A Histochemical Technique for the Detection of Annonaceous Acetogenins.

Annonaceous acetogenins (ACGs) are molecules with carbon numbers C35-C37, usually with tetrahydrofuran and tetrahydropyran rings and one terminal γ-lactone (usually α,ß-unsaturated), in a large aliphatic chain that is varyingly hydroxylated, acetoxylated or ketonized. ACGs have ecological functions as insecticides and are pharmacologically promising due to their cytotoxic and antitumoral properties. They are found in the seeds, leaves, roots, flowers and fruits of annonaceous plants and can be detected during isolation via thin-layer chromatography using Kedde's reagent, which reacts with the unsaturated lactone. This chapter describes the location in situ of ACGs in fresh sections of annonaceous seeds using Kedde's reagent.The acetogenins are located in the idioblasts, in the endosperm and in the embryonic axis during differentiation. This method can aid in the detection of ACGs with a terminal unsaturated γ-lactone in organs and tissues.

Argentatin B Inhibits Proliferation of Prostate and Colon Cancer Cells by Inducing Cell Senescence.

Argentatin B has been shown to inhibit the growth of colon HCT-15, and prostate PC-3 cancer cells. However, the mechanism by which argentatin B inhibits cell proliferation is still unknown. We aimed to investigate the mechanism by which argentatin B inhibits cell proliferation. The cell cycle was studied by flow cytometry. Apoptosis was evaluated by Annexin-V-Fluos, and Hoechst 33342 dye staining. Cell senescence was evaluated by proliferation tests, and staining for SA-ß-galactosidase. Senescence-related proteins (PCNA, p21, and p27) were analyzed by Western blotting. Potential toxicity of argentatin B was evaluated in CD-1 mice. Its effect on tumor growth was tested in a HCT-15 and PC-3 xenograft model. Argentatin B induced an increment of cells in sub G1, but did not produce apoptosis. Proliferation of both cell lines was inhibited by argentatin B. Forty-three percent HCT-15, and 66% PC-3 cells showed positive SA-ß-galactosidase staining. The expression of PCNA was decreased, p21 expression was increased in both cell lines, but p27 expression increased only in PC-3 cells after treatment. Administration of argentatin B to healthy mice did not produce treatment-associated pathologies. However, it restricted the growth of HCT-15 and PC-3 tumors. These results indicate that treatment with argentatin B induces cell senescence.