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Abstract
We have determined the presence and distribution of intracellular progesterone receptors (PRs) and glucocorticoid receptors (GRs) in the lung of adult female rabbits using immunohistochemistry. The effects of ovariectomy and administration of oestradiol benzoate (10 μg for 3 consecutive days) upon PR and GR immunoreactivity were also studied. The results demonstrated the presence of both steroid hormone receptors in the female rabbit lung. PR and GR immunoreactivity was predominantly nuclear and located in alveolar epithelial cells and various interstitial cells such as polymorphonuclear leucocytes. Tissue distribution of both receptors was similar in all cases. Oestradiol treatment induced a marked increase in the number of PR immunoreactive cells compared with intact and ovariectomized female animals. Neither ovariectomy nor oestradiol treatment modified the number of GR immunoreactive cells. The presence and localization of intracellular PRs and GRs in several lung cell types suggest that they may play an important role in mediating the effects of progesterone and glucocorticoids in various physiological processes in the rabbit lung. The data also indicated an oestrogen regulation of PRs in the rabbit lung.
Journal of Endocrinology (1994) 142, 311–316
Facultad de Química and
Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacan 04510, D F México, México
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Facultad de Química and
Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacan 04510, D F México, México
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Facultad de Química and
Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacan 04510, D F México, México
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Facultad de Química and
Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacan 04510, D F México, México
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Facultad de Química and
Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacan 04510, D F México, México
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Facultad de Química and
Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacan 04510, D F México, México
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Beta-cell apoptosis is responsible for the development of insulin-dependent diabetes mellitus in the streptozotocin (STZ) rat model. It has been demonstrated that steroid hormones possess antioxidant and protective antiapoptotic effects in many tissues. The aim of the present study was to investigate the early apoptotic damage induced by STZ in rat pancreas, and the effect of testosterone in preventing apoptosis of pancreatic β cells. Intact and castrated adult male Wistar rats were subjected to a unique injection of STZ 60 mg/kg (body weight) in citrate buffer, and the kinetics of apoptosis in β cells was assessed. Insulin and glucose were measured by RIA and a glucometer respectively, and in pancreatic tissue by immunohistochemistry. At 6 h after STZ injection, a marked increase in apoptotic β cells was detected; however, glucose and insulin serum levels were not significantly different from the controls. The castrated animals presented higher percentages of apoptotic β cells (65.75 ± 5.42%) than intact males (20.6 ± 4.38%) and castrated, testosterone-substituted males (30.66 ± 1.38%). The decrease in apoptotic β cells induced by testosterone was reversed by the antiandrogen flutamide (67.69 ± 3.45%). The overall results indicate that early apoptotic damage produced by STZ in castrated animals was reversed by testosterone, suggesting that this hormone exerts a natural protective effect in rat pancreas. This effect could help to explain some sexual differences in diabetes mellitus incidence in man, reinforcing the idea that new approaches in steroid hormone therapies should be considered for treatment of this disease.
