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Selenium attenuates docetaxel-induced apoptosis and mitochondrial oxidative stress in kidney cells

Baş, Ercana; Naziroğlu, Mustafab,c

doi: 10.1097/CAD.0000000000000723

Docetaxel (DTX) is a chemotherapeutic agent, and it is used for the treatment of several cancers including prostate and glioblastoma, but it results in many adverse effects in normal tissues, including kidney. The cytoprotective properties of selenium (Se) against adverse effects of DTX were reported in several normal cells, except kidney cell lines. The purpose of this study was to investigate the effects of Se on DTX-induced nephrotoxicity in normal kidney cell lines. The human embryonic kidney 293 (HEK293) cells were divided into four groups as control, Se (200 nmol/l for 10 h), DTX (10 nmol/l for 48 h), and DTX+Se. Laser confocal microscope fluorescence intensity of apoptosis (annexin V and propidium iodide), mitochondrial membrane depolarization, reactive oxygen species production, and lipid peroxidation levels were increased in the cells by the DTX treatments, although cell number, cell viability, reduced glutathione and glutathione peroxidase values were decreased by the treatments. The fluorescence intensities and values were recovered in the DTX+Se group of the cells by Se treatment. In conclusion, DTX-induced adverse effects were recovered through inhibition of apoptosis and mitochondrial oxidative stress through upregulation of reduced glutathione and glutathione peroxidase in the normal kidney (HEK293) cells. Combination therapy of DTX and Se could be used as an effective strategy for protection of kidney cells against adverse effects of DTX.

aDepartment of Urology, Faculty of Medicine

bNeuroscience Research Center, Suleyman Demirel University

cDrug Discovery and Development Research Group, BSN Health, Analysis and Innovation Inc., Goller Bolgesi Teknokenti, Isparta, Turkey

Correspondence to Mustafa Naziroğlu, PhD, Neuroscience Research Center, Suleyman Demirel University, Isparta TR-32260, Turkey Tel: +90 246 211 3641; fax: +90 246 237 1165; e-mail:

Received August 6, 2018

Accepted November 5, 2018

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