RESUMEN
CONTEXT: Exposure to Electomagnetic radiation fields of cell phones causes thyroid dysfunction and a previous study revealed that nesfatin-1 may affect functions of the thyroid gland. OBJECTIVE: To study the role of nesfatin-1 on functions of rat's thyroid gland exposed to EMRF. MATERIALS AND METHODS: Thirty adult male rats were divided equally into 3 groups as group I, group II and group III. The experiment extended for 30 days then the plasma nesfatin-1 level, thyroid functions, and thyroid tissue oxidative stress were assessed. Also; histological and immunohistochemical study studies were done to evaluate structural and apoptotic changes of the thyroid gland. RESULTS: There was a significant decrease in plasma nesfatin-1 level and thyroid functions with an increase in oxidative stress and apoptosis. Interestingly, there was a correlation between nesfatin-1 level and markers of thyroid function, oxidative stress and apoptosis. CONCLUSION: Nesfatin-1 plays a role in thyroid dysfunctions of rats exposed to mobile phone radiation.
Asunto(s)
Teléfono Celular , Glándula Tiroides , Animales , Ratas , Masculino , Estrés Oxidativo , ApoptosisRESUMEN
CONTEXT: Oestrogen deficiency is linked with pulmonary fibrosis. Additionally, it may lead to over-activation of the renin-angiotensin system (RAS), which worsens lung fibrosis. OBJECTIVE: The present study aims to investigate the role of RAS on lung fibrosis associated with oestrogen deficiency in ovariectomised rats. MATERIALS AND METHODS: Serum 17ß-oestradiol (E2), arterial blood gases, plasma angiotensin II levels, lung tissue hydroxyproline content, and transforming growth factor beta 1 (TGF-ß1) concentration, the mRNA expression of angiotensin type 1 receptor (AT1R), and angiotensin-converting enzyme (ACE1) were evaluated. Moreover, lung tissues were examined by histopathology and immunohistochemistry. RESULTS: Hydroxyproline content, TGF-ß1 concentration, plasma angiotensin II, the relative mRNA expression of ACE1, and AT1R is found to increase in ovariectomised rats. The mentioned changes can be largely rescued by administration of RAS blockers. CONCLUSION: Oestrogen deficiency activates RAS, which consequently increases the expression of pro-fibrotic factors and stimulates the fibrotic cascade causing lung fibrosis.