title: Growth and physiological responses to toxicosis in lines of mice selected for resistance or susceptibility to endophyte-infected tall fescue in the diet.
abstract: In three experiments, mice from lines selected for resistance (R) or susceptibility (S) to growth depression from endophyte-infected fescue seed in the diet were fed diets containing infected (E+) or non-infected (E-) seed. Activities of liver enzymes known to participate in oxidation, reduction, or hydrolysis or in conjugation of xenobiotics were measured in these mice. In all experiments, E+ caused greater reduction in initial ADG of S than of R mice. In Exp. 1, liver cytochromes P450 and b5 activities were not affected by line, diet, or their interaction. These enzymes were not evaluated in subsequent experiments. In all experiments, glutathione-S-transferase (GST) and uridine diphosphate glucuronosyltransferase (GRT) activities differed between lines. Resistant mice had significantly higher GST activity on both diets in Exp. 1, on E- in Exp. 2, and on E+ in Exp. 3. Resistant mice had higher GRT activities on E+ in Exp. 1, on E- in Exp. 2, but after 4 wk on either diet in Exp. 3. Before test diets were imposed in Exp. 3, GST and GRT activities were higher in R-line mice. Divergent selection created lines that differed in response to tall fescue in the diet. Postweaning growth of resistant mice was less severely depressed by E+, although susceptible mice later expressed compensatory gain. Activities of two detoxification enzymes generally were higher in livers from R-line mice, suggesting a biochemical mechanism for the difference. Using such traits, it may be possible to select ruminants for resistance to fescue toxicosis.
authors.affiliation: Department of Animal and Poultry Science, Virginia Polytechnic Institute, Blacksburg 24061-0306, USA.
authors.forename: W D
authors.initials: WD
authors.lastname: Hohenboken
authors.forename: D J
authors.initials: DJ
authors.lastname: Blodgett
mesh_terms: D000818:Animals; D001947:Breeding; D005260:Female; D020022:Genetic Predisposition to Disease; D005982:Glutathione Transferase / Q000032:analysis; D006128:Growth / Q000235:genetics / Q000502:physiology; D006868:Hydrolysis; D008099:Liver / Q000201:enzymology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR / Q000235:genetics* / Q000254:growth & development / Q000502:physiology*; D008954:Models, Biological; D010084:Oxidation-Reduction; D010939:Plant Poisoning / Q000503:physiopathology / Q000517:prevention & control / Q000662:veterinary*; D006109:Poaceae / Q000382:microbiology*; D012641:Selection, Genetic; D015430:Weight Gain / Q000502:physiology
chemical_list: D005982:Glutathione Transferase