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Protective Mechanisms Of Dimethyl Sulfoxide On Depleted Uranium Induced Damage In Cultured Human Bronchial Epithelial Cells

Posted on:2007-03-05Degree:MasterType:Thesis
Country:ChinaCandidate:Y WangFull Text:PDF
GTID:2144360185968490Subject:Radiation Medicine
Abstract/Summary:PDF Full Text Request
Objective: To investigate toxicity of depleted uranium (DU) on cultured human bronchial epithelial cells (BEAS-2B) and its protection by dimethyl sulfoxide (DMSO).Methods: Human bronchial epithelial cells (BEAS-2B) were divided into 4 groups, namely normal group (NC), DMSO control groups (DMSO), DU treated with or without DMSO groups (DU and DU+DMSO). The fractions of survival, apoptosis and necrosis cells were detected by fluorescent photometry. Changes of cellular localization and ultrastructure were observed by transmission electron microscopy (TEM). The total and phosphorylated ERK1/2 or p38-MAPK was detected by Western bolting.Results: (1) After DU treatment, cell survival decrease, cell apoptosis and necrosis increased, and DMSO could reduce cell damage induced by DU. (2) Under TEM, cells of NC and DMSO groups showed normal structure, while that of DU treated without DMSO (DU group), numerous organelle altered presenting apoptosis and/or necrosis, endoplasmic reticulum vesiculated, mitochondria destroyed, especially the cells there were DU particles inside or outside. However, in DMSO+DU group, though some ultrastructural changes similar to DU group were appeared, amount and extension of alterations distinctly reduced, and presenting not any pathological features. (3) DU could inhibit not only ERK1/2 and p38 expression but also ERK activation. DMSO could modify the phosphorylation of ERK1/2 and p38, and partially increase MAPK signaling to attenuate DU induced necrotic and/or apoptoticConclusion: DU could induce cell apoptosis and necrosis, and severe alterations of cell altrastructure, and DMSO could reduce these damages.
Keywords/Search Tags:Depleted uranium (DU), Dimethyl sulfoxide (DMSO), Apoptosis and necrosis, Cellular ultrastructure, MAPK signaling pathway
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