Pre-natal glucocorticoids are used in women at risk of preterm delivery to induce foetal lung maturation. However, glucocorticoids can produce negative outcomes for other tissues such as the reproductive system. We therefore tested the effects of pre-natal betamethasone on testicular morphology and apoptotic protein immune expression during pre- and post-natal development. Pregnant ewes (n = 42) bearing singleton male foetuses were randomly allocated to receive intramuscular injections of saline or betamethasone (0. 5 mg/kg) at 104, 111 and 118 days of gestation (DG). Testes were collected at 121 and 132 DG, and at 45 and 90 post-natal days (PD) and subjected to morphometric analysis (volume densities of sex cords and interstitial tissues; sex cord diameter). Immunohistochemistry (% stained area) was used to assess active caspase-3, Bax, Bcl-2 and cell-cycle proteins (PCNA). Compared with control values, betamethasone treatment decreased sex cord diameter at 121 DG, 45 and 90 PD, and sex cord volume at 90 PD. Active caspase-3 was decreased by betamethasone at 121 DG and 90 PD, but Bax was increased in all betamethasone groups. Bcl-2 and PCNA decreased in the betamethasone groups at 121 DG and 45 PD, but increased at 132 DG and 90 PD. We conclude that high levels of pre-natally administered glucocorticoid reduce foetal testicular development, perhaps via changes in the balance between pro- and anti-apoptotic proteins and cell-cycle proteins. These outcomes could compromise the future spermatogenic potential of male offspring.
Toxic honeydew produced by Flatidae Epormenis cestri in Uruguay has been shown to cause among honeybees (Apis mellifera) colonies a massive larva death called “River disease”, but the intrinsic mechanisms are still unknown. Because fat body cells, oenocytes and trophocytes, are known to regulated larvae metabolism, and to be affected by xenobiotics, we tested whether apoptosis of these cells can be an underlying cause of larvae death. Ten colonies were divided into two groups and fed with common honey or toxic honeydew obtained from colonies affected by “River disease”. Five-dayold larvae were collected and processed for histology and immunohistochemistry for caspase-3. The area, diameter, and immunostaining area in oenocytes and trophocytes were measured. The oenocyte and trophocyte cellular area decreased in the treated group (p=0.002; p<0.001 respectively) compared to the control group. The diameter of oenocytes (p=0.0002) and trophocytes (p<0.0001) decreased in the treated group. Caspase-3 was detected in cytoplasm in the control group but in the cytoplasm and nucleus in the treated group. The caspase-3 immunostaining area increased in oenocytes (p<0.002) and trophocytes (p<0.0001) of the treated group. The ingestion of toxic honeydew altered the morphology, localization and immunoexpression of caspase-3 in fat body cells, which suggests that the deregulation of the apoptotic mechanism affected the normal development in A. mellifera larvae.
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