The purposes of this study were to investigate the effects of strenuous exercise on apoptosis of the gastrocnemius and soleus muscle fibers and clarify the role of oxidative metabolism in the strenuous exercise-induced apoptosis. The experiment was designed with 49 (n = 49) male, 24-week-old, L. Wistar albino rats. Strenuous exercise model was applied to 42 (n = 42) rats and seven (n = 7) rats served as rested controls. All rats were randomly assigned to one of the following groups (n = 7): rested control (C), immediately after exercise (0 h) and 3, 6, 12, 24, and 48 h after exercise. Apoptotic nuclei were shown by single stranded DNA (ssDNA) determination. Oxidative damage in mitochondrial fractions of the muscle tissues was evaluated by malondialdehyde (MDA) levels and reduced/oxidized glutathione (GSH/GSSG) ratios. Caspase-9, -8 and -3 activities and the level of cytochrome c (Cyt c) were measured in the cytosolic fractions of muscle tissues to follow mitochondrial-dependent (intrinsic) or ligand-mediated death receptor (extrinsic) pathways of apoptosis. Plasma interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) levels were also determined. Based on our results, apoptosis is significantly triggered in muscle fibers by strenuous exercise (P < 0.05). Apoptosis in the soleus muscle tissues mostly depends on the intrinsic pathway and may be triggered by increased oxidative stress. In contrast, extrinsic pathway of apoptosis was predominant in the gastrocnemius muscle and increases of TNF-alpha and IL-6 may play a significant role.
1. This study compared the effect of dietary supplementation with organic or inorganic selenium (Se) sources plus control amounts or large amounts of vitamin E (alpha-tocopherol acetate) in broilers raised at control (20 to 24 degrees C) or low (14.5 to 16.8 degrees C) temperatures after 2 weeks of age. 2. The following dietary treatments were used from one day old. Diet 1, the control diet, comprised a commercial diet containing 0.15 mg/kg inorganic Se and 50 mg vitamin E/kg feed. Diet 2 was the same as diet 1, supplemented with 0.15 mg/kg inorganic Se. Diet 3 was the same as diet 2 but was supplemented with 200 mg/kg vitamin E. Diet 4 was the same as diet 1, but inorganic Se was replaced with 0.30 mg/kg organic Se. Diet 5 was the same as diet 4, supplemented with 200 mg/kg vitamin E. 3. Low temperature reduced the growth rate of broilers; however, at 6 weeks, there were no differences in the body weights of birds fed on organic Se supplemented diets housed at low or control temperature. The feed conversion ratio was significantly affected by low temperature but not by diet. The heterophil/lymphocyte ratio was higher in chicks after one week in the cold, indicating mild stress. Blood triiodothyronine levels were significantly higher in birds after 1 and 4 weeks in the cold but thyroxin was not affected. 4. Organic Se supplementation increased relative lung weight at the control temperature, which might lead to greater respiratory capacity. Relative spleen weight significantly decreased in broilers fed diets supplemented with inorganic Se under cold conditions, a possible indication of chronic oxidative stress. 5. At the low temperature, supplementation with organic Se alone, or with inorganic Se and vitamin E increased glutathione peroxidase (GSHPx) activity and glutathione (GSH) concentration in the liver of broilers, which may indicate increased activity of birds' antioxidant defence against suboptimal environments.
In this study, we have investigated the antiproliferative effect of quercetin on human papillary thyroid cancer cells and determined the apoptotic mechanisms underlying its actions. We have used different concentrations of quercetin to induce apoptosis and measured cell viability. Apoptosis and cell cycle analysis was determined by flow cytometry using Annexin V and propidium iodide. Finally, we have measured changes in caspase-3 and cleaved poly(ADP-ribose) polymerase (PARP) protein expression levels as hallmarks of apoptosis and Hsp90 protein expression level as a marker of proteasome activity in treated and control cells. Quercetin treatment of human papillary thyroid cancer cells resulted in decreased cell proliferation and increased rate of apoptosis by caspase activation. Furthermore, it was demonstrated that quercetin induces cancer cell apoptosis by downregulating the levels of Hsp90. In conclusion, we have shown that quercetin induces downregulation of Hsp90 expression that may be involved in the decrease of chymotrypsin-like proteasome activity which, in order, induces inhibition of growth and causes cell death in thyroid cancer cells. Thus, quercetin appears to be a promising candidate drug for Hsp90 downregulation and apoptosis of thyroid cancer cells.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.