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  1. Article ; Online: p66

    Pérez, Hernán / Finocchietto, Paola Vanesa / Alippe, Yael / Rebagliati, Inés / Elguero, María Eugenia / Villalba, Nerina / Poderoso, Juan José / Carreras, María Cecilia

    Oxidative medicine and cellular longevity

    2018  Volume 2018, Page(s) 8561892

    Abstract: Programmed and damage aging theories have traditionally been conceived as stand-alone schools of thought. However, the ... ...

    Abstract Programmed and damage aging theories have traditionally been conceived as stand-alone schools of thought. However, the p66
    MeSH term(s) Aging/metabolism ; Animals ; Brain/metabolism ; Homeostasis ; Mice ; Mice, Knockout ; Mitochondria/metabolism ; Reactive Nitrogen Species/metabolism ; Sirtuin 3/metabolism ; Src Homology 2 Domain-Containing, Transforming Protein 1/metabolism
    Chemical Substances Reactive Nitrogen Species ; Shc1 protein, mouse ; Sirt3 protein, mouse ; Src Homology 2 Domain-Containing, Transforming Protein 1 ; Sirtuin 3 (EC 3.5.1.-)
    Language English
    Publishing date 2018-03-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2455981-7
    ISSN 1942-0994 ; 1942-0994
    ISSN (online) 1942-0994
    ISSN 1942-0994
    DOI 10.1155/2018/8561892
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Cardiac-specific overexpression of thioredoxin 1 attenuates mitochondrial and myocardial dysfunction in septic mice.

    Sánchez-Villamil, Juana P / D'Annunzio, Verónica / Finocchietto, Paola / Holod, Silvia / Rebagliati, Inés / Pérez, Hernán / Peralta, Jorge G / Gelpi, Ricardo J / Poderoso, Juan J / Carreras, María C

    The international journal of biochemistry & cell biology

    2016  Volume 81, Issue Pt B, Page(s) 323–334

    Abstract: Sepsis-induced myocardial dysfunction is associated with increased oxidative stress and mitochondrial dysfunction. Current evidence suggests a protective role of thioredoxin-1 (Trx1) in the pathogenesis of cardiovascular diseases. However, it is unknown ... ...

    Abstract Sepsis-induced myocardial dysfunction is associated with increased oxidative stress and mitochondrial dysfunction. Current evidence suggests a protective role of thioredoxin-1 (Trx1) in the pathogenesis of cardiovascular diseases. However, it is unknown yet a putative role of Trx1 in sepsis-induced myocardial dysfunction, in which oxidative stress is an underlying cause. Transgenic male mice with Trx1 cardiac-specific overexpression (Trx1-Tg) and its wild-type control (wt) were subjected to cecal ligation and puncture or sham surgery. After 6, 18, and 24h, cardiac contractility, antioxidant enzymes, protein oxidation, and mitochondrial function were evaluated. Trx1 overexpression improved the average life expectancy (Trx1-Tg: 36, wt: 28h; p=0.0204). Sepsis induced a decrease in left ventricular developed pressure in both groups, while the contractile reserve, estimated as the response to β-adrenergic stimulus, was higher in Trx1-Tg in relation to wt, after 6h of the procedure. Trx1 overexpression attenuated complex I inhibition, protein carbonylation, and loss of membrane potential, and preserved Mn superoxide dismutase activity at 24h. Ultrastructural alterations in mitochondrial cristae were accompanied by reduced optic atrophy 1 (OPA1) fusion protein, and activation of dynamin-related protein 1 (Drp1) (fission protein) in wt mice at 24h, suggesting mitochondrial fusion/fission imbalance. PGC-1α gene expression showed a 2.5-fold increase in Trx1-Tg at 24h, suggesting mitochondrial biogenesis induction. Autophagy, demonstrated by electron microscopy and increased LC3-II/LC3-I ratio, was observed earlier in Trx1-Tg. In conclusion, Trx1 overexpression extends antioxidant protection, attenuates mitochondrial damage, and activates mitochondrial turnover (mitophagy and biogenesis), preserves contractile reserve and prolongs survival during sepsis.
    Language English
    Publishing date 2016-12
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1228429-4
    ISSN 1878-5875 ; 1357-2725
    ISSN (online) 1878-5875
    ISSN 1357-2725
    DOI 10.1016/j.biocel.2016.08.045
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Mitochondrial respiration in muscle and liver from cold-acclimated hypothyroid rats.

    Zaninovich, Angel A / Rebagliati, Ines / Raices, Marcela / Ricci, Conrado / Hagmuller, Karl

    Journal of applied physiology (Bethesda, Md. : 1985)

    2003  Volume 95, Issue 4, Page(s) 1584–1590

    Abstract: The effects of long-term cold exposure on muscle and liver mitochondrial oxygen consumption in hypothyroid and normal rats were examined. Thyroid ablation was performed after 8-wk acclimation to 4 degrees C. Hypothyroid and normal controls remained in ... ...

    Abstract The effects of long-term cold exposure on muscle and liver mitochondrial oxygen consumption in hypothyroid and normal rats were examined. Thyroid ablation was performed after 8-wk acclimation to 4 degrees C. Hypothyroid and normal controls remained in the cold for an additional 8 wk. At the end of 16-wk cold exposure, all hypothyroid rats were alive and normothermic and had normal body weight. At ambient temperature (24 degrees C), thyroid ablation induced a 65% fall in muscle mitochondrial oxygen consumption, which was reversed by thyroxine but not by norepinephrine administration. After cold acclimation was reached, suppression of thyroid function reduced muscle mitochondrial respiration by 30%, but the hypothyroid values remained about threefold higher than those in hypothyroid muscle in the warm. Blockade of beta- and alpha1-adrenergic receptors in both hypothyroid and normal rats produced hypothermia in vivo and a fall in muscle, liver, and brown adipose tissue mitochondria respiration in vitro. In normal rats, cold acclimation enhanced muscle respiration by 35%, in liver 18%, and in brown adipose tissue 450% over values in the warm. The results demonstrate that thyroid hormones, in the presence of norepinephrine, are major determinants of thermogenic activity in muscle and liver of cold-acclimated rats. After thyroid ablation, cold-induced nonshivering thermogenesis replaced 3,5,3'-triiodothyronine-induced thermogenesis, and normal body temperature was maintained.
    MeSH term(s) Adipose Tissue, Brown/metabolism ; Adrenergic Antagonists/pharmacology ; Adrenergic Uptake Inhibitors/pharmacology ; Animals ; Body Weight ; Cold Temperature ; Drug Combinations ; Female ; Hypothyroidism/metabolism ; Hypothyroidism/pathology ; Hypothyroidism/physiopathology ; Male ; Mitochondria/metabolism ; Mitochondria, Liver/metabolism ; Mitochondria, Muscle/metabolism ; Norepinephrine/pharmacology ; Oxygen Consumption/drug effects ; Prazosin/pharmacology ; Propranolol/pharmacology ; Rats ; Rats, Wistar ; Reserpine/pharmacology ; Temperature ; Thermogenesis/drug effects
    Chemical Substances Adrenergic Antagonists ; Adrenergic Uptake Inhibitors ; Drug Combinations ; Reserpine (8B1QWR724A) ; Propranolol (9Y8NXQ24VQ) ; Norepinephrine (X4W3ENH1CV) ; Prazosin (XM03YJ541D)
    Language English
    Publishing date 2003-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 219139-8
    ISSN 1522-1601 ; 8750-7587 ; 0021-8987 ; 0161-7567
    ISSN (online) 1522-1601
    ISSN 8750-7587 ; 0021-8987 ; 0161-7567
    DOI 10.1152/japplphysiol.00363.2003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Brown fat thermogenesis in cold-acclimated rats is not abolished by the suppression of thyroid function.

    Zaninovich, Angel A / Raíces, Marcela / Rebagliati, Inés / Ricci, Conrado / Hagmüller, Karl

    American journal of physiology. Endocrinology and metabolism

    2002  Volume 283, Issue 3, Page(s) E496–502

    Abstract: The effects of long-term cold exposure on brown adipose tissue (BAT) thermogenesis in hypothyroid rats have been examined. Thyroid ablation was performed in normal rats after 2 mo of exposure to 4 degrees C, when BAT hypertrophy and thermogenic activity ... ...

    Abstract The effects of long-term cold exposure on brown adipose tissue (BAT) thermogenesis in hypothyroid rats have been examined. Thyroid ablation was performed in normal rats after 2 mo of exposure to 4 degrees C, when BAT hypertrophy and thermogenic activity were maximal. After ablation, hypothyroid and normal controls remained in the cold for 2 additional months. At the end of the 4-mo cold exposure, all untreated hypothyroid rats were alive, had normal body temperature, and had gained an average 12.8% more weight than normal controls. Long-term cold exposure of hypothyroid rats markedly increased BAT weight, mitochondrial proteins, uncoupling protein (UCP)-1, mRNA for UCP-1, and oxygen consumption to levels similar to those seen in cold-exposed normal rats. The results indicate that thyroid hormones are required for increased thermogenic capacity to occur as an adaptation to long-term cold exposure. However, cold adaptation can be maintained in the absence of thyroid hormone.
    MeSH term(s) Acclimatization ; Adipose Tissue, Brown/physiology ; Adipose Tissue, Brown/physiopathology ; Animals ; Antithyroid Agents/pharmacology ; Body Weight ; Carrier Proteins/metabolism ; Cold Temperature ; Female ; Glyceraldehyde-3-Phosphate Dehydrogenases/metabolism ; Hypothyroidism/metabolism ; Hypothyroidism/physiopathology ; Ion Channels ; Isoenzymes/metabolism ; Male ; Membrane Proteins/metabolism ; Methimazole/pharmacology ; Mitochondria/metabolism ; Mitochondrial Proteins ; Oxygen Consumption ; RNA, Messenger/metabolism ; Rats ; Rats, Wistar ; Thermogenesis ; Thyroid Gland/physiology ; Thyroid Gland/physiopathology ; Time Factors ; Uncoupling Protein 1
    Chemical Substances Antithyroid Agents ; Carrier Proteins ; Ion Channels ; Isoenzymes ; Membrane Proteins ; Mitochondrial Proteins ; RNA, Messenger ; Ucp1 protein, rat ; Uncoupling Protein 1 ; Methimazole (554Z48XN5E) ; Glyceraldehyde-3-Phosphate Dehydrogenases (EC 1.2.1.-)
    Language English
    Publishing date 2002-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603841-4
    ISSN 1522-1555 ; 0193-1849
    ISSN (online) 1522-1555
    ISSN 0193-1849
    DOI 10.1152/ajpendo.00540.2001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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