Open AccessDetection of mitomycin C‐induced testicular toxicity by micronucleus assay in mice
Author(s) -
Nakagawa Soichi,
Mori Chisato
Publication year - 2003
Publication title -
reproductive medicine and biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.005
H-Index - 22
eISSN - 1447-0578
pISSN - 1445-5781
DOI - 10.1046/j.1445-5781.2003.00023.x
Subject(s) - spermatocyte , mitomycin c , apoptosis , biology , micronucleus test , microbiology and biotechnology , spermatogenesis , comet assay , dna damage , andrology , micronucleus , germ cell , cancer research , dna , toxicity , genetics , meiosis , medicine , endocrinology , gene
Background, Aims and Methods: Mitomycin C is a promising cancer agent that has been shown to inhibit DNA synthesis. Our previous study showed that mitomycin C induces spermatogenic cell apoptosis in the mouse testis. By using TdT‐mediated dUTP‐biotin nick‐end labeling in the study, we confirmed that apoptotic cell death was most commonly found in the spermatogonia and less frequently found in spermatocytes in mitomycin C‐treated mice. We therefore hypothesized that the spermatogenic cell apoptosis induced by mitomycin C occurred as the result of a mechanism to eliminate male germ cells with DNA damage or chromosomal aberrations. To test our hypothesis, we used a micronucleus assay for the detection of chromosomal damage induced in the spermatogonia or spermatocyte stages. Results and Conclusions: The frequency of micronuclei was clearly increased in the mitomycin C‐treated animals, and the number of micronuclei was greater at the spermatogonia or early spermatocyte stage than at the secondary spermatocyte stage. These results revealed that apoptosis and chromosomal aberration in the mouse testis after mitomycin C treatment occurred in the same cell types, that is, spermatogonia and spermatocytes. These findings indicate that chromosomal aberration of the spermatogenic cells induced by mitomycin C may have caused the spermatogenic cell apoptosis. (Reprod Med Biol 2003; 2 : 69–73)