Endocrinology, Vol 114, 922-929, Copyright © 1984 by Endocrine Society
The dark mink: a model of male infertility
KS Tung, LE Ellis, GV Childs and M Dufau
Breeding mink for a fine dark fur has coselected male infertility, which
may be manifest at the onset of breeding (primary infertility) or after one
or more fertile breeding seasons (secondary infertility). Mink with primary
infertility have low LH and testosterone levels. However, they respond to
exogenous GnRH with increases in LH production and in the number and size
of LH and FSH positive gonadotropes in the anterior pituitary. Exogenous
human CG also induces testosterone secretion. Thus, mink with primary
infertility are probably defective in GnRH secretion, which is due either
to abnormal hypothalamic function or its control mechanisms. Autoimmune
orchitis with testicular immune complexes are frequent in mink with
secondary infertility, suggesting an autoimmune etiology. In contrast,
fertile dark mink and fertile mink with the opaline and pastel fur have
normal serum LH and testosterone levels; their testes are also normal. In
mink with secondary infertility, the frequency and degree of orchitis and
testicular immune complexes increased from March (peak sexual activity) to
April (onset of testicular regression). Thus, testicular autoimmunity most
likely develops during testicular regression. Antisperm antibodies also
increased in frequency during testicular regression in the fertile dark
mink and in dark mink with primary and secondary infertility. Thus,
antisperm antibody per se is insufficient to induce autoimmune orchitis. It
is concluded that the infertile mink is a useful model of human male
infertility, involving both endocrinological and immunological mechanisms.
