Effects of lycopene from guava (Psidium guajava L.) derived products on breast cancer cells.

Polyphenols, condensed tannins, total flavonoids, total carotenoids, lycopene and ascorbic acid were determined besides verifying antioxidant capacity of peel, pulp and desserts (with and without sugar) of red guava (Psidium guajava L.) as well as the effects of lycopene on cytotoxicity, cell cycle and apoptosis on breast cancer cell line MCF-7. Guava peel contains 90% of the total ascorbic acid and heat treatment does not modify bioactive compounds content and antioxidant capacity. Sugar addition decreased guava pulp functional capacity. After heat treatment, lycopene content was stable, but sugar addition reduced its concentration by 57%. Lycopene (10 µM) extracted from guava and standard presented the same cytotoxic effect on MCF-7 cells. Lycopene influenced over G2-M transition check-point of the cell cycle and increased apoptotic cells percentages compared to untreated cells. The consumption of in natura guava, especially with peel can be considered an important source of bioactive compounds.

Estradiol modulates TGF-ß1 expression and its signaling pathway in thyroid stromal cells.

The higher prevalence of thyroid disease in women suggests that estrogen (E2) might be involved in the pathophysiology of thyroid dysfunction. To approach the question of the effect of stromal cells in the modulation of thyroid epithelial cells activity, we established and characterized a homogeneous stromal cell population (TS7 cells) of rat thyroid gland. These fibroblastic cells synthesize the cytoskeleton proteins α-smooth muscle actin and vimentin, produce basement membrane components and express the cytokine transforming growth factor beta 1 (TGF-ß1). Here, we hypothesized that the effects of E2 on follicular thyroid cells are mediated by TGF-ß1 synthesis and secretion by stromal cells (paracrine action). Thus we investigated the effect of E2 on TGF-ß1 synthesis and its signaling pathway in TS7 cells. In addition, we analyzed the role of TGF-ß1 signaling pathway as mediator of TS7-PC CL3 thyroid epithelial cells interactions. We report that TS7 stromal cells expressed α and ß estrogen receptors (ERα and ERß). Further, both isoforms of TGF-ß1 receptors, TGFRI and TGFRII, were also identified in TS7 cells, suggesting that these cells might be a target for this cytokine in vitro. Treatment of TS7 cells with E2 induced both synthesis and secretion of TGF-ß1. This event was followed by phosphorylation of the transcription factor Smad2, a hallmark of TGF-ß1 pathway activation. Co-culture of PC CL3 cells onto TS7 cells monolayers yielded round aggregates of PC CL3 cells surrounded by TS7 cells. TS7 cells induced a decrease in iodide uptake by PC CL3 cells, probably by a mechanism involving TGF-ß1. Moreover, E2 affected synthesis and organization of the extracellular matrix (ECM) components, tenascin C and chondroitin sulfate, in these co-culture cells. Our results point to the TGF-ß1/Smad-2 signaling pathway as a putative target of estrogen actions on thyroid stromal cells and contribute to understanding the interplay between stromal and follicular cells in thyroid physiology.