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 degrees 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 microU/L vs. 15.5 +/- 6.2; P < 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 < 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 microU/L vs. 15.5 +/- 6.2; P < 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.
Frangioni
Giuliano
G
Department of Animal Biology and Genetics, University of Florence, via Romana 17, I-50125 Florence, Italy. giuliano.frangioni@unifi.it
Atzori
Antonio
A
Balzi
Manuela
M
Fuzzi
Giancarlo
G
Ghinassi
Andrea
A
Pescosolido
Nicoletta
N
Bianchi
Stefano
S
Borgioli
Gianfranco
G
D000818:Animals; D005234:Fatty Liver / Q000097:blood / Q000378:metabolism; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006651:Histocytochemistry; D000860:Hypoxia / Q000097:blood / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism; D008297:Male; D008548:Melanosis / Q000378:metabolism; D010902:Pituitary Gland / Q000378:metabolism; D012455:Salamandridae / Q000097:blood / Q000378:metabolism*; D013312:Stress, Physiological / Q000097:blood / Q000209:etiology / Q000378:metabolism; D013961:Thyroid Gland / Q000378:metabolism*; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
D014284:Triiodothyronine; D013972:Thyrotropin; D013974:Thyroxine