Kupffer Cell Function in Thyroid Hormone-Induced Liver Oxidative Stress in the Rat

Tapia, Gladys; Pepper, Inés; Smok, G; Videla, Luis A.

doi:10.3109/10715769709097805

Cited by 62 publications

(81 citation statements)

References 25 publications

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“…1). Interestingly, T 3 -induced changes in hepatic oxidative stress-related parameters are significantly diminished by GdCl 3 pretreatment (29,65), thus raising the possibility of upregulation of redox-sensitive gene transcription at the Kupffer cell level (8)(9)(10)12).…”

Section: Kupffer Cell Activity In Hyperthyroid Statementioning

confidence: 99%

“…1; 25, 26). In addition to T 3 -induced liver mitochondrial ROS production, hyperthyroid state in rats is associated with enhancement in other ROS-generating systems, including the highly pro-oxidant microsomal cytochrome P450 2E1 (27), cytosolic enzymes such as xanthine oxidase (28), peroxisomal fatty acid b-oxidation (25), and the respiratory burst activity of Kupffer cells involving NADPH oxidase activity (29). In addition, Kupffer cells isolated from acutely T 3 -treated rats exhibited upregulation of UCP2 mRNA, which may limit mitochondrial ROS production by these cells (30).…”

Section: T 3 -Induced Enhancement Of Liver O 2 Consumption and Oxidatmentioning

confidence: 99%

“…This pro-oxidant state induced in the liver of experimental animals by thyroid hormone administration is considered as a mild redox alteration, considering the lack of occurrence of morphological changes in liver parenchyma, except for significant hyperplasia and hypertrophy of Kupffer cells ( Fig. 2A), the resident macrophages of the liver (29,39). In man, hyperthyroidism is characterized by significant changes in circulating parameters related to oxidative stress, including (i) higher levels of lipid peroxidation indicators (40)(41)(42)(43)(44)(45)(46)(47)(48)(49); (ii) enhancement in hydrogen peroxide and lipid hydroperoxide levels (49); and (iii) diminished levels of antioxidants such as a-tocopherol (41), coenzyme Q (44), ascorbic acid (41), and reduced thiols (42,46,50).…”

Section: T 3 -Induced Enhancement Of Liver O 2 Consumption and Oxidatmentioning

confidence: 99%

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Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Videla

2010

IUBMB Life

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SummaryThyroid hormone (L-3,3 0 ,5-triiodothyronine, T 3 ) exerts calorigenic effects by accelerating mitochondrial O 2 consumption through transcriptional activation of respiratory genes, with consequent increased reactive oxygen species (ROS) production. In the liver, ROS generation occurs at different sites of hepatocytes and in the respiratory burst of Kupffer cells, triggering the activation of the transcription factors nuclear factor-jB, signal transducer and activator of transcription 3, and activating protein 1. Under these conditions, the redox upregulation of Kupffer cell-dependent expression of cytokines [tumor necrosis factor-a, interleukin (IL)-1, and IL-6] is achieved, which upon interaction with specific receptors in hepatocytes trigger the expression of antioxidant enzymes (manganese superoxide dismutase, inducible nitric oxide synthase), antiapoptotic proteins (Bcl-2), and acute-phase proteins (haptoglobin, b-fibrinogen). These responses and the promotion of hepatocyte and Kupffer cell proliferation observed represent hormetic effects re-establishing redox homeostasis, promoting cell survival, and protecting the liver against ischemia-reperfusion (IR) injury. It is proposed that hormesis underlying T 3 action may constitute a novel preconditioning strategy for IR injury during liver surgery in man or in liver transplantation using reduced-size grafts from living donors, considering that (i) with the exception of the controversial ischemic preconditioning, all other studied strategies have failed to reach the clinical setting and (ii) T 3 is a well-tolerated therapeutic agent that either lacks major adverse effects or has minimal and controlled side effects. IUBMBIUBMB Life, 62(6): [460][461][462][463][464][465][466] 2010

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Section: Kupffer Cell Activity In Hyperthyroid Statementioning

confidence: 99%

Section: T 3 -Induced Enhancement Of Liver O 2 Consumption and Oxidatmentioning

confidence: 99%

Section: T 3 -Induced Enhancement Of Liver O 2 Consumption and Oxidatmentioning

confidence: 99%

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Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Videla

2010

IUBMB Life

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“…(B) Kupffer cells are the resident macrophages of the liver. TH stimulation in vivo results in Kupffer cell hyperplasia and enhanced phagocytosis (Tapia et al 1997, Valencia et al 2004. TH transporter and receptor expression in Kupffer cells have not yet been studied.…”

Section: Effects Of Extracellular Thyroid Hormone Levels On Macrophagmentioning

confidence: 99%

“…Several studies by the same group have analysed the effect of TH administration on rat liver and the role of Kupffer cells in this process. T 3 administration induces oxidative stress in the liver (Tapia et al 1997, 2006, 2010, Valencia et al 2004, Fernandez et al 2005, 2007a,b, 2008. This is thought to be mediated via Kupffer cells, which demonstrate hyperplasia, increased phagocytic capacity, increased ROS generation and tumour necrosis factor α (TNFα) production in response to T 3 administration in vivo (Fig.…”

Section: Thyroid Hormone Metabolism In Tissue-resident Macrophagesmentioning

confidence: 99%

Thyroid hormone metabolism in innate immune cells

Spek

Fliers

Boelen

2017

Journal of Endocrinology

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Thyroid hormone (TH) metabolism and thyroid status have been linked to various aspects of the immune response. There is extensive literature available on the effects of thyroid hormone on innate immune cells. However, only recently have authors begun to study the mechanisms behind these effects and the role of intracellular TH metabolism in innate immune cell function during inflammation. This review provides an overview of the molecular machinery of intracellular TH metabolism present in neutrophils, macrophages and dendritic cells and the role and effects of intracellular TH metabolism in these cells. Circulating TH levels have a profound effect on neutrophil, macrophage and dendritic cell function. In general, increased TH levels result in an amplification of the pro-inflammatory response of these cells. The mechanisms behind these effects include both genomic and non-genomic effects of TH. Besides a pro-inflammatory effect induced by extracellular TH, the cellular response to pro-inflammatory stimuli appears to be dependent on functional intracellular TH metabolism. This is illustrated by the fact that the deiodinase enzymes and in some cell types also thyroid hormone receptors appear to be crucial for adequate innate immune cell function. This overview of the literature suggests that TH metabolism plays an important role in the host defence against infection through the modulation of innate immune cell function.

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Nrf2‐regulated phase‐II detoxification enzymes and phase‐III transporters are induced by thyroid hormone in rat liver

2013

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Thyroid hormone (T₃)-induced calorigenesis triggers the hepatic production of reactive oxygen species (ROS) and redox-sensitive nuclear transcription factor erythroid 2-related factor 2 (Nrf2) activation. The aim of this study was to test the hypothesis that in vivo T₃ administration upregulates the expression of phase II and III detoxification proteins that is controlled by Nrf2. Male Sprague-Dawley rats were given a single intraperitoneal dose of 0.1 mg T₃/kg or T₃ vehicle (controls). After treatment, rectal temperature of the animals, liver Nrf2 DNA binding (EMSA), protein levels of epoxide hydrolase 1 (Eh1), NADPH-quinone oxidoreductase 1 (NQO1), glutathione-S-transferases Ya (GST Ya) and Yp (GST Yp), and multidrug resistance-associated proteins 2 (MRP-2) and 4 (MRP-4) (Western blot), and MRP-3 (RT-PCR) were determined at different times. T₃ significantly rose the rectal temperature of the animals in the time period studied, concomitantly with increases (P < 0.05) of liver Nrf2 DNA binding at 1 and 2 h after treatment, which was normalized at 4-12 h. Within 1-2 h after T₃ treatment, liver phase II enzymes Eh1, NQO1, GST Ya, and GST Yp were enhanced (P < 0.05) as did phase III transporters MRP-2 and MRP-3, whereas MRP-4 remained unchanged. In conclusion, enhancement of liver Nrf2 DNA binding elicited by in vivo T₃ administration is associated with upregulation of the expression of detoxification and drug transport proteins. These changes, in addition to antioxidant protein induction previously observed, may represent cytoprotective mechanisms underlying T₃ preconditioning against liver injury mediated by ROS and chemical toxicity.

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Kupffer Cell Function in Thyroid Hormone-Induced Liver Oxidative Stress in the Rat

Cited by 62 publications

References 25 publications

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Thyroid hormone metabolism in innate immune cells

Nrf2‐regulated phase‐II detoxification enzymes and phase‐III transporters are induced by thyroid hormone in rat liver

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