Causal role of oxidative stress in liver preconditioning by thyroid hormone in rats

Fernández, Virgínia; Tapia, Gladys; Varela, Patricia; Gaete, Leonardo; Vera, G; Mora, Catalina; Vial, M; Videla, Luis A.

doi:10.1016/j.freeradbiomed.2008.01.010

Cited by 39 publications

(38 citation statements)

References 43 publications

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“…1; 12). The nongenomic actions of thyroid hormones may in turn influence gene transcription by different pathways involving either antioxidant-sensitive NF-jB, AP-1, and STAT3 activation (67,80) or TR and STAT phosphorylation (19,85). Furthermore, CREB-binding protein and the related protein p300 activating liganded TRs in the classical genomic pathway of T 3 action (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…This contention was evaluated in the 1-h ischemia-20-h reperfusion model, which elicited substantial liver damage with increased serum aspartate aminotransferase and TNF-a levels, higher liver oxidative stress status, loss of the DNA binding capacity of NF-jB and STAT3 implying loss of cytoprotective potential, and enhancement in AP-1 activation (78) as a major determinant of hepatotoxicity (79). These changes were normalized by a single dose of T 3 given 48 h before the IR protocol (78), a hormetic effect that was sensitive to the antioxidant N-acetylcysteine (80) or the Kupffer cell inactivator GdCl 3 given prior to T 3 , with enhanced hepatocyte proliferation compensating for liver cells lost due to IR-induced hepatocellular necrosis (68). Alternate hormetic responses induced by T 3 may involve (i) the transcriptional upregulation of uncoupling protein genes affording lower mitochondrial ROS generation (23,30) and export of peroxidized unsaturated fatty acid anions (81); (ii) acceleration of substrate cycles such as ATP cycling that increases mitochondrial oxidative phosphorylation and lowers ROS production, and/or NADPH cycling that favors antioxidants reduction, thus promoting ROS scavenging (82); and (iii) activation of the Nrf2 defense pathway (unpublished), upregulating antioxidant proteins and phase 2 detoxifying enzymes and transporters (83,84).…”

Section: Hormetic Nature Of Kupffer Cell-dependent Redox Upregulationmentioning

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: Discussionmentioning

confidence: 99%

Section: Hormetic Nature Of Kupffer Cell-dependent Redox Upregulationmentioning

confidence: 99%

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

Videla

2010

IUBMB Life

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“…development of transient and reversible oxidative stress (Fernandez et al 2008(Fernandez et al , 2009.…”

Section: :2mentioning

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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“…4). These mechanisms are effective in protecting the liver against IRI [5,6], the beneficial actions of thyroid hormones being also observed in ischemic injury of the heart [26], kidney [27], and brain [28] or in the repair of organs subjected to several types of injury other than IRI [29]. Data presented indicate that a protocol comprising the administration of single daily doses of 0.1 mg T 3 /kg to rats on three consecutive days underlies an enhanced liver ROS generation coupled to T 3 -induced increase in oxygen consumption as a result of the calorigenic effect achieved, leading to significant lipid peroxidation and protein oxidation responses and concomitant GSH depletion.…”

Section: Discussionmentioning

confidence: 99%

Causal role of oxidative stress in unfolded protein response development in the hyperthyroid state

Videla

Fernández

Cornejo

et al. 2015

Free Radical Biology and Medicine

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Causal role of oxidative stress in liver preconditioning by thyroid hormone in rats

Cited by 39 publications

References 43 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

Causal role of oxidative stress in unfolded protein response development in the hyperthyroid state

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