Thyroid hormone-induced oxidative stress in rodents and humans: A comparative view and relation to redox regulation of gene expression

Fernández, Virgínia; Tapia, Gladys; Varela, Patricia; Romanque, Pamela; Cartier-Ugarte, Denise; Videla, Luis A.

doi:10.1016/j.cbpc.2005.10.007

Cited by 61 publications

(62 citation statements)

References 66 publications

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“…However, in other pathophysiological conditions, it has been found that oxidative stress is associated with increased mRNA levels of TNF-α, IL-10, MMP-2 and MMP-9 (Rajagopalan et al 1996;Tapia et al 2003). The differences between the findings obtained here and those present in the literature may be due to the fact that development of oxidative stress might induce different cellular responses, depending on the level of free oxygen radicals achieved and the time of exposure (Droge 2002;Fernandez et al 2006). It is known that reactive oxygen species play an important role in cellular signalling and in the regulation of gene expression, but in their excess they are very toxic, impairing the cellular components.…”

Section: Resultscontrasting

confidence: 51%

“…As mentioned above, TNF-α plays an important role in liver regeneration (Schwabe & Brenner, 2006). Oxidative stress induced by thyroid hormone in the liver, caused mRNA expression of the NF-κB-responsive genes for TNF-α and IL-10 (Fernandez et al 2006). In the IL-10 knockout mice, apoptosis was found to be increased in a model of lipopolysaccharide-induced apoptosis (Zhong et al 2006), suggesting that IL-10 could inhibit liver apoptosis.…”

Section: Resultsmentioning

confidence: 96%

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Copper decreases gene expression of TNF-α, IL-10, and of matrix metalloproteinases MMP-2 and MMP-9 in isolated perfused rat livers

et al. 2007

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Abstract:Copper is known to induce oxidative stress in a number of models. It was shown that many pathophysiological events were associated with oxidative stress. Further, oxidative stress can increase gene expression of cytokines and of metalloproteinases. We previously found that copper toxic effects in isolated perfused rat livers were associated with significant oxidative stress (as assessed by lipid peroxidation, protein oxidation and oxidative DNA damage, particularly at concentration of 0.03 mM of Cu 2+ in the perfusate). Here we investigated gene expression of tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10), matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) in frozen liver tissue samples by the real-time PCR assay. Compared to controls, copper at concentration of 0.01 mM did not affect gene expression of TNF-α, IL-10, MMP-2 and MMP-9, whereas copper at concentration of 0.03 mM significantly decreased gene expression of all the four TNF-α, IL-10, MMP-2 and MMP-9 by 69%, 81%, 43%, and 62%, respectively. These results suggest that copper-induced oxidative stress in the isolated rat liver can lead to the suppression of gene expression. Because TNF-α and metalloproteinases are involved also in liver regeneration, the suppression of these genes by copper may be one of the mechanisms by which acute intoxication of animals and humans with copper may impair regenerative capability of the liver.

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Section: Resultscontrasting

confidence: 51%

Section: Resultsmentioning

confidence: 96%

Copper decreases gene expression of TNF-α, IL-10, and of matrix metalloproteinases MMP-2 and MMP-9 in isolated perfused rat livers

et al. 2007

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“…Fernandez et al found that thyroid calorigenesis is a hormonal stimulus for the REDOX activation of NFB, a response that is triggered in Kupffer cells having higher respiratoryburst activities (Fernandez et al, 2006). These findings are in agreement with studies showing that the NFB activation can be achieved by physiological levels of the ROS, which are produced during the respiratory burst after stimulation of isolated or cultured macrophages (Kaul & Forman, 1996) and in carbon-stimulated Kupffer cells in the isolated, perfused rat liver (Romanque et al, 2003).…”

Section: Hyperthyroidism and The Ros-steady Statesupporting

confidence: 60%

The Relationship Between Thyroid States, Oxidative Stress and Cellular Damage

Cano-Europa¹,

Blas-Valdivia²,

Franco-Colín³

et al. 2012

Oxidative Stress and Diseases

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“…The increase of some antioxidant enzymes activities such as SOD, GPx and CAT, which are the main antioxidants in the body may be indicative of the failure of compensating the induced oxidative stress [207,208]. These enzymes may scavenge excess O2 ‾ and H2O2, and peroxides ROOH produced by free radicals.…”

Section: Antioxidant Statusmentioning

confidence: 99%