RESUMO
Tertiary trisomic males, carrying the small translocation chromosome from the T(1;13)7OH reciprocal mouse translocation as the extra chromosome, are oligospermic. Uterine and oviductal sperm counts were congruent to 10% of normal. Of the uterine spermatozoa, 77-2% were morphologically abnormal compared with 24-6% in the oviduct. Oligospermy in the tertiary trisomic males leads to delayed fertilization; 34-8% of the 109 eggs scored between 5-5--9-5 hr after mating were fertilized compared with 52-1% (n=343) at Day 2. Of the 179 morulae/blastocysts recovered at Day 4, 46-9% contained the small marker chromosome, which agrees with earlier cytological studies on secondary spermatocytes. These results indicate that euploid and aneuploid spermatozoa are formed in about equal numbers and there is no relationship between sperm morphology and karyotype.
PIP: Studies on sperm function and viability of eggs fertilized by tertiary trisomic male mice carrying the small translocation chromosome t(1; 13)7 OH were conducted. These males are oligospermic: 10 percent of normal sperm numbers were found in uterus and oviduct. 77.2 percent of uterine and 24.6 percent of oviduct spermatozoa were abnormal, usually having aberrant tail attachment and symmetrical heads. Delayed fertilization was suggested since only 34.8 percent of eggs were fertilized by 5.5-9.5 hours after mating, compared with 100 percent in contols; control eggs were in a more advanced stage of development; and on Day 2 50.1 percent of trisomic and 95.5 percent of control eggs were fertilized. Of 179 morulae or blastocysts karyotyped on Day 4, 46.9 percent contained the marker chromosome, indicating 1:1 segregation of meiosis. The sex ratio determined by C-banding was 103.5 males per 100 females. The trisomic males became less fertile with age. Those with abnormal incisors produced smaller litters. The results indicate that eupoloid and aneuploid spermatozoa are formed in equal numbers, and sperm karyotype does not effect sperm morphology or function.
