ABSTRACT
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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Subject(s)
Animals , Rats , Hypothyroidism/physiopathology , Carbohydrate Metabolism/physiology , Disease Models, Animal , Adrenal Glands/physiopathology , Lectins/metabolism , Histocytochemistry/methods , Rats, WistarABSTRACT
Diabetes mellitus (DM) currently belongs to the most widespread human pathologies, affecting about 4% of the world adult population. Despite the pivotal role of the liver in the development of metabolic disorders, the influence of DM on hepatic glycoconjugates remains obscure. The aim of the present investigation was to use a set of lectins with different carbohydrate affinities to investigate impairment in rat liver glycoconjugates influenced by streptozotocin-induced diabetes mellitus. The lectin panel included 7 conventional lectins - Con A, SNA, RCA, WGA, PNA, SBA, and HPA, supplemented with the original fucose-specific lectin preparation from Laburnum anagyroides bark (LABA). Tissue samples were fixed in 4% neutral formalin, embedded in paraffin, and subjected to lectin-peroxidase-diaminobenzidine staining. In control rats a strong reactivity against Con A, LABA, SBA and SNA with cytoplasmic granularities of hepatocytes was detected, while RCA, WGA and HPA showed a strong reactivity with vascular endothelium, and WGA and HPA with bile capillaries. Experimental diabetes was associated with a redistribution of Con A and LABA receptor sites from centrolobular hepatocytes to hepatocytes with peripheral localization. Among the most remarkable observations was DMinduced exposure of lectin reactivity with hepatocyte and endothelial cell nuclei. The endothelial lining of sinusoidal hemocapillaries, of central veins, and portal tract vessels also displayed a significant and differential rearrangement of carbohydrate determinants when influenced by DM. Diabetes-induced activation of Kupffer cells was accompanied by the expression of SNA, PNA and SBA receptor sites within the cytoplasm of these cells, which was lectin-negative in control specimens. The results reported provide a new insight into the pathogenesis of DM-induced impairment of hepatic carbohydrates, and demonstrate the applicability of the original fucose-specific lectin preparation to experimental histopathology (AU)
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