Spermatogenesis inFasciola hepatica:an ultrastructural comparison of the effects of the anthelmintic, thiabendazole (“Fasinex”) and the microtubule inhibitor, tubulozole

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Abstract
Summary The normal sequence of spermatogenesis in Fasciola hepatica has been established. The single-celled primary spermatogonium—after three mitotic divisons and one meiotic division, accompanied by incomplete cytokinesis—gives rise to a rosette of 32 spermatid cells from which the spermatozoa differentiate. Rosette formation begins to develop at the tertiary spermatogonial stage and leads to individual cells being joined together via a central “cytophore”. As revealed by transmission electron microscopy (TEM), spermatogenesis is readily disrupted by the active sulphoxide metabolite of triclabendazole (TCBZSX), a relatively new benzimidazole anthelmintic. Following short incubation times in this drug (3 h onwards), the spermatogonial stages become mitotically inactive and detached from their normal position close to the wall of the tubule. The rosette stages become increasingly disrupted, with fragmentation of the cytoplasmic cytophore. After longer time periods (12–24 h) the testis tubules were almost completely empty with few spermatogenic stages or mature spermatozoa present. The ultrastructural effects of TCBZ-SX bear some resemblance to those observed after treatment with tubulozole, a potent microtubule inhibitor. The results with the two drugs are discussed in relation to the mode of action of triclabendazole, which at present is unknown.