Influence of hyperthyroidism on hepatic antioxidants and cytokines Levels: An Experimental Study

Abstract

Objective: Thyroid diseases greatly affect the liver. Hyperthyroidism can affect the function of the liver. This study aimed to investigate the possible change of antioxidant and pro-inflammatory cytokines levels in liver tissue in hyperthyroid rats.
 Material and Methods: This study was carried out with 2 experimental groups. Hyperthyroid group was fed with 4 mg/kg L-thyroxine added standard fodder. Control group was fed with standard rat fodder. Liver selenium (Se) levels were measured by inductively coupled plasma optical emission spectrophotometer (ICP-OES). The antioxidant markers such as Selenoprotein P (SelP), and glutathione peroxidase (GPx), and the pro-inflammatory cytokines such as Interleukin (IL)-18, and Tumor necrosis factor-α (TNF-α) levels were studied in liver tissues by ELISA. All markers levels of liver samples were measured in tissue homogenates.
 Results: Se, SelP, and GPx levels of the hyperthyroidism group were lower than the control group. (p=0.038, p=0.046, p=0.008 respectively). There was a significant increase in IL-18 and TNF-α levels in hyperthyroidism group when compared to control group (p=0.002, p=0.023 respectively). There was positive correlation between FT3 and FT4, IL-18 and TNF-α (r=0.761, r=0.843, and r=0.826 respectively), but there was negative correlation between FT3 and Se, SelP, and GPx (r=-0.833, r=-0.754, and r=-0.778 respectively).
 Conclusion: Our findings showed that antioxidant marker levels were decreased, and pro-inflammatory cytokine levels were increased in liver tissues of hyperthyroid rats. These findings suggest that impaired antioxidant and pro-inflammatory status may play a role in liver pathogenesis due to hyperthyroidism.

Melissa officinalis extract palliates redox imbalance and inflammation associated with hyperthyroidism-induced liver damage by regulating Nrf-2/ Keap-1 gene expression in γ-irradiated rats

“…Lyu et al [ 65 ] revealed overexpression of hepatic pro-inflammatory genes (IL-6 and TNF-α) due to hepatic deficiency of Nrf2. Owing to this, the excessive production of pro-inflammatory cytokines in the hepatic tissues of the hyperthyroid rats is assured by the upregulated mRNA expression of both TNF-α and MCP1 which is consistent with the results of Bahtiyar et al [ 44 ] and Ashry et al [ 52 ]. Queck et al [ 66 ] reported that activation of the hepatic macrophage during liver injury was associated with upregulation of the hepatic MCP-1 which in turn activates fibrogenic hepatic stellate cells (HSCs) [ 67 ].…”

“…This was confirmed by the damaged structural integrity of the liver manifested by hepatocyte degeneration and coagulative necrosis. The hepatic dysfunction associated with hyperthyroidism was attributed to improper exposure to high levels of thyroid hormones, hepatocyte anoxia and apoptosis resulting from excessive energy demand associated with hypermetabolic state provoking mitochondrial generation of the reactive oxygen species (ROS) as well as mitochondrial apoptotic pathway, hepatocytes degeneration subsequent to degradation of glycogen and protein in addition to hepatic necrosis following thyrotoxicosis cardiac failure [ 44 , 45 ]. On the contrary, treating the hyperthyroid rats with MO Extract remarkably alleviated the hepatic structure and dysfunction appeared clearly by the significant reduction in the activities of the serum transaminases (AST and ALT) coupled with enhancement of the levels of the hepatic proteins.…”

Vitamin D improves oxidative stress and histopathological damage in rat ovaries caused by hyperthyroidism

“…9 The effectiveness of some antioxidants, such as melatonin and selenium on oxidative stress developed by hyperthyroidism in tissues, such as testicles and liver has been investigated in various studies. 10,11 The aim of this study is to investigate the histopathological and biochemical efficacy of vitamin D on oxidative damage and fibrosis in rat ovary with hyperthyroidism induced experimentally.…”