Date of Award:

5-1-1981

Document Type:

Dissertation

Degree Name:

Doctor of Philosophy (PhD)

Department:

Biology

Department name when degree awarded

Life Sciences:Biology

Committee Chair(s)

LeGrande C. Ellis

Committee

LeGrande C. Ellis

Committee

Jim Gessaman

Committee

Ray Sanders

Committee

Ross Smart

Committee

Steve Oberg

Abstract

A series of investigations were undertaken to ascertain the cause(s) of excessive male infertility and neonatal kit mortality in finely-bred dark mink. Two mechanisms of testicular sperm transport were examined, testicular capsular contractions and seminiferous tubular contractions, and found to be the same in fertile and infertile dark mink. Spontaneous testicular capsular contractions were absent in both groups of mink. Seminiferous tubular contractions were present in both groups and this appears to be the primary means of sperm transport in the mink testis. Epididymides from infertile animals were devoid of sperm and showed signs of epithelial degeneration (i.e., sperm granuloma). Histological sections of the testes demonstrated degeneration of the germinal epithelium in some animals and failure of the testis to mature in others. Two conditions were described: Primary infertility in which mink were infertile in their first reproductive season and secondary infertility in which mink were fertile for one or more seasons and then were infertile a subsequent year. The etiology of the two conditions was found to differ. Secondary infertile animals exhibited a high incidence of autoimmune testicular orchitis. This condition was infrequent in the primary infertile animals. Testicular and epididymal monamine oxidase, Phospholipase A2 and prostaglandin dehydrogenase activities were compared for fertile and infertile animals. Phospholipase A2 and monoamine oxidase activities were depressed in the testes of the infertile animals. Alpha-melanocyte-stimulating hormone stimulated phospholipase A2 activity in vitro while monamine oxidase activity was depressed. Monoamine oxidase activity was enhanced by beta-melanocyte-stimulating hormone in vitro. Plasma alpha-melanocyte-stimulating hormone levels were higher in dark males when compared to pastel males in February and April. Plasma alpha-melanocyte-stimulating hormone levels were highest in September, diminished in December and lowest in February just prior to breeding. Serum testosterone levels were low in September and December but were high in February. Dark mink had much lower testosterone levels than did pastel or opal males in February. A negative correlation was observed between alpha-melanocyte-stimulating hormone and testosterone levels. Pancreatic glucagon in dark moribund kits was elevated while extra-pancreatic levels were depressed when compared to healthy control animals. No significant differences in pancreatic or extra-pancreatic somatostatin were observed for these two groups of mink. Dark moribund kits exhibited depressed liver glycogen levels and lower pancreatic MAO activity than did the healthy animals. Mortality rates during the first 48-hour postpartum were found to be higher for the dark than for pastel, demi or opal mink. Litter size at birth was smaller in the darks than the other mutant color phases. Dark mink kits were also found to be more sensitive to heat stress than the other color phases. In addition, dark mink whelped earlier than either pearl or sapphire mink. Mortality data on two different strains of dark mink suggested genetic differences between the two groups of animals. The above observations indicate that dark mink are analogous to selected rodent strains that exhibit genetically-determined high incidences of infertility, embryonic death, small body size and other morphological abnormalities. It was suggested that careful selective breeding could eliminate the genes responsible for the negative traits through recombination as has been demonstrated in rodents.

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