Jc. Chapman et al., The differential effect of injecting estradiol-17 beta, testosterone, and hydrocortisone during the immune adaptive period on the fertility of femalemice, AM J REPROD, 46(4), 2001, pp. 288-297
PROBLEM: Female mice injected with estradiol-17 beta (E-2) and testosterone
during the immune adaptive period are infertile as adults. Study I examine
d the effect of the day of injection of E-2 and testosterone on the inciden
ce of infertility in two strains of mice. Study 2 examined the effect of hy
drocortisone on E-2-induced infertility.
METHOD OF STUDY: Study 1: Neonatal (C57BL/6J x A/J)F-1 B6A and (C3H/ HeJ x
129J)F-1 C31 female mice were injected from 0 to 3 and from 3 to 6 days of
age with either 20 mug E-2 or 20 mug testosterone. Animals were tested for
fertility by mating with fertile males. Study 2: Neonatal B6A females were
injected with 20 mug E-2 with/without 1000 mug hydrocortisone on days 1, 3,
5, 7, and 10. At adulthood, ovaries were examined for the presence of corp
ora lutea (CLs).
RESULTS: Study 1: The incidence of E-2-induced infertility in adult B6A and
C31 females decreased over three consecutive matings. In contrast, the inc
idence of testosterone-induced infertility in adult B6A and C31 females inc
reased. E-2 caused the highest incidence of infertility in C31 females when
injected prior to 3 days of age. In B6A mice, E-2 caused the highest incid
ence of infertility when injected after 3 days of age. Study 2: When hydroc
ortisone was injected with E-2, 90% of the B6A females had ovaries with CLs
at 100 days of age. Without hydrocortisone, only 16% of the B6A females in
jected with E-2 had ovaries with CLs.
CONCLUSION: Study 1: The incidence of infertility caused by injections of E
-2 is dependent on the strain of mice and the day(s) injected. The incidenc
e of infertility caused by injections of testosterone is independent of the
strain of mice. Study 2: Hydrocortisone prevents E-2-induced infertility.
It is proposed that injections of E-2 during the immune adaptive period alt
er T-cell maturation, which contributes to E-2-induced infertility.