Search

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. To study the role of nesfatin-1 on functions of rat's thyroid gland exposed to EMRF. 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. 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. Nesfatin-1 plays a role in thyroid dysfunctions of rats exposed to mobile phone radiation. [ABSTRACT FROM AUTHOR]

Oestrogen deficiency is linked with pulmonary fibrosis. Additionally, it may lead to over-activation of the renin-angiotensin system (RAS), which worsens lung fibrosis. The present study aims to investigate the role of RAS on lung fibrosis associated with oestrogen deficiency in ovariectomised rats. Serum 17β-oestradiol (E2), arterial blood gases, plasma angiotensin II levels, lung tissue hydroxyproline content, and transforming growth factor beta 1 (TGF-β1) 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. Hydroxyproline content, TGF-β1 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. Oestrogen deficiency activates RAS, which consequently increases the expression of pro-fibrotic factors and stimulates the fibrotic cascade causing lung fibrosis. [ABSTRACT FROM AUTHOR]

This study was designed to evaluate the effect of acute overdose of acetaminophen exposure, and determine the curative effect of carvedilol and explore the role of endogenous H2S. Four groups of rats (n=10): groups I: control group, group II: acetaminophen (APAP) hepatotoxictoxic group, group III: APAP hepatotoxictoxic + carvedilol (CVD) treated group and group IV: APAP hepatotoxictoxic + CVD + hydrogen sulfide (H2S) blocker; dl-propargylglycine (PAG) treated group. Animals of groups II, III, IV were given a single overdose of APAP; (2 g/kg) by oral gavages. Groups III and IV received CVD (10 mg/kg/day) by oral gavages, treatment was started 1 hr before APAP administration for 14 days. Animals of group IV received intraperitoneal injection of PAG (45 μmol/kg/day) for 14 days before CVD administration. On the 15th day, blood samples were obtained for estimation of liver enzymes activity levels and animals were sacrificed. Liver was extracted for histological examination and estimation of antioxidant enzymes activity and malondialdhyde (MDA) levels in liver tissue homogenate. Serum liver enzymes activity and MDA levels were significantly higher with significantly lower antioxidant enzymes activity in group II than in groups I and III. Serum liver enzymes activity and MDA levels were significantly higher with reduced antioxidant enzymes activity in group IV than in group III. We concluded that acute acetaminophen exposure destroyed hepatic architecture and altered enzymes activity. Carvedilol has a curative effect through preserved activity of antioxidants. Endogenous H2S significantly contributes to carvedilol mediated effect. [ABSTRACT FROM AUTHOR]

Obesity has various effects on hepatic function. There is little information available for effects of exercise on biochemical and histopathological changes in the liver of obese rats. In addition the prevalence of cigarette smoking (CS) is increased among obese subjects, who are susceptible to develop fatty liver disease. The purpose of this study was to determine the effect of exercise and passive smoking on body mass index, serum lipid profile (LDL and HDL cholesterol), blood glucose, aspartate aminotransferase (AST), alanine aminotransferase (ALT), albumin level and liver histology in rats fed high-sucrose diet. The rats were classified into 5 main groups: Group I, Control Group; Group II, High Sucrose Untrained Group Not Exposed to Passive Smoking; Group III, High Sucrose Trained Group; Group IV, High Sucrose Group Exposed to Passive Smoking; Group V, High Sucrose Trained Group Exposed to Passive Smoking. The findings from this study indicate that obesity induced by high sucrose diet caused significant increase in body mass index, serum triglycerides, total cholesterol, LDL-C, blood glucose, AST, and ALT as well as a significant decrease in albumin and serum HDL-C with significant changes in liver histology. All these effects were counteracted by exercise and were ameliorated by smoking. Preventing and treating obesity will be a key measure in preventing and controlling this epidemic of fatty liver disease. [ABSTRACT FROM AUTHOR]