[Genotoxic effects of pesticide fipronil in somatic and generative cells of mice].

The pronounced genotoxic effect of fipronil in all used doses (4.75, 9.50, 19.00, and 31.70 mg/kg) at a single exposure in the liver, lungs and spleen was ascertained by the Comet assay. Organ specificity of genotoxic effects of the pesticide was revealed. The liver was the most sensitive to fipronil. Fipronil at a dose of 9.50 mg/kg in a single and repeated exposure (within 10 days) induced aberrations in mouse bone marrow cells with the frequency exceeding the spontaneous mutation rate (p < 0.01 and p < 0.001, respectively). Fipronil also showed genotoxic activity in the germ cells of the experimental animals, causing abnormalities of the structure of synaptonemal complexes in the spermatocytes.

[The effect of mutation dominant spotting-Yurlovo (KitW-Y) on spermatogenesis, early embryogenesis, and fertility of C57BL/6JY mice].

The effect of mutation KitW-Y found in C57BL/6 mice on fertility, spermatogenesis, and early embryogenesis of mice have been studied. If heterozygotes KitW-Y/+ are crossed with wild-type mice, fertility decreases by 20%. Homozygotes Kitw-Y/KitW-Y and compounds KitW-Y/KitSsm are nonviable. The study of spermatogenesis in KitW-Y/+ mice has demonstrated a negative effect of this mutation on spermatocytes. Histological examination of the testes of mutant males has shown local empty spaces in seminal ducts. Electron microscopic examination of synaptonemal complexes have demonstrated desynapsis disturbance in some nuclei at the diplotene stage of meiotic prophase I. However, these disturbances do not cause a decrease in the number of fertilized oocytes/ova. The decrease in fertility is accounted for disturbances of early embryogenesis. In vivo and in vitro analyses of early embryogenesis have demonstrated that cleavage divisions are asynchronous in KitW-Y/+ heterozygous embryos. Some of these embryos die before implantation, and others cleave more rapidly than wildtype embryos, which give them selective advantage during the postimplantation period of embryogenesis. The pattern of KitW-Y expression during spermatogenesis and embryogenesis mimics potential human pathology, which makes these mutants an interesting and valuable object for genetics and developmental biology.

Destructive effect of DNA topoisomerase II inhibitor vepesid on mouse spermatogenesis.

Inhibition of DNA topoisomerase II with vepesid induced structural and functional reorganization of chromatin in meiotically dividing spermatocytes I, which later led to the block of their differentiation and long-lasting disorders in spermatogenesis. Vepesid induced decondensation of spermatocyte I chromatin, block of desynapsis, and elongation of lateral elements of spermatocyte autosome synaptonemal complexes during late pachytene and diplotene of meiosis. This confirms the involvement of type II DNA topoisomerase in chromatin condensation and homologous chromosome desynapsis at the stage of diplotene and the role of this enzyme in structural organization of the synaptonemal complex. Vepesid induced the formation of dichotomy and breaks of the pericentromer regions of subelements of lateral elements of the autosomal synaptonemal complexes; the number of cells with associations of axial elements of sex chromosomes with autosomal synaptonemal complexes increased, univalents of autosomes and sex chromosomes appeared. Mesna, a modifier of toxic effects of antitumor drugs, had no toxic effect on spermatogenic cells. Mesna reduced the lethal effect of vepesid during combined treatment, but did not ensure long-term protection of spermatogenesis.

Damaging effect of taxol on mouse spermatogenesis.

Taxol produced a specific effect on mouse spermatocytes I and on stem spermatogonia, which leads to overall degeneration of spermatocytes I and long lasting disorders of spermatogenesis. Breaks of the axial and lateral elements of the synaptonemal complex, aneuploidies in spermatocytes in early, middle, and late pachytene, and accumulation of cells with associations of sex chromosomes and autosomes were observed, which attested to blockade of spermatogenesis in late pachytene and diplotene of meiosis prophase I. Mesna, a chemoprotective agent, reduced total toxicity and lethal effects of taxol, but did not prevent destruction of the testes.

[The condition of mitochondria in experimental viral carcinogenesis]. / O sostoianii mitokhondrii pri éksperimental'nom virusno kantserogeneze

A parallel histoenzymatic and electron-microscopy study of the state of mitochondria in experimental viral cancerogenesis induced by adenovirus of monkeys SA7(C8) and virus of Rous sarcoma in soft tissues of hamster was carried out. It was shown that the earliest changes in the cell in the process of its tumorous transformation were those in mitochondria. The character of deposits of diformazin at an early stage of viral cancerogenesis corresponded to the trend to the linear arrangement of mitochondria and to initial phenomena of their swelling. Progressive swelling of mitochondria in the process of tumorous growth was established, which correlated with histochemically revealed changes in the relationships of a number of reduction-oxidation enzymes.

[Ultrastructure of experimental virus-induced hemangiopericytomas]. / Ul'trastruktura éksperimental'nykh virusindutsirovannykh gemangioperitsitom

Electron-microscopy studies of malignant low-differentiated hemangiopericytomas, induced by adenovirus of monkeys SA7(C8) and bovine adenovirus type 3 were, carried out. At earlier stages of the development of these tumours in tumourous cells located around capillaries there were observed the ultrastructural characteristics typical of pericytes and cells of human hemangiopericytis: the presence of the basal layer and fibrills as thick as 40 A. As differentiation proceeded, tumorous cells acquired an elongated form, and in some of them there appeared myofilaments typical of smooth-muscle cells, with local thickenings, as well as multitude of pinicytic vacules along the plasmatic membranes of cells. The foregoing confirms the assumption of hemangiopericytomas as a prestage of leio-(angioleio-) myosarcomas. Moreover, the tumour cells revealed the presence of cilia, fibrills as thick as 100A, 75A, annulate lamelae, and myelin-like formations.