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.

Toward the Development of a Single-Round Infection Assay Based on EGFP Reporting for Anti-HIV-1 Drug Discovery

Background: The rapid increase of HIV-1 strains resistant to current antiretroviral drugs is a challenge for successful AIDS therapy. This necessitates the development of novel drugs, and to this end, availability of screening systems for in vitro drug discovery is a priority. Herein, we report the modification of a previously developed system for increased sensitivity, ease of use, and cost-efficiency, based on the application of the EGFP marker. Methods: A PCR-amplified gfp gene (gfp) was cloned into pmzNL4-3, the plasmid already designed to produce single-cycle replicable virions, in frame with the reverse-transcriptase gene to construct the pmzNL4-3/GFP plasmid. GFP-mzNL4-3 pseudo-typed virions, as the first progeny viruses, were recovered from the culture supernatant of HEK293T cells co-transfected with pmzNL4-3/GFP and the helper plasmids pSPAX2 and pMD2G, which respectively encode HIV-1 Gag-Pol and vesicular stomatitis virus glycoprotein. Single-cycle replication and virion production were assessed by syncytia formation, p24 antigen assays, and electron and fluorescence microscopy. Results: The incorporation of EGFP into the viral particles allowed their quantification by fluorometry, flow-cytometry, and fluorescence microscopy; however, this modification did not affect the single-round infectivity or production rate of the GFP fluorescence-emitting virions. Conclusions: Our results certify the development of a rapid, inexpensive, and safe GFP-reporting single-cycle replicable system for anti-HIV drug discovery. Further experiments are needed to measure the validity and robustness of the assay