Miyajima
authors.forename: K
authors.initials: K
authors.lastname: Umegaki
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001205:Ascorbic Acid / Q000378:metabolism; D004249:DNA Damage; D018753:Diet, Protein-Restricted; D004044:Dietary Proteins / Q000008:administration & dosage; D005978:Glutathione / Q000378:metabolism; D007501:Iron / Q000378:metabolism; D050356:Lipid Metabolism; D008055:Lipids / Q000528:radiation effects; D008099:Liver / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009929:Organ Size / Q000528:radiation effects; D018384:Oxidative Stress / Q000528:radiation effects; D011506:Proteins / Q000378:metabolism / Q000528:radiation effects; D011836:Radiation Tolerance; D013154:Spleen / Q000473:pathology / Q000528:radiation effects; D014810:Vitamin E / Q000378:metabolism; D014916:Whole-Body Irradiation
chemical_list: D000975:Antioxidants; D004044:Dietary Proteins; D008055:Lipids; D011506:Proteins; D014810:Vitamin E; D007501:Iron; D005978:Glutathione; D001205:Ascorbic Acid