Prof. Dr. Joseph Caruso
Professor University of Cincinnati
Member of the advisory board of Metallomics.
Local: Auditório Audimax (Prédio 16, centro de Educação)
Hora e Data: às 14:00 h, terça-feira, 16 de dezembro de 2014
The effect of selenium on modulating arsenic cytotoxicity is well known in mammals, but not well understood. Acute cell cytotoxicity and reactive oxygen (ROS) changes were determined in combinations of As(III) and selenomethionine (SeMet) or methyl-selenocysteine toxic mixes on, HEK293, human kidney cells, HUVEC cells and fibroblasts. For HEK cells, cell growth is readily restored from 20% to 60% when switching from 30 µM As(III) as toxin to a mix of 30 µM As(III) and 100 µM SeMet. Importantly, SeMet induces lower ROS levels at the same concentrations used to modulate As(III) cytotoxicity (IC50). Elevated ROS is important to As(III) cytotoxicity, and minimizing it is accomplished with organoselenium species as antagonists. Changes in cell signaling, through analysis of differential protein phosphorylation to uncover molecular level changes occurring in HEK293 human kidney cells show the appearance of proteins favorable to cell health when the organoselenium antagonist is part of the cell growth media.1 Interesting data on selenium containing or selenoproteins will be presented.
Changes in the protein phosphorylation, often suggest cell-signaling changes to produce proteins beneficial to cell health. Three samples were separated into fractions using size exclusion chromatography-ICPMS via 31P+. Phosphorylated proteins unique to the As(III)/Se antagonism mixture were then identified. This study with the HEK cell has been extended to the other cell types as well as utilizing MeSeCys as antagonist. The results show that selenium antagonism is an antioxidant in this system, which induces molecular changes in the proteome that confer cell survival.