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Objectives Betahistine is a histamine analog commonly prescribed for symptomatic treatment of vertiginous symptoms. In vitro studies have shown that betahistine was not toxic at the prescribed doses in a nasal epithelial cell line. However, the effect of betahistine on other cell types has not been studied. In this study, we aimed to investigate some of the physiological effects of betahistine on L929 fibroblast, A549 lung cancer, human umbilical vein endothelial (HUVEC), and Ishikawa endometrial cell lines. Materials and methods Cellular proliferation was assed assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, apoptosis was evaluated by acridine orange-ethidium bromide staining, and cellular migration was assed assessed by scratch assay. Results Betahistine treatment (0.1-0.5 mg/mL, 24 hours) can inhibit cell proliferation and induce apoptosis in HUVEC, A549, Ishikawa, and L929 cell lines. Betahistine (≥0.1 mg/mL) significantly increased the number of apoptotic cells (HUVEC: 26.3%, A549: 17.3%, L929: 8.6%, and Ishikawa: 2.3%). Betahistine at doses over 0.1 mg/mL significantly suppressed the cell migration rate in all of the cell lines. In contrast, exposure to a low dose of betahistine (0.025 mg/mL) induced migration rates of HUVEC and Ishikawa cells by 81% and 48%, respectively. Conclusion Betahistine may alter the processes of cellular proliferation, apoptosis, and cellular migration in a cell line- and dose-dependent manner. In this sense, proliferative and metastatic properties of certain cancer cells can potentially be altered in response to betahistine treatment.

OBJECTIVES: Dehydroepiandrosterone (DHEA) is an endogenous hormone that acts as a ligand for several cellular receptors. An age-dependent decline in circulating levels of DHEA is linked to changes in various physiological functions. In gynecological clinical practice, DHEA is commonly prescribed to induce ovulation. Some clinical studies report a positive association between high serum concentrations of DHEA and an increased risk of developing ovarian cancer. However, the in vitro physiological effects of DHEA on ovarian cancerous cells have not been explored thus far. In this study, we aimed to investigate the physiological effects of DHEA treatment (0-200 μM, 24-72 hours) on MDAH-2774 human ovarian cancer cell line and primary HuVeC human endothelial cells. MATERIALS AND METHODS: The physiological effects of DHEA treatment (0-200 μM, 24-72 hours) on MDAH-2774 human ovarian cancer cell line and primary HuVeC human endothelial cells were investigated with the (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) test, acridine orange/ethidium bromide staining, and scratch assay. RESULTS: DHEA treatment promoted proliferation of the MDAH-2774 cancer cell line in a dose-dependent manner (r=0.6906, p