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Thyroid and hypoxic stress in the newt Triturus carnifex

When specimens of the newt Triturus carnifex, under anaesthesia by submersion in a 0.2% chlorbutol solution for 25 min, are isolated in a respiratory chamber at 18°C containing water with only 1.3 ppm of oxygen, they consume the oxygen completely in about 3 hr, but they can stay alive for many more...

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Published in:Journal of experimental zoology. Part A, Comparative experimental biology Comparative experimental biology, 2006-03, Vol.305A (3), p.225-232
Main Authors: Frangioni, Giuliano, Atzori, Antonio, Balzi, Manuela, Fuzzi, Giancarlo, Ghinassi, Andrea, Pescosolido, Nicoletta, Bianchi, Stefano, Borgioli, Gianfranco
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container_title Journal of experimental zoology. Part A, Comparative experimental biology
container_volume 305A
creator Frangioni, Giuliano
Atzori, Antonio
Balzi, Manuela
Fuzzi, Giancarlo
Ghinassi, Andrea
Pescosolido, Nicoletta
Bianchi, Stefano
Borgioli, Gianfranco
description When specimens of the newt Triturus carnifex, under anaesthesia by submersion in a 0.2% chlorbutol solution for 25 min, are isolated in a respiratory chamber at 18°C containing water with only 1.3 ppm of oxygen, they consume the oxygen completely in about 3 hr, but they can stay alive for many more hours and wake up with no apparent exterior consequences. Hypoxia induces rapid onset of hepatic steatosis and melanosis, as well as a controlled haemolytic process involving a pool of red blood cells of the same order of size as that held as a reserve in the spleen by animals in an aerial habitat. At the origin of the phenomena is an intense response by the hypophysis, histologically detectable 1 hr from the onset of treatment and confirmed 2 hr later by a highly significant increase in the plasma thyroidstimulating hormone (TSH) concentration compared with the controls (41.5±13.7 µU/L vs. 15.5±6.2; P
doi_str_mv 10.1002/jez.a.268
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Hypoxia induces rapid onset of hepatic steatosis and melanosis, as well as a controlled haemolytic process involving a pool of red blood cells of the same order of size as that held as a reserve in the spleen by animals in an aerial habitat. At the origin of the phenomena is an intense response by the hypophysis, histologically detectable 1 hr from the onset of treatment and confirmed 2 hr later by a highly significant increase in the plasma thyroidstimulating hormone (TSH) concentration compared with the controls (41.5±13.7 µU/L vs. 15.5±6.2; P&lt;0.005). The thyroid follicles react by reabsorbing their colloid, but instead of an increase in the plasma free T3 and T4 concentrations, fT3 falls significantly (1.5±0.3 pg/mL vs., the 2.4±0.7; P&lt;0.05), whereas fT4 remains stationary (4.0±0.5 pg/mL vs. 4.6±0.8; N.S.). After 6 hr, the plasmatic TSH concentration is still higher than in the controls (27.0±3.0 µU/L vs. 15.5±6.2; P&lt;0.05), whereas fT3 and fT4 remain stable (1.5±0.3 and 4.4±0.5 pg/mL, respectively). If T3 or T4 labelled with 125I is administered prior to hypoxia, after 6 hr of treatment the radioactivity is found to be limited exclusively to the liver and kidney; the thyroid, gall bladder and gut result negative, and this does not agree with hypotheses of hormone inactivation by deiodination, sulphation or glucuronidation. This apparently peculiar endocrine path has not been observed in previous studies on hypoxia in vertebrates, because the experiments were always designed to analyse plasma hormone levels after at least 24 hr of hypoxia or during chronic treatments, losing the most interesting phases of the endocrine response. The possibility that the hypoxic newt possesses alternative or complementary metabolic pathways to anaerobic glycolysis to sustain steatogenesis and melanogenesis and maintain the same cardiac activity as the controls is briefly discussed. J. Exp. 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Part A, Comparative experimental biology</title><addtitle>J. Exp. Zool</addtitle><description>When specimens of the newt Triturus carnifex, under anaesthesia by submersion in a 0.2% chlorbutol solution for 25 min, are isolated in a respiratory chamber at 18°C containing water with only 1.3 ppm of oxygen, they consume the oxygen completely in about 3 hr, but they can stay alive for many more hours and wake up with no apparent exterior consequences. Hypoxia induces rapid onset of hepatic steatosis and melanosis, as well as a controlled haemolytic process involving a pool of red blood cells of the same order of size as that held as a reserve in the spleen by animals in an aerial habitat. At the origin of the phenomena is an intense response by the hypophysis, histologically detectable 1 hr from the onset of treatment and confirmed 2 hr later by a highly significant increase in the plasma thyroidstimulating hormone (TSH) concentration compared with the controls (41.5±13.7 µU/L vs. 15.5±6.2; P&lt;0.005). The thyroid follicles react by reabsorbing their colloid, but instead of an increase in the plasma free T3 and T4 concentrations, fT3 falls significantly (1.5±0.3 pg/mL vs., the 2.4±0.7; P&lt;0.05), whereas fT4 remains stationary (4.0±0.5 pg/mL vs. 4.6±0.8; N.S.). After 6 hr, the plasmatic TSH concentration is still higher than in the controls (27.0±3.0 µU/L vs. 15.5±6.2; P&lt;0.05), whereas fT3 and fT4 remain stable (1.5±0.3 and 4.4±0.5 pg/mL, respectively). If T3 or T4 labelled with 125I is administered prior to hypoxia, after 6 hr of treatment the radioactivity is found to be limited exclusively to the liver and kidney; the thyroid, gall bladder and gut result negative, and this does not agree with hypotheses of hormone inactivation by deiodination, sulphation or glucuronidation. This apparently peculiar endocrine path has not been observed in previous studies on hypoxia in vertebrates, because the experiments were always designed to analyse plasma hormone levels after at least 24 hr of hypoxia or during chronic treatments, losing the most interesting phases of the endocrine response. The possibility that the hypoxic newt possesses alternative or complementary metabolic pathways to anaerobic glycolysis to sustain steatogenesis and melanogenesis and maintain the same cardiac activity as the controls is briefly discussed. J. Exp. 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At the origin of the phenomena is an intense response by the hypophysis, histologically detectable 1 hr from the onset of treatment and confirmed 2 hr later by a highly significant increase in the plasma thyroidstimulating hormone (TSH) concentration compared with the controls (41.5±13.7 µU/L vs. 15.5±6.2; P&lt;0.005). The thyroid follicles react by reabsorbing their colloid, but instead of an increase in the plasma free T3 and T4 concentrations, fT3 falls significantly (1.5±0.3 pg/mL vs., the 2.4±0.7; P&lt;0.05), whereas fT4 remains stationary (4.0±0.5 pg/mL vs. 4.6±0.8; N.S.). After 6 hr, the plasmatic TSH concentration is still higher than in the controls (27.0±3.0 µU/L vs. 15.5±6.2; P&lt;0.05), whereas fT3 and fT4 remain stable (1.5±0.3 and 4.4±0.5 pg/mL, respectively). If T3 or T4 labelled with 125I is administered prior to hypoxia, after 6 hr of treatment the radioactivity is found to be limited exclusively to the liver and kidney; the thyroid, gall bladder and gut result negative, and this does not agree with hypotheses of hormone inactivation by deiodination, sulphation or glucuronidation. This apparently peculiar endocrine path has not been observed in previous studies on hypoxia in vertebrates, because the experiments were always designed to analyse plasma hormone levels after at least 24 hr of hypoxia or during chronic treatments, losing the most interesting phases of the endocrine response. The possibility that the hypoxic newt possesses alternative or complementary metabolic pathways to anaerobic glycolysis to sustain steatogenesis and melanogenesis and maintain the same cardiac activity as the controls is briefly discussed. J. Exp. 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subjects Animals
Fatty Liver - blood
Fatty Liver - metabolism
Female
Heart Rate - physiology
Histocytochemistry
Hypoxia - blood
Hypoxia - metabolism
Kidney - metabolism
Male
Melanosis - metabolism
Pituitary Gland - metabolism
Salamandridae
Salamandridae - blood
Salamandridae - metabolism
Stress, Physiological - blood
Stress, Physiological - etiology
Stress, Physiological - metabolism
Thyroid Gland - metabolism
Thyrotropin - blood
Thyroxine - blood
Triiodothyronine - blood
Triturus carnifex
title Thyroid and hypoxic stress in the newt Triturus carnifex
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