EFFECTS OF HEAT-STRESS ON MOUSE TESTICULAR CELLS AND SPERM CHROMATIN STRUCTURE

Scrotal regions of mice were exposed to a 38.0, 40.0, or 42.0 degrees C (+/-0.1) H2O bath for 60 minutes to determine the effects of elevate d temperatures on testicular cells and sperm chromatin structure. Mice were killed on various days after exposure, and ratios of acridine or ange-stained testicular cell populations were determined by flow cytom etry. Testicular weights of mice exposed to 42.0 degrees C decreased s ignificantly day 1 (P < 0.01) through 35 (P < 0.001). Also, a signific ant relative decrease in testicular haploid cells was seen on days 3-3 5 (P < 0.001) with a corresponding increase in the diploid population (P < 0.001). Testicular analyses of mice exposed to 38.0 degrees C wer e not significantly different from control values, Testis weights of m ice exposed to 40.0 degrees C were not affected, but a relative decrea se in percent haploid cells occurred on days 11 and 14 (P < 0.001), Th e sperm chromatin structure assay (SCSA) was used to measure the susce ptibility of cauda epididymal sperm DNA to in situ denaturation at low pH. Caudal epididymides of mice exposed to 42.0 degrees C had no sper m. Caudal epididymal sperm from mice exposed to 40.0 degrees C were mo st susceptible to acid-induced DNA denaturation on days 3 (P < 0.05), 7, 11, and 14 (all P < 0.001). The 38.0 degrees C exposed mice showed some minor sperm chromatin abnormalities at later time points (days 11 -35). When compared to sperm head morphology measurements, SCSA parame ters were more sensitive indicators of heal-induced sperm abnormalitie s. These results show that mouse spermatogenesis is disrupted by scrot al exposure to environmental temperatures several degrees over normal physiological temperature and, of more biological interest, that some thermal ranges above normal allowed production of sperm with compromis ed nuclear chromatin structure.