Name: PRISCILA OLIVEIRA DA CRUZ

Publication date: 04/10/2024

Examining board:

Namesort descending Role
ALESSANDRA SIMAO PADILHA Examinador Interno
DANIELLA BONAVENTURA Examinador Externo

Summary: The impacts of tributyltin (TBT) on marine biota were evidenced by evidence of changes in
the anatomy of the gastropod Nucella lapillus, with the emergence of male sexual organs in
females (Imposex). Despite being banned, recent investigations have indicated a wide
distribution of TBT in different ecosystems. Considering the biomagnification and
bioaccumulation capacity of this pollutant, the occurrence of damage to important systems of
our body, possibly the vascular system, is not ruled out. Therefore, the objective of this study
was to investigate the possible effects of TBT treatment on endothelium-dependent coronary
vascular reactivity in rats. Our hypothesis is that TBT treatment impairs
endothelium-dependent vascular vasodilation in these rats. Wistar rats, 12 weeks old
(200–270 g), were used in protocols previously approved by CEUA-UFES (#19/2022). The
animals were divided into two groups: control (CON) and treated (TBT). Treatment was
performed via the orogastric route with tributyltin solution, 100 ng/kg for 15 days. The
estrous cycle and systolic blood pressure (SBP) were evaluated. The vascular reactivity of the
coronary bed was examined using the modified Langendorff method. The coronary arteries
were collected for histological analysis. The results were expressed as mean ± standard error
of the mean (S.E.M.) and p-values < 0.05 were considered significant. TBT was able to
promote changes in the estrous cycle of rats, increasing the duration of the metestrus-diestrus
phase, followed by a prolongation of the estrous cycle. There was also a reduction in the
weight of the uterus and an increase in the weight of its associated parametrial fat, due to its
effects as an endocrine disruptor. In coronary artery reactivity, TBT treatment was able to
modify the pathway through which endothelium-dependent relaxation occurs, increasing the
participation of NO in this response, and this difference was accompanied by morphological
changes in the thickness of the tunica media of the coronary arteries, where the treatment
promoted morphological damage, causing atrophy of smooth muscle cells. Taken together,
our results suggest that exposure to TBT can be considered a potential cardiovascular risk
factor.

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