In utero and lactational exposure of the male Holtzman rat to 2,3,7,8-tetrachlorodibenzo-p-dioxin: decreased epididymal and ejaculated sperm numbers without alterations in sperm transit rate.

Decreased daily sperm production (DSP) and cauda epididymal sperm number (CESN) are some of the most sensitive effects of in utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure. The reduction in CESN cannot be fully accounted for by decreased spermatogenesis. To explain the decrease in CESN it was hypothesized that TCDD exposure increases the rate of sperm transit through the excurrent duct system, thereby decreasing the number of sperm in the system at any given time. Pregnant Holtzman rats were administered a single dose of TCDD (1.0 microgram/ kg,po) or vehicle on gestation day 15 and offspring were weaned on postnatal day (PND) 21. On PND 50, testicular sperm were labeled in five males per litter, from 30 control and 26 TCDD-exposed litters, by injecting 15 microCi [3H]thymidine into each testis, under general anesthesia. Sperm movement through the excurrent duct system was monitored daily 35-64 days post [3H]thymidine injection. On PNDs 92-93, TCDD exposure significantly decreased DSP/testis, corpus and cauda epididymis sperm numbers, vas deferens sperm number, and ejaculated sperm number by 28, 30, 36, 39, and 46%, respectively. The decreases in sperm number in the distal excurrent duct system were greater than the decrease in DSP, consistent with the hypothesis that TCDD exposure causes an effect other than decreased DSP that reduced epididymal and ejaculated sperm numbers. However, in utero and lactational TCDD exposure did not alter radiolabeled sperm transit time through the whole epididymis (15 days). With TCDD exposure causing no obvious alteration in sperm transit rate, a plausible explanation for the sperm loss is an increase in sperm phagocytosis in the excurrent duct system.