Colchicine causes prenatal cell toxicity and increases tetraploid risk

Abstract

Background Colchicine is a clinical medicine used for relief from gout and familial Mediterranean fever. Because of its toxic effects, intravenous injection of colchicine has been banned, but it is still widely administered orally. We assayed the toxic effects of colchicine in cultured primary chorionic villus cells and amniotic fluid cells to interpret its influence on the placenta and foetus. Methods Bright field record and cell count kit 8 were used to value cell viability. Flow cytometer was used to identify cells markers, cell cycle and cell apoptosis. G-banding was used for karyotype analysis for sample genetic and drug effect evaluation. Results Chorionic villus cells and amniotic fluid cells were characterized as mesenchymal cells that share most cell surface markers and have a similar response to colchicine. Colchicine did not induce a decline in cell viability at low concentrations but suppressed cell proliferation by arresting the cell cycle in the G2/M phase and increased the risk of tetraploid generation in a small subset of cases. Conclusions Our study revealed the results of a colchicine-induced toxicity test in prenatal cells and determined the anti-mitotic biologically functional dose and manner of administration that might reduce the risk of tetraploid generation.

Duloxetine-Induced Neural Cell Death and Promoted Neurite Outgrowth in N2a Cells

“…In this study, we tested duloxetine’s neural cell toxicity in the mouse neuroblastoma cell line N2a and mouse C17.2 neural stem cells. These specific cells were good models for the evaluation of clinical drug toxicity (Wang et al 2019 ). The results showed significant cell toxicity in both cell lines when they were exposed to 100 μM duloxetine, and the C17.2 cells were more sensitive than the N2a cells as shown by the induction of cell death by a lower dose.…”