We found a significant increase in ROS and an increase in the genomic and protein expression of the antioxidant enzymes catalase (CAT) and glutathione peroxidase-1 (GPx-1) in lymph node and spleen cells of hyperthyroid mice.
Hyperthyroid rats presented lower sperm motility, higher levels of lipid hydroperoxides and thiobarbituric reactive substances, lower catalase and glutathione peroxidase activities and higher glutathione-S-transferase activity in their testes than control animals.
Translated products of AOGs showed differential expression in the liver of hyperthyroid rats, where Cu/Zn SOD (SOD1), CAT and GR were decreased in contrast to Mn SOD (SOD2) and GPx1.
MOK acupuncture significantly increased hepatic GSH levels and decreased the expression of SOD and catalase in the liver, heart, and brain tissues of hyperthyroidism rats.
Translated products of AOGs showed differential expression in the liver of hyperthyroid rats, where Cu/Zn SOD (SOD1), CAT and GR were decreased in contrast to Mn SOD (SOD2) and GPx1.
We found a significant increase in ROS and an increase in the genomic and protein expression of the antioxidant enzymes catalase (CAT) and glutathione peroxidase-1 (GPx-1) in lymph node and spleen cells of hyperthyroid mice.
Translated products of AOGs showed differential expression in the liver of hyperthyroid rats, where Cu/Zn SOD (SOD1), CAT and GR were decreased in contrast to Mn SOD (SOD2) and GPx1.
Based on a literature search regarding all published TSHR mutations, this review covers several mutations which are clearly associated with a hyperthyroidism-phenotype, but interestingly show a lack of constitutive activity determined by in vitro characterization.
Thyroid-infiltrating activated T cells may lead to cell-mediated immunity, thyroid injury and eventually hypothyroidism, whereas humoral immunity via TSHR-stimulating antibodies may give rise to hyperthyroidism.
These mice showed severe hyperthyroidism in a manner very similar to that described above for mice immunized with the mouse TSHR or human TSHR, and exhibited significant weight loss, with average weight for treatment groups ranging from 20.6 to 21.67 g, while controls weighed 24.2 g. Early after onset of the disease, histopathological examination of thyroids showed enlargement of colloids and thinning of epithelial cells without inflammation.
GTT was defined as hyperthyroidism (free thyroxine [FT4] level: ≥95th percentile) in the early pregnancy, which normalized in mid-pregnancy without thyroid-stimulating hormone receptor antibodies.
However, the comparison of the LRA values of sporadic TSHR mutations with LRA values of familial TSHR mutations does show a significantly higher median LRA value for sporadic as compared to familial autosomal dominant hyperthyroidism.
Curcumin differentially regulates the expression of superoxide dismutase in cerebral cortex and cerebellum of L-thyroxine (T₄)-induced hyperthyroid rat brain.
Although hereditary nonautoimmune overt hyperthyroidism is very rare, TSHR activating mutations as a cause of subclinical hyperthyroidism may be more common and should be considered in the differential diagnosis, especially if familial.
Previously, in an induced mouse model, injecting TSHR A-subunit protein attenuated hyperthyroidism by diverting pathogenic TSHR Abs to a nonfunctional variety.
In addition, patients harboring the same mutation of the TSHr gene may show wide phenotypic variability with respect to the age at onset, and severity of hyperthyroidism and thyroid growth.
It usually presents as a component of the syndrome known as Graves' disease where loss of immune tolerance to the thyrotropin receptor (TSHR) results in the generation of activating antibodies against that protein and hyperthyroidism.
To test the possibility that hyperthyroid cats develop antibodies that stimulate the autologous receptor, transfected cells expressing the feline TSHR were treated with sera or purified IgG obtained from 16 hyperthyroid cats.