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

We tested whether resistance of lymphocytes to heat stress is modified by breed, intracellular glutathione content, and extracellular antioxidants. In the first experiment, lymphocytes from Angus (Bos taurus, non-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 for 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 (HSP70). 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 phytohemagglutinin- stimulated lymphocytes, heating to 42 degrees C reduced [H-3]thymidine incorporation equally for all breeds. Viability at the end of culture was affected (P <.001) by a breed x temperature interaction because 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 concentrations of HSP70, but there was no interaction of temperature with breed. In another experiment (with lymphocytes harvested from three Holstein cows), buthionine sulfoximine, a glutathione synthesis inhibitor, inhibited (P <.01) proliferation of phytohemagglutinin-stimulated lymphocytes at 38.5 and 42 degrees C. Addition of the antioxidants glutathione 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 effect is caused by differential HSP70 synthesis. Although intracellular antioxidant status affected lymphocyte proliferation, exogenous glutathione or thioredoxin did not overcome the effects of heat shock.