Ultrastructural and functional alterations of the rat thyroid gland produced by polychlorinated biphenyls compared with iodide excess and deficiency, and thyrotropin and thyroxine administration

Collins, William T.; Capen, Charles C.

doi:10.1007/bf02899183

Cited by 65 publications

(27 citation statements)

References 19 publications

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“…Idiopathic follicular atrophy was a primary degenerative disease of the thyroid and 191. differed distinctly from the trophic atrophy of follicular cells secondary to diminished secretion of thyrotropin. Under these conditions, thyroid follicles were lined by a low cuboidal epithelium and distended by uniformly dense PAS-positive colloid, with little evidence of endocytosis in response to diminished thyrotropin secretion [2]. Ultrastructurally, the progressive degeneration of follicular cells in idiopathic follicular atrophy and formation of microfollicles in individual cells were different lesions from those reported in trophic atrophy of follicular cells as a result of diminished thyrotropin stimulation [2].…”

Section: Discussionmentioning

confidence: 92%

Histologic and Ultrastructural Evaluation of Thyroid Lesions Associated with Hypothyroidism in Dogs

1981

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Abstract. Thyroid lesions in 16 pet dogs with hypothyroidism were evaluated by light and electron microscopy. Lymphocytic thyroiditis, found in seven dogs, was characterized by diffuse infiltration of the thyroid gland by lymphocytes, plasma cells and macrophages with formation of some lymphoid nodules and destruction of follicles, progressing to replacement of most of the thyroid by fibrous connective tissue. The basement membrane around follicles was thick and had electron-dense deposits. The morphology of the thyroid lesions and the presence of circulating thyroglobulin autoantibodies suggested that lymphocytic thyroiditis was immune-mediated.Idiopathic follicular atrophy, found in nine dogs, was characterized by loss of thyroid parenchyma and replacement by adipose connective tissue. Degeneration of individual follicular cells was present in the early stage, with exfoliation into the colloid and interfollicular area. Most of the thyroid gland consisted of adipose connective tissue with either interspersed small follicles or individual follicular cells that had dilated rough endoplasmic reticulum, large Golgi apparatus, and intracytoplasmic microfollicles in the advanced stage. Follicular atrophy was a degenerative lesion of follicular cells of unknown cause, not associated with inflammatory destruction in the thyroid gland.Hypothyroidism in pet dogs is a metabolic disorder that can result from primary diseases of the thyroid gland or be secondary to long-standing pituitary or hypothalamic lesions that interfere with the release of thyrotropin or thyrotropin-releasing hormone. Hypothyroid dogs have a gradual decline in vigor and physical activity, and often are "heat seekers" [ 12). Varied degrees of alopecia and epidermal atrophy were reported in 48% of hypothyroid dogs [17]. Hypothyroidism in pet dogs was associated with a low level of serum triiodothyronine (38.7 k 4.1 ng/dl) and thyroxine (0.8 k 0.07 pg/dl); circulating thyroid hormone concentrations did not increase significantly after thyrotropin stimulation [7]. These changes in thyroid function were specific for hypothyroid dogs compared to dogs with other endocrinopathies or normal pet dogs. Thyroglobulin autoantibodies were found in 48% (12 of 25) pet dogs with hypothyroidism, and may be related to the cause of thyroiditis [7]. Laboratory beagles with naturally occurring lymphocytic thyroiditis also have circulating thyroid autoantibodies [ 141, but the focal thyroiditis was not associated with 299

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Section: Discussionmentioning

confidence: 92%

Histologic and Ultrastructural Evaluation of Thyroid Lesions Associated with Hypothyroidism in Dogs

1981

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“…Previous studies have demonstrated that these environmental contaminants can alter various aspects of thyroid function in several vertebrate species (e.g., Brouwer et al 1989;Byrne et al 1987;Chiba et al 2001;Collins et al 1977;Collins and Capen 1980a, 1980b, 1980cDesaulniers et al 1999;Langer et al 1998;Schumacher et al 1993;Sepkovic and Byme 1984;Tryponas et al 1984). The cellular mechanisms involved in thyroid pathology are poorly known.…”

Section: Discussionmentioning

confidence: 99%

“…Much of the toxicological work on laboratory animals has reported a negative correlation between organohalogens and serum levels of hormones. Experimental PCB exposure on rats revealed low T4 levels in the serum combined to hypertrophy of follicular cells, extensive dilation of rough endoplasmic reticulum, only occasional colloid droplets, and limited lysosome-colloid droplets interaction (Collins and Capen 1980c;Kazka et al 1978). PCBs depress plasma levels of T4 in seals and in polar bears (Braathen et al 2004;Brouwer et al 1989;Reijnders 1986).…”

Section: Discussionmentioning

confidence: 99%

Interfollicular Fibrosis in the Thyroid of the Harbour Porpoise: An Endocrine Disruption?

Das

Vossen

Tolley

et al. 2006

Arch Environ Contam Toxicol

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Abstract. Previous studies have described high levels of polychlorobiphenyls (PCB), polybrominated diphenylether (PBDE), toxaphene, p,p 0 -dichlorodiphenyltrichloroethane (DDT), and p,p 0 -dichlorodiphenyldichloroethylene (DDE) in the blubber of the harbour porpoise from the North Sea raising the question of a potential endocrine disruption in this species. In the present study, the thyroids of 57 harbour porpoises from the German and Danish (North and Baltic Seas), Norwegian, and Icelandic coasts have been collected for histological and immunohistological investigations. The number of follicles and the relative distribution of follicles, connective, and solid tissues (%) were quantified in the thyroid of each individual. Then, the potential relationship between the thyroid morphometry data and previously described organic compounds (namely, PCB, PBDE, toxaphene, DDT, and DDE) was investigated using factor analysis and multiple regressions. Thyroid morphology differed strongly between sampling sites. Porpoises from the German (North and Baltic Seas) and Norwegian coasts displayed a high percentage of connective tissues between 30 and 38% revealing severe interfollicular fibrosis and a high number of large follicles (diameter >200 lm). A correlation-based principal component analysis (PCA) revealed two principal components explaining 85.9% of the total variance. The variables PCB, PBDE, DDT, and DDE compounds loaded highest on PC1 whereas toxaphene compound loaded most on PC2. Our results pointed out a relationship between PC1 (PCBs, PBDE, DDE, and DDT compounds) and interfollicular fibrosis in the harbour porpoise thyroids. Such an association is not alone sufficient for a cause-effect relationship but supports the hypothesis of a contaminant-induced thyroid fibrosis in harbour porpoises raising the question of the longterm viability in highly polluted areas.

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“…PCBs have been reported to reduce thyroid hormone concentrations 100,101) . Seo et al (1995) compared the effects of PCBs and TCDD on thyroid hormone, by administering TCDD (0.025 or 0.1 µg/kg/day), PCB 77 (3,3',4,4'-tetrachlorobiphenyl, 2 or 8 mg/kg/day, based on the 1997 WHO TEF of PCB 77 as 0.0001, which are equivalent to 0.2 or 0.8 µg TEQ/kg/day, respectively), or PCB126 (3,3',4,4',5-pentachlorobiphenyl, 0.25 or 1 µg/kg/ day, based on TEF = 0.1, which is equivalent to 0.025 or 0.1 µg TEQ/kg/day, respectively), to SD rats on GD 10 to GD 16 96) .…”

Section: Disruption Of Thyroxin Function By Pcb Exposurementioning

confidence: 99%

Developmental Neurotoxicity of Dioxin and Its Related Compounds.

Kakeyama

Tohyama

2003

INDUSTRIAL HEALTH

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This manuscript reviewed the neurotoxicity of dioxins and related compounds with an emphasis on maternal exposure. The brain during developmental period is thought to be highly sensitive to dioxin and its related compounds that affect a broad range of brain functions from the advanced brain function to the reproduction-controlling function, even at low doses. It is suggested that dioxins exhibit endocrine-disrupting action on the gonadal and thyroid hormone axes, as well as the 'neural-disrupting action' on neural transmission and neural network formation. From behavioral toxicological studies as well as studies on the underlying mechanisms of dioxins' toxicity, dioxins affect some specific functions in particular regions or cells of the brain at critical windows during the developmental period.

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Ultrastructural and functional alterations of the rat thyroid gland produced by polychlorinated biphenyls compared with iodide excess and deficiency, and thyrotropin and thyroxine administration

Cited by 65 publications

References 19 publications

Histologic and Ultrastructural Evaluation of Thyroid Lesions Associated with Hypothyroidism in Dogs

Histologic and Ultrastructural Evaluation of Thyroid Lesions Associated with Hypothyroidism in Dogs

Interfollicular Fibrosis in the Thyroid of the Harbour Porpoise: An Endocrine Disruption?

Developmental Neurotoxicity of Dioxin and Its Related Compounds.

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