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Rycina z artykułu: Mechanizmy działania...
 
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Wprowadzenie i cel:
Bisfenol A (BPA) należy do najlepiej poznanych związków zaburzających funkcjonowanie układu hormonalnego, tzw. dysruptorów endokrynnych. Ze względu na podobieństwo strukturalne do hormonów endogennych BPA i jego analogi mogą oddziaływać ze szlakami wewnątrzkomórkowymi, w tym z tymi zależnymi od hormonów tarczycy. Celem niniejszego przeglądu jest przedstawienie mechanizmów działania bisfenoli oraz ocena, w jaki sposób mogą one wpływać na funkcję tarczycy.

Opis stanu wiedzy:
BPA i jego analogi są szeroko rozpowszechnione w środowisku, co od lat skłania do badania ich potencjalnego wpływu na fizjologię tarczycy. Badania epidemiologiczne wskazują, że wyższe stężenia BPA w moczu lub surowicy mogą wiązać się ze zmianami stężeń T4, T3 i TSH, choć wyniki badań przeprowadzonych w różnych populacjach są niejednoznaczne. Dane z badań komórkowych i modeli zwierzęcych dodatkowo potwierdzają te obserwacje, wskazując, że BPA może zaburzać syntezę hormonów tarczycy oraz modyfikować ekspresję genów regulowanych przez hormony T3. Wykazano również, że BPA może zakłócać działanie receptorów hormonów tarczycy, modyfikując dalsze etapy sygnalizacji. Podobne efekty odnotowano dla kilku zamienników BPA, w tym BPS i BPF.

Podsumowanie:
Dostępne dane sugerują, że BPA oraz jego analogi mogą wpływać na sygnalizację hormonów tarczycy na kilku poziomach. Badania pokazują zaburzenia aktywności receptorów, sygnalizacji niegenomowej i lokalnego metabolizmu hormonów, a te przeprowadzone na modelach zwierzęcych potwierdzają występowanie takich efektów in vivo. Dane pochodzące z badań u ludzi są niespójne i sugerują zależności o niewielkim nasileniu, bez jednoznacznych implikacji klinicznych.

Introduction and objective:
Bisphenol A (BPA) is among the most extensively studied endocrine-disrupting chemicals. Because its chemical structure resembles that of endogenous hormones, BPA and its analogues are capable of interacting with intracellular pathways, including those governed by thyroid hormones. The this aim of the review is to outline the molecular mechanisms through which bisphenols exert their effects, and to evaluate how these interactions may influence thyroid function.

Brief description of the state of knowledge:
BPA and its structural analogues are widely present in the environment, which has stimulated ongoing interest in their potential effects on thyroid physiology. Epidemiological studies suggest that higher concentrations of urinary or serum BPA may be linked to changes in T4, T3 and TSH levels, although findings remain inconsistent across populations. Experimental evidence from cellular and animal models provides additional support, showing that BPA can impair thyroid hormone synthesis, alter glandular architecture, and influence the expression of genes essential for hormone production. BPA has also been shown to interfere with thyroid hormone receptor activity, thereby modifying downstream signalling. Comparable effects have been observed for several BPA substitutes, including BPS and BPF.

Summary:
Available evidence indicates that BPA and its analogues can interfere with thyroid hormone signalling through multiple molecular mechanisms. Experimental studies demon-strate effects on receptor activity, non-genomic signalling and local hormone metabolism, while animal models support thyroid related effects in vivo. Human data remain heteroge-neous and suggest modest associations, underscoring the need for well designed longitudinal studies to clarify clinical relevance.
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