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Abstract The first changes in rat testicle haemomicrocircular channel links ultrastructural arrangement are noticed already in a 2-week run of streptozotocin-induced diabetes mellitus, and accumulate throughout next periods of the experiment. Angiopathy is a trigger mechanism for diabetic development of testicle structural changes. This finding is a basis for further morphologist and clinicist surveys for the purpose of new diabetic testicle pathology diagnostics, prevention, and elaboration of treatment techniques.
The implication of apoptosis in the cytotoxicity of cadmium (Cd) on rat thymus, testicle and liver was investigated. Four days after Cd injection (1.5 and 3.0 mg/kg b.w. i.p) the testicle and thymus relative weight decreased but that of liver increased significantly in a dose-dependent manner. In vitro, 6 h incuba­tion of thymocytes in the presence of 10-3M Cd resulted in a typical degradation of DNA into oligonucle­otide fragments similar to that observed in the presence of the dexamethasone, suggesting the induction of apoptosis in the cells. The addition of 1 mM ZnSO4, a metallic antioxidant, prevented this fragmentation. Nick end-labeling method confirmed the involvement of apoptosis in the thymus and revealed a high per­centage of TUNEL-positive cells 48 h following Cd administration mainly in the cortical zone. An apoptot- ic effect was also observed in the testicle where TUNEL-positive cells were present, primarily in late stages of gametogenesis. In contrast, the liver of Cd-treated rats failed to exhibit significant levels of apoptosis and all hepatocytes showed strictly negative TUNEL-labeled nuclei. In contrast, centrilobular-necrosis was observed reflecting species differences in target cells. These findings suggest that the apoptotic mechanism in thymus and testicle, but not in liver, may contribute to the toxicity of cadmium in rats.
The objective of this study was to determine the effect of oxidative stress caused by exposure to ozone on the activity of 17-β-hydroxysteroid dehydrogenase and alkaline phosphatase, and testosterone concentrations in male rats, and to investigate the possible protective effect of easily available antioxidants such as vitamins E and C. The experiment was conducted on adult Wistar-Hannover rats. One group of animals was exposed to ozone without vitamin cover, and the remaining animals were administered vitamins E and C in various combinations and doses. Ozone exposure in the group of rats not receiving vitamin injections caused oxidative stress manifested by elevated MDA concentrations in the blood plasma and testicular tissue. An increase in MDA levels was also observed in the group of animals administered vitamins, excluding the animals receiving low- and average-dose combinations of vitamins E and C. A drop in the activity of 17-β-hydroxysteroid dehydrogenase was reported in animals exposed to ozone, but this effect was not noted in the groups exposed to ozone and receiving vitamins. The lowest blood testosterone levels were observed in rats exposed to ozone and in the groups receiving low- and average-dose combinations of vitamins E and C.
Alterations in the genetic apparatus of mice bone marrow cells and testicles caused by Hymenolepis nana, Ascaris suum and Toxocara canis metabolites have been investigated by means of micronuclear test application. The activity of spermatogenesis has been investigated at experimental hymenolepidosis, migrating ascariasis and toxocarosis with the use of ³H-timidine. Helminths metabolites have been established to exert a mutagenie effect on somatic cells of bone marrow, spermatogonies and also on the generative cells (spermatides) of helminths in invaded mice. The concurrent increase in micronucleus number in erythrocytes, spermatogonies and in spermatides (to a lesser degree) of invaded mice has been revealed. The decrease in spermatogenesis activity has been established in experimental hymenolepidosis, migrating ascariasis and toxocarosis in invaded mice.
Rats were fed a copper fortified diet (10 times the level in a standard diet) for a 4-week period and were concomitantly exposed to cadmium at a dose corresponding to 10 mg Cd/kg diet. The contents of cadmium in the carcass, and liver, kidneys, muscles and testicles and corresponding AUC values, calculated with respect to concentration-time curve, indicate that the copper supplement increased the absorption of cadmium from the gastrointestinal tract and the bodily and organ cadmium burden. On the other hand, an increase in body weight gain produced by the copper supplemental diet suggested that the toxic action of cadmium was limited.
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