Blocking of KC1O4-induced metamorphosis in premetamorphic sea lampreys by exogenous thyroid hormones (TH); effects of KC1O4 and TH on serum TH concentrations and intestinal thyroxine outer-ring deiodination.
Immediately premetamorphic larval sea lampreys (Petromyzon marinus) (>/=120 mm in length) were treated for 4, 8, or 16 weeks with one of two concentrations of either exogenous thyroxine (T4; 1 or 0.5 mg/L) or 3,5,3'-triiodothyronine (T3; 1 or 0.25 mg/L) in the presence or absence of the goitrogen potassium perchlorate (KC1O4; 0.05%) as well as with KC1O4 alone. Larvae from all treatments were examined for signs of metamorphosis, changes in serum T4 and T3 concentrations (serum T4 and serum T3), and changes in intestinal T4 outer-ring (5') deiodination to T3 (T4ORD). KC1O4 depressed both serum T4 and T3 and induced metamorphosis in 80% of larvae treated for 8 weeks or longer. However, neither effect was observed in larvae exposed to KC1O4 combined with either thyroid hormone (TH). These data confirm previous suggestions that exogenous TH blocks KC1O4-induced metamorphosis by elevating serum TH concentrations, and provide evidence that declines in serum TH concentrations are mandatory for precocious metamorphosis. Serum T4, but not serum T3, was elevated following exogenous T4 treatment in the presence or absence of KC1O4. This maintenance of serum T3 at control levels, in the presence of a T4 challenge, was not due to decreases in intestinal T4ORD activity, since T4ORD activity was not affected by any treatments in the study. Exogenous T3 elevated both serum T4 and T3. However, serum T3 in T3-treated larvae decreased with time, suggesting a stringent T3 regulation. Elevation of serum T4 following T3 treatment may have been a result of either inhibition of T4 metabolism, or stimulation of T4 secretion by the endostyle. Based on these results, we conclude that (i) exogenous TH blocks KClO4-induced metamorphosis in sea lampreys and (ii) serum T3 is maintained at control levels despite elevations in serum T4 (its immediate precursor), but this does not involve any changes in intestinal T4ORD activity.
Manzon
R G
RG
Division of Life Sciences, University of Toronto at Scarborough, 1265 Military Trail, Scarborough, Ontario, M1C 1A4, Canada.
Eales
J G
JG
Youson
J H
JH
D000818:Animals; D007422:Intestines / Q000201:enzymology; D007453:Iodide Peroxidase / Q000378:metabolism*; D007798:Lampreys / Q000254:growth & development*; D008675:Metamorphosis, Biological / Q000187:drug effects*; D008861:Microsomes / Q000201:enzymology; D010472:Perchlorates / Q000494:pharmacology*; D017680:Potassium Compounds / Q000494:pharmacology*; D013963:Thyroid Hormones / Q000097:blood* / Q000494:pharmacology*; D013974:Thyroxine / Q000097:blood / Q000378:metabolism / Q000494:pharmacology; D014284:Triiodothyronine / Q000097:blood / Q000494:pharmacology
D010472:Perchlorates; D017680:Potassium Compounds; D013963:Thyroid Hormones; D014284:Triiodothyronine; C009006:potassium perchlorate; D007453:Iodide Peroxidase; D013974:Thyroxine