Polychlorinated biphenyl (PCB)-contaminated fish induces vitamin A and thyroid hormone deficiency in the common seal (Phoca vitulina)

1989 ◽  
Vol 15 (1) ◽  
pp. 99-105 ◽  
Author(s):  
A. Brouwer ◽  
P.J.H. Reijnders ◽  
J.H. Koeman
2021 ◽  
Author(s):  
Wissal Abassi ◽  
Nejmeddine Ouerghi ◽  
Anissa Bouassida

Hypothyroidism refers to the common pathological disorder of thyroid hormone deficiency. The successful therapy for hypothyroidism is levothyroxine (LT4) administration, which is the same as thyroxine but produced synthetically. Serum thyrotropin (TSH) normalization with LT4 replacement therapy in hypothyroidism is generally needed to restore a euthyroid state. The daily dose of thyroxine therapy depends on various factors, such as body weight, age, and severity. It also differs from hypothyroidism during pregnancy to congenital hypothyroidism. The presence of various comorbidities may exist such as myxoedema coma, coronary artery disease, obesity, anemia and COVID-19 which necessitate individualized treatment. LT4 intolerance manifested with sympathetic hyperactivity may appear during the first hours after the LT4 administration. It requires starting with very low doses of LT4 that should be increased gradually, and reaching normal TSH may take several months. The sympathetic hyperactivity may be attributable to the presence of uncorrected iron-deficiency anemia that worsens by the use of thyroid hormone.


2006 ◽  
Vol 114 (7) ◽  
pp. 1024-1031 ◽  
Author(s):  
Maki Tabuchi ◽  
Nik Veldhoen ◽  
Neil Dangerfield ◽  
Steven Jeffries ◽  
Caren C. Helbing ◽  
...  

2009 ◽  
Vol 34 (2) ◽  
pp. 366-374 ◽  
Author(s):  
Liqun Zhang ◽  
Klas Blomgren ◽  
H. Georg Kuhn ◽  
Christi M. Cooper-Kuhn

1993 ◽  
Vol 38 (4) ◽  
pp. 419-434 ◽  
Author(s):  
G. A. H. Heussen ◽  
G. J. Schefferlie ◽  
M. J. G. Talsma ◽  
H. van Til ◽  
M. J. W. Dohmen ◽  
...  

2008 ◽  
Vol 294 (1) ◽  
pp. E69-E77 ◽  
Author(s):  
Nathalie Koulmann ◽  
Lahoucine Bahi ◽  
Florence Ribera ◽  
Hervé Sanchez ◽  
Bernard Serrurier ◽  
...  

The present experiment was designed to examine the effects of hypothyroidism and calcineurin inhibition induced by cyclosporin A (CsA) administration on both contractile and metabolic soleus muscle phenotypes, with a novel approach to the signaling pathway controlling mitochondrial biogenesis. Twenty-eight rats were randomly assigned to four groups, normothyroid, hypothyroid, and orally treated with either CsA (25 mg/kg, N-CsA and H-CsA) or vehicle (N-Vh and H-Vh), for 3 wk. Muscle phenotype was estimated by the MHC profile and activities of oxidative and glycolytic enzymes. We measured mRNA levels of the peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), the major regulator of mitochondrial content. We also studied the expression of the catalytic A-subunit of calcineurin (CnA) both at protein and transcript levels and mRNA levels of modulatory calcineurin inhibitor proteins (MCIP)-1 and -2, which are differentially regulated by calcineurin activity and thyroid hormone, respectively. CsA-administration induced a slow-to-fast MHC transition limited to the type IIA isoform, which is associated with increased oxidative capacities. Hypothyroidism strongly decreased both the expression of fast MHC isoforms and oxidative capacities. Effects of CsA administration on muscle phenotype were blocked in conditions of thyroid hormone deficiency. Changes in the oxidative profile were strongly related to PGC-1α changes and associated with phosphorylation of p38 MAPK. Calcineurin and MCIPs mRNA levels were decreased by both hypothyroidism and CsA without additive effects. Taken together, these results suggest that adult muscle phenotype is primarily under the control of thyroid state. Physiological levels of thyroid hormone are required for the effects of calcineurin inhibition on slow oxidative muscle phenotype.


2002 ◽  
Vol 80 (9) ◽  
pp. 1511-1519 ◽  
Author(s):  
Lizzy Mos ◽  
Peter S Ross

Vitamin A is a nutrient essential to all mammals for growth and development, as well as for the maintenance of reproductive, endocrine, and immune systems. Environmental contaminant-related disruption of vitamin A has been observed in many wildlife species and can therefore be used as a biomarker of toxic effects. However, the natural processes regulating vitamin A uptake, storage, and distribution among compartments are poorly understood in marine mammals. In this study, 20 young healthy harbour seals (Phoca vitulina) were captured to establish a compartment-based model providing a foundation for a mechanistic understanding of vitamin A physiology and disruption. Vitamin A (retinol, retinyl palmitate, and (or) retinoic acid) was quantified in blood plasma and in biopsy samples of liver, blubber, and skin. Although the highest concentrations of vitamin A were found in liver, blubber represents a more important storage depot, with an estimated 66% of the total retinoid content of the compartments measured. We suggest that vitamin A physiology in the precocious harbour seal has evolved to deal with high vitamin A availability during a short nursing period and to sustain growth during the postweaning fast. Positive correlations in vitamin A concentrations among liver, blubber, and skin support the use of less invasive biopsy sampling of just blubber or skin, which can provide physiologically relevant information in biomarker studies of free-ranging marine mammals.


2006 ◽  
Vol 24 (7) ◽  
pp. 445-453 ◽  
Author(s):  
V. Younes‐Rapozo ◽  
J. Berendonk ◽  
T. Savignon ◽  
A.C. Manhães ◽  
P.C. Barradas

1994 ◽  
Vol 143 (1) ◽  
pp. 107-120 ◽  
Author(s):  
H Wallace ◽  
K McLaren ◽  
R Al-Shawi ◽  
J O Bishop

Abstract The herpes simplex type 1 virus thymidine kinase (HSV1-TK) reporter gene was coupled to a bovine thyroglobulin promoter (TG-tk construct). Within the thyroid glands of transgenic mice expression was confined to thyroid follicle cells. Infusion of Ganciclovir (9-[(1,3-dihydroxy-2-propoxy)methyl]guanine) to 8 to 12 week transgenic females led to the complete loss of thyroid HSV1-TK activity (at 3 to 4 days) and thyroid follicles (between 7 and 14 days). During the first 5 days of treatment a single reciprocal oscillation in circulating thyroxine (T4) and TSH levels occurred. By 14 days the circulating triiodothyronine (T3) and T4 levels of all treated animals were below the detection limits of the assays, while TSH levels were elevated ten-fold and continued to increase thereafter. During 14 days of treatment the thyroids regressed, protein content fell by 80–90% and the C cells, normally dispersed within the central region of each gland, came together in aggregates. Pituitary GH levels in females rose and fell back to normal within 14 days and between 14 and 28 days fell to a level comparable with that of GH-deficient lit/lit mice. The levels of hepatic GH receptor mRNA and the predominant 6·6 kb T3 receptor mRNA were unaffected by thyrocyte ablation. Thyrocyte ablation had no effect on the level of prolactin (Prl) receptor mRNA in females, but increased Prl receptor mRNA levels in males and eliminated group 1 major urinary protein (MUP) mRNA in females. T4 replacement reversed the effects of thyrocyte ablation on MUP mRNA in females and on Prl receptor mRNA in males. Despite the many physiological changes induced by thyrocyte ablation, ablated mice have been maintained for up to 1 year without thyroid hormone supplementation. T4-deficient females were normally fertile and carried pups to term. Although transgenic males expressed HSV1-TK ectopically in spermatids and spermatozoa at levels similar to thyrocyte levels, a rate of Ganciclovir infusion which successfully ablated the thyrocytes did not affect the testis. As an alternative to infusion by minipump, thyrocyte ablation could be achieved by 6 twice-daily injections of Ganciclovir, at a level of 112 μg Ganciclovir/g body weight per day, and fetuses in utero could be thyrocyte ablated by administering 50 or 15 μg/g body weight per day to pregnant females between days 14 and 18 of gestation. These data demonstrate the potential value of transgenic thyrocyte ablation in the study of the effects of thyroid hormone deprivation. Journal of Endocrinology (1994) 143, 107–120


2019 ◽  
Vol 88 (3) ◽  
pp. 257-264 ◽  
Author(s):  
Olga Aniołek

This research aimed to evaluate the effect of thyroid hormone deficiency on the erythrocytic system in dogs. Dogs with clinical symptoms of hypothyreosis such as obesity, hyperpigmentation, and lethargy were selected. The dogs demonstrating breed predisposition to hypothyreosis were incorporated in the analysis: Dachshunds, Retrievers, and mixed-breed dogs. A detailed history was taken and clinical, hormonal, biochemical and haematological blood tests were performed. Peripheral blood samples were taken from 53 dogs. Finally, the dogs with the initial T4 (thyroxine) concentration < 1.3 µg/dl and animals demonstrating clinical improvement after a 2-month therapy with levothyroxine at a dose of 10 µg/kg administeredper ostwo times a day were qualified. The animals between 10 months to 13 years of age were divided into two groups: clinically healthy (control group, n = 35) and dogs presenting clinical symptoms of hypothyreosis (experimental group, n = 18). In this research, the broadly described normocytic normochromic non-regenerative anaemia was not diagnosed in dogs with hypothyreosis. However, a positive correlation between T4 and red blood cell indices such as the average mass of haemoglobin per red blood cell, concentration of haemoglobin in a given volume of packed red blood cells as well as a negative correlation with haematocrit value was discovered in the experimental group after the 2-month therapy with levothyroxine. These results point to the influence of thyroid hormones on erythropoiesis. This observation is partially consistent with other studies, which noted the casual link between the changes in red blood cell system and the function of thyroid in dogs and humans.


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