title: Copper metabolism disorders affect testes structure and gamete quality in male mice.
abstract: In the present study, animals with a genetic defect in copper metabolism were used as a model organism to study the role of copper in reproduction and to determine whether the disturbances in copper and zinc metabolism affect the testicular tissue and gamete quality in males. Mice with an X-linked mosaic mutation (Atp7a(mo-ms)) exhibit pathological features characteristic of affected copper metabolism. This mutation usually leads to lethality of the mutant males which generally expire on about day 16. Only 4% of mutant animals survive the critical period, achieve maturity, and become fertile. To improve the mutants' viability they were treated with subcutaneous injections of cupric chloride. We measured copper and zinc concentration in the gonads of young (14-day-old) and adult (5-month-old) mutant and control males. Results indicate that copper content was increased but zinc was decreased in the mutant testes. Analysis of the morphology of the testis of the young animals indicate that apoptosis (characteristic for the gonads of young males) was increased in the gonads of the 14-day-old mutants. This process was less advanced in the group of 14-day-old copper treated control males. Apoptosis was also increased in the testes of the adult mutants. Moreover in adult mutants we observed pathological changes in testes morphology (atrophic and sclerotic tubules). Copper and zinc disorders also negatively influenced semen quality parameters, including sperm motility, head morphology, tail cytoplasmic membrane integrity, and number of viable spermatozoa. Poor semen quality of the mutant males seems to be responsible for affected in vivo fertilization efficiency. Treatment with cupric chloride did not influence semen quality except in maturation rate, which was even slower in both mutant and control males after treatment. Additionally, in mutants, copulatory plugs and fertile copulation outcome were decreased after copper treatment.
authors.affiliation: Department of Genetics and Evolution, Institute of Zoology, Jagiellonian University, Ingardena 6, Krakow, Poland.
authors.forename: Małgorzata
authors.initials: M
authors.lastname: Kowal
authors.forename: Małgorzata
authors.initials: M
authors.lastname: Lenartowicz
authors.forename: Anna
authors.initials: A
authors.lastname: Pecio
authors.forename: Aniela
authors.initials: A
authors.lastname: Gołas
authors.forename: Teresa
authors.initials: T
authors.lastname: Błaszkiewicz
authors.forename: Jozéfa
authors.initials: J
authors.lastname: Styrna
mesh_terms: D000251:Adenosine Triphosphatases / Q000235:genetics*; D000818:Animals; D017209:Apoptosis; D027682:Cation Transport Proteins / Q000235:genetics*; D003300:Copper / Q000378:metabolism* / Q000494:pharmacology; D000073840:Copper-Transporting ATPases; D008297:Male; D008664:Metal Metabolism, Inborn Errors / Q000503:physiopathology*; D051379:Mice; D009929:Organ Size; D055101:Semen Analysis; D012726:Sexual Behavior, Animal; D013737:Testis / Q000033:anatomy & histology / Q000473:pathology*; D015032:Zinc / Q000378:metabolism
chemical_list: C486201:Atp7a protein, mouse; D027682:Cation Transport Proteins; D003300:Copper; D000251:Adenosine Triphosphatases; D000073840:Copper-Transporting ATPases; D015032:Zinc; C029892:cupric chloride