Thioacetamide (TAA) is widely used in the production of drugs, pesticides and dyeing auxiliaries. Moreover, it is a chemical that can cause liver damage and cancer. TAA has recently been identified to cause bone damage in animal models. However, the type of bone damage that TAA causes and its potential pathogenic mechanisms remain unclear. The toxic effects of TAA on the femurs of New Zealand white rabbits and the underlying toxicity mechanism were investigated in this study. Serum samples, the heart, liver, kidney and femurs were collected from rabbits after intraperitoneal injection of TAA for 5 months (100 and 200 mg/kg). The New Zealand white rabbits treated with TAA showed significant weight loss and femoral shortening. The activities of total bilirubin, total bile acid and gamma-glutamyl transpeptidase in the serum were increased following treatment with TAA. In addition, the cortical bone became thinner, and the trabecular thickness decreased significantly in TAA-treated rabbits, which was accompanied by significantly decreased mineral density of the cortical and trabecular bone. Moreover, there was a significant decrease in modulus of elasticity and maximum load on bone stress in TAA-treated rabbits. The western blotting results showed that the expression of phosphorylated (p)-p38 and p-ERK in femur tissues of rabbits were increased after TAA administration. Collectively, these results suggested that TAA may lead to femoral damage in rabbits by activating the p38/ERK signaling pathway.
The aim of the study was to examine the potential impacts of bisphenol A (BPA) and its analogues BPB, BPF, and BPS on mice TM3 Leydig cells, with respect to basal cell viability parameters such as metabolic activity, cell membrane integrity, and lysosomal activity after 48-h exposure. In addition, monitoring of potential bisphenol´s actions included evaluation of ROS production and gap junctional intercellular communication (GJIC) complemented by determination of testosterone secretion. Obtained results revealed significant inhibition in mitochondrial activity started at 10 µg/ml of bisphenols after 48-h exposure. Cell membrane integrity was significantly decreased at 5 µg/ml of BPA and BPF and 10, 25, and 50 µg/ml of BPA and BPS. The lysosomal activity was significantly affected at 10, 25, and 50 µg/ml of applied bisphenols. A significant overproduction of ROS was recorded mainly at 5 and 10 µg/ml of tested compounds. In addition, significant inhibition of GJIC was observed at 5 µg/ml of BPB followed by a progressive decline at higher applied doses. In the case of testosterone production, a significant decline was confirmed at 10, 25 and 50 µg/ml.
The toxicity of cadmium and zinc at concentrations ranging from 0.1 to 100 µg/l was investigated against the activity of Diplostomum spathaceum (Rudolphi, 1819) cercariae. Over a 24 h exposure period a significant reduction in cercarial activity occurred in solutions of cadmium, zinc, and a mixture of cadmium and zinc at all concentrations. Reduced cercarial activity also occurred in all toxicant solutions compared with controls after only 6 h exposure indicating that cercariae were vulnerable during the period of maximum cercarial infectivity (0-5 h). The mechanisms of metal toxicity and their importance to parasite transmission are discussed.
The oogonia and oocytes in the ovaries of Toxocara canis are joined to a cytoplasmic process called the rachis. The rachis is a muchbranched cytoplasmic mass without cell components in the germinal zone. At the end of the germinal zone and in the growth zone the cytoplasmic mass is formed into a central axial cylinder, containing small dense granules, lipid drops and glycogen. Throughout the growth zone shell granules similar to those present in the oocytes are also present in the rachis. Anterior to the opening of the ovaries into the oviduct the rachis disappears. The ovarian wall is composed of epithelial cells, adjoining the basal lamina. They are characterized by the presence of large numbers of mitochondria, especially in the germinal zone. The epithelial cells in the growth zone also contain rough endoplasmic reticulum, ribosomes and bundles of microfibrils. A dense tubular material occurs between the basal membrane of the epithelial cells and the basal lamina as well as in the wall intercellular spaces in the ovarian growth zone. Multivesicular labyrinthlike formations can also be observed in the epithelial intercellular spaces in the central portion of the T. canis ovary.
The fine structure of the oviduct, oviduct-uterine junction and uterus of the nematode Toxocara canis (Werner, 1782) is described. Columnar-type epithelioid cells with numerous microvilli at the apical membrane border the oviduct lumen. Many electron dense secretory products are present in these cells. The cells lining the oviduct-uterine junction have no microvilli. They are coated with an electron-dense layer and contain numerous membrane-bound dense material containing bodies. Externally, the cells are surrounded by a basal lamina and muscle cells. The epithelial cells lining the greater part of the paired uteri appear to be rather flat. The oocytes inside the oviduct are covered with a dense thick plasma membrane and contain lipid droplets, dense granules and glycogen. The morphology of the oocytes before the fertilization inside the oviduct-uterine junction resembles that of the oocyte in the oviduct. After the fertilization the egg shell formation takes place. The egg shell of T.canis is composed of four layers: uterine, vitelline, middle chitinous and inner layer. The differences between the fine structure of the egg shell of T. canis and other related nematodes are discussed.
The apicomplexan Toxoplasma gondii (Nicolle et Manceaux, 1908) secretes a group of serine/threonine kinases from rhoptries, which play vital roles in boosting intracellular infection. Toxoplasma gondii rhoptry organelle protein 17 (ROP17) is one of these important kinase proteins. Nevertheless, its function remains unclear. Here, we showed that ROP17 induced autophagy in vitro and in vivo. The autophagy of small intestine tissues of T. gondii tachyzoite (RH strain)-infected mice was detected by the immunohistochemistry staining of LC3B, Beclin 1 and P62. ROP17 overexpression augmented starvation-induced autophagy in HEK 293T cells as measured by MDC staining, transmission electron microscopy (TEM), fluorescence microscopy and Western blot analysis. Moreover, the interaction of ROP17 and Bcl-2 was confirmed using co-immunoprecipitation analysis, and the data demonstrated that ROP17 had an autophagic role dependent on the Beclin 1-Bcl-2 pathway, which was also revealed in an in vivo model through immunohistochemical staining. Pearson coefficient analysis showed that there existed strong positive correlations between the expression of ROP17 and LC3B, Beclin 1 and phosphorylation of Bcl-2, while strong negative correlations between the expression of ROP17 and p62 and Bcl-2. Collectively, our findings indicate that ROP17 plays a pivotal role in maintaining T. gondii proliferation in host cells via the promotion of autophagy-dependent survival.
Toxoplasma gondii reportedly manipulates rodent behaviour to increase transmission to its definitive feline host. We compared the effects of mouse infection by two Type II strains of T. gondii, Prugniaud (PRU) and ME49, on attraction to cat odour, locomotor activity, anxiety, sensorimotor gating, and spatial working and recognition memory 2 months post-infection (mpi). Attraction to cat odour was reassessed 7 mpi. At 2 mpi, mice infected with either strain exhibited significantly more attraction to cat odour than uninfected animals did, but only PRU-infected mice exhibited this behaviour 7 mpi. PRU-infected mice had significantly greater body weights and hyperactivity, while ME49-infected mice exhibited impaired spatial working memory. No differences in parasite antibody titres were seen between PRU- and ME49-infected mice. The present data suggest the effect of T. gondii infection on mouse behaviour is parasite strain-dependent.
A convincing body of evidence now exists, from both human and animal studies, and encompassing epidemiological to experimental, to indicate that the common protozoan Toxoplasma gondii can cause specific behavioural changes in its host. Such behavioural alterations are likely to be the product of strong selective pressures for the parasite to enhance transmission from its intermediate host reservoir, primarily rodent, to its feline definitive host, wherein sexual reproduction can occur and the parasite's life cycle completed. Here we consider what the available data to date may reveal about the potential mechanisms involved, the future research that needs to be performed, and the subsequent implications for animal and human health.
Background - There is growing interest in the role of microbial agents in the causation of psychiatric disorders. The neurotropic protozoan parasite Toxoplasma gondii is one of the main candidates and has been associated with various psychiatric conditions, including schizophrenia. Methods - A narrative review of the literature from the main medical databases (Medline, PubMed, PsycINFO), Google Scholar and Google using combinations of applicable terms. Results - T. gondii affects the brain in both the acute and the latent stages of infection causing apparent brain pathologies in infected rodents and both immuno-compromised and immuno-competent humans. In immuno-competent individuals, behavioural disorders are primarily related to the latent stages of the illness. Behavioural/mental disorders that include schizophrenia, mood disorders, personality changes and cognitive impairments may be related to infection with T. gondii. Evidence for a behavioural effect of T. gondii comes from observational reports in animal models and controlled behavioural analysis in humans. Indirect clues of infection also come from raised seroprevalence or serotitres of antitoxoplasma antibodies among those with mental disorders. The pathophysiologic mechanism through which T. gondii may exert its effect is not clear, but direct impact on the brain and changes in neuroimmunomodulation, neurotransmission and some gene-environment interactions are postulated. Conclusion - There is evidence supporting a potential role of T. gondii infection in the onset of some behavioural disorders. Confirmation of such a role would prove a significant breakthrough in the search for the aetiology, treatment and prevention of behavioural disorders, such as schizophrenia. However, the associations remain preliminary.