RESPONSES OF BOVINE LYMPHOCYTES TO HEAT-SHOCK AS MODIFIED BY BREED AND ANTIOXIDANT STATUS

Citation
La. Kamwanja et al., RESPONSES OF BOVINE LYMPHOCYTES TO HEAT-SHOCK AS MODIFIED BY BREED AND ANTIOXIDANT STATUS, Journal of animal science, 72(2), 1994, pp. 438-444
Citations number
33
Categorie Soggetti
Agriculture Dairy & AnumalScience
Journal title
ISSN journal
00218812
Volume
72
Issue
2
Year of publication
1994
Pages
438 - 444
Database
ISI
SICI code
0021-8812(1994)72:2<438:ROBLTH>2.0.ZU;2-8
Abstract
We tested whether resistance of lymphocytes to heat stress is modified by breed, intracellular glutathione content, and extracellular antiox idants. In the first experiment, lymphocytes from Angus (Bos taurus, n on-heat-tolerant), Brahman (B. indicus, heat-tolerant), and Senepol (B . taurus, heat-tolerant) heifers (12 heifers per breed) were cultured at 45 degrees C for 3 h to evaluate thermal killing, at 42 degrees C f or 12 h in a 60-h phytohemagglutin-induced proliferation test, and at 42 degrees C for 1 h to measure induction of heat shock protein 70 (HS P70). Killing at 45 degrees C was affected by breed x temperature (P < .01); the decrease in viability caused by a temperature of 45 degrees C was greater for Angus than for Brahman or Senep ol. For phytohemaggl utinin- stimulated lymphocytes, heating to 42 degrees C reduced [H-3]t hymidine incorporation equally for all breeds. Viability at the end of culture was affected (P <.001) by a breed x temperature interaction b ecause the decrease in viability caused by culture at 42 degrees C was greatest for lymphocytes from Angus heifers. Heat shock for 1 h at 42 degrees C caused a two- to threefold increase in intracellular concen trations of HSP70, but there was no interaction of temperature with br eed. In another experiment (with lymphocytes harvested from three Hols tein cows), buthionine sulfoximine, a glutathione synthesis inhibitor, inhibited (P <.01) proliferation of phytohemagglutinin-stimulated lym phocytes at 38.5 and 42 degrees C. Addition of the antioxidants glutat hione or thioredoxin to culture did not reduce the effects of heating to 42 degrees C on proliferation. In summary, lymphocyte resistance to heat shock differed between breeds. There was no evidence that this e ffect is caused by differential HSP70 synthesis. Although intracellula r antioxidant status affected lymphocyte proliferation, exogenous glut athione or thioredoxin did not overcome the effects of heat shock.