The effect of hyperthyroidism on the levels of liver enzymes in adult male Wistar rats

 Thyrotoxicosis is a condition in which tissues are stimulated by increased secretion of thyroid hormone. The most common cause is diffuse toxic goiter and toxic multi-nodular goiter. For more reviews on this disease, the effects of hyperthyroidism on liver enzyme levels were studied. A total of 30 adult male Wistar rats weighing about 190 g were purchased from the Pasteur Institute of Iran. In this study, rats were divided into control group, the group receiving vitamin E, the group receiving levothyroxine, the group receiving levothyroxine treated with vitamin E; blood was taken from all groups over a period of 10 days after injection, and measurement of thyroid hormones and liver tests was made. The findings obtained in this study show that Isolated systolic hypertension (ISH) hormone levels in rats treated with levothyroxine, Treatment with vitamin E may reduce serum levels of ISH , Hormone levels of T4 in the rats treated with levothyroxine were increased compared to normal rates. Treatment with vitamin E reduces serum levels of T4 compared to the first hyper group. T4 hormone levels in rats treated with levothyroxine were reduced compared to normal rates. Treatment with vitamin E may reduce serum levels of T4 compared with the first hyper group. Asparagine Transferase (AST) enzyme levels in rats treated with levothyroxine were increased compared, Treatment with vitamin E may reduce serum levels of AST , Alanine transferase (ALT) enzyme levels in rats treated with levothyroxine were increased , Treatment with vitamin E may increase serum levels of ALT , alkaline phosphatase (ALP) enzyme levels in rats treated with levothyroxine has been increased compared with normal rates. Treatment with vitamin E resulted in serum levels of ALT not to be increased compared with the first group. According to the results of hyperthyroidism and levels of liver enzymes, it can be concluded that hyperthyroidism induced by levothyroxine can increase the levels of hormones T3, T4 and Thyroid Stimulating Hormone (TSH), and then increase the levels of liver enzymes. Treatment of empirical samples with vitamin E is likely to reduce liver damages and prevent the increased levels of liver enzymes compared to empirical samples of hyperthyroidism which have been treated with vitamin E.

The Effects of Cytotoxic Dose of Testosterone on Bax , Bcl2, and CD82/KAI1 Genes Expression in Colorectal Adenocarcinoma (HT29) and Brain Glioblastoma Cells(A172)

Background and Objectives: Studies have shown that sex steroids affect cancer cells at cellular and molecular level. The objective of this study was to investigate the effects of cytotoxic dose of testosterone on the expression of Bax, Bcl2, and CD82/KAI1 genes in adenocarcinoma colorectal (HT29) and brain glioblastoma cells (A172).   Methods: In this laboratory-experimental study, HT29 and A172 cells, were divided into control group and groups exposed to cytotoxic dose of testosterone (1 and 0.1 mg/ml for HT29 and A172, respectively). Real time PCR was used to evaluate the expression levels of Bax, Bcl2, and CD82/KAI1 genes. The data were statistically analyzed between groups using one way ANOVA statistical test.   Results: The expression levels of BCL-2 and Bax genes significantly increased and decreased in HT29 cells exposed to cytotoxic dose of testosterone, respectively (p<0.001), but, expression level of CD82/KAI1 gene did not significantly change. The expression levels of Bax and CD82/KAI1 genes significantly increased (p<0.01) and decreased (p<0.001) in A172 cells received cytotoxic dose of testosterone, respectively; however, BCL-2 gene expression level did not significantly change. Conclusion: Based on the results of this study, the cytotoxic concentration of testosterone in colorectal adenocarcinoma and brain glioblastoma cells induces Bax gene-related apoptosis. Also, it had no antimetastatic effect in adenocarcinoma colorectal cells. Whereas, in the brain glioblastoma cells, it decreases the expression level of CD82/KAI1 anti-metastatic gene, which may also increase the metastatic potential

Lipoprotein lipase gene variants: Association with acute myocardial infarction and lipid profiles

Background: Studies showed that lipid metabolism disorders are significant risk factors for myocardial infarction and coronary artery disease (CAD). Therefore, genes involved in lipid and lipoprotein metabolism pathways such as lipoprotein lipase (LPL), are proper candidates for susceptibility to CAD. Aim: To investigate the possible association between LPL gene variants (HindIII (rs320) and PvuII (rs285)), acute myocardial infarction (AMI) and serum lipid levels. Subjects and methods: The study population consisted of 211 patients with a diagnosis of premature AMI, and 203 age-matched individuals with normal coronary angiograms as controls. Genotyping of HindIII and PvuII polymorphisms was done by the PCR-RFLP technique. Results: Although the H+ and P+ alleles were more observed among the patients, there were no significant differences in genotype distributions and allele frequencies of HindIII and PvuII polymorphisms between patient and control subjects (P > 0.05). Triglyceride levels were found to be significantly elevated in H+H+ and P+P+ genotypes compared to others (P < 0.05). However, there was no association between HindIII and PvuII genotypes and HDL-C, LDL-C and cholesterol levels. Conclusion: Our findings indicate that LPL-HindIII and PvuII polymorphisms are not associated with acute myocardial infarction but with triglyceride levels