RESUMO
Thyroid disorders are currently among the most widespread endocrine pathologies, affecting about 3% of the worlds population. Although the thyroid gland interacts with other endocrine organs, including the pituitary and adrenals, the many details of these feedback mechanisms remain obscure. In the relevant literature, no data concerning hypothyroidism-induced remodelling of adrenal gland glycoconjugates were found. Therefore, the aim of the present investigation was to study the effects of experimental hypothyroidism on exposure of glycoepitopes in rat adrenal glands by means of lectin histochemistry. Hypothyroidism was induced by daily diet supplementation of experimental animals with 5 mg/kg mercazolil (1-methyl-2-mercapto-imidazole) for 30 days. Formalin-fixed, paraffin-embedded adrenal glands were labelled by lectin-peroxidase conjugates, with subsequent visualization by diaminobenzidine-tetrahydrochloride. The lectin panel included 12 lectins with different carbohydrate affinities (Con A, PSA, LCA, GNA, PFA, LABA, SNA, RCA, WGA, PNA, SBA, HPA).The most significant effects of hypothyroidism were detected in blood vessels. They included dilation of the adrenal medulla vascular bed, perivascular oedema, and increased LABA reactivity of the vascular endothelium of both the cortex and medulla. Hypothyroidism induced decreased exposure of αDMan/αLFuc with simultaneous accumulation of βDGal/ DGalNAc sugar determinants within the cells of the adrenal parenchyma; this phenomenon apparently was dependent on incomplete glycosylation patterns - i.e. impairments in the processing of oligomannosidic type N-glycans and of fucose-containing glycoconjugates. There was also an increased count of spider-like cells with strongly lectin-reactive cytoplasmic granularity in the cortical region of the adrenal glands, presumably due to hypothyroidism-induced uncoupling of biosynthesis and secretion, with subsequent retention of bioactive compounds within these cells. It can be concluded that hypothyroidism has significant effects on adrenal gland glycoconjugates, inducing decreased αDMan/αLFuc and enhanced βDGal/ DGalNAc determinant exposure, accompanied by an imbalance in the synthesis and secretion of physiologically active substances
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