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http://www.sciencedirect.com/science...87233312000720
Lung epithelial cell death induced by oil-dispersant mixtures
He Wanga, b, Corresponding author contact information, E-mail the corresponding author,
Yongli Shia, b,
Danielle Majora,
Zhanjun Yanga, c
a Department of Global Environmental Health Science, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA 70112, USA
b Cancer Center, Tulane University, New Orleans, LA 70112, USA
c Department of Human Anatomy, BaoTou Medical College, Science and Technology University, Inner Mongolia, China
Abstract
The dispersants used in oil spill disasters are claimed to be safe, but increased solubility of high-molecular-weight components in crude oil is of public health concern. The water-accommodated fractions (WAF) of crude oil mixed with dispersants may become airborne and cause lung epithelial damage when inhaled. This study was designed to examine the cell death and related death pathways of lung epithelial cells in response to WAF. Cultured A549 cells were treated for 2 or 24 h with different concentrations of WAF. The WAF was prepared by mixing each of the dispersants (Corexit EC9527A, Corexit EC9500A and Corexit EC9580A) with crude oil for extraction with PBS. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide MTT assay, lactate dehydrogenase assay, morphology and cleaved caspase 9 protein, and microtubule-associated protein 1 light chain 3 were all used to measure cell viability, necrosis, apoptosis and autophagy quantitation, respectively. Results showed that the WAF of oil-dispersant mixtures caused cell death in the lung epithelial cells, in a dose-dependent manner, with the major cellular pathways of necrosis and apoptosis involved. Autophagy also occurred in cells exposed to WAF mixtures at lower concentrations before any detectable cell death, indicating greater sensitivity to WAF exposure. The three types of cell behavior, namely necrosis, apoptosis and autophagy, may play different roles in oil spill-related respiratory disorders.
Copyright ? 2012 Elsevier B.V. All rights reserved.
He Wanga, b, Corresponding author contact information, E-mail the corresponding author,
Yongli Shia, b,
Danielle Majora,
Zhanjun Yanga, c
a Department of Global Environmental Health Science, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA 70112, USA
b Cancer Center, Tulane University, New Orleans, LA 70112, USA
c Department of Human Anatomy, BaoTou Medical College, Science and Technology University, Inner Mongolia, China
Abstract
The dispersants used in oil spill disasters are claimed to be safe, but increased solubility of high-molecular-weight components in crude oil is of public health concern. The water-accommodated fractions (WAF) of crude oil mixed with dispersants may become airborne and cause lung epithelial damage when inhaled. This study was designed to examine the cell death and related death pathways of lung epithelial cells in response to WAF. Cultured A549 cells were treated for 2 or 24 h with different concentrations of WAF. The WAF was prepared by mixing each of the dispersants (Corexit EC9527A, Corexit EC9500A and Corexit EC9580A) with crude oil for extraction with PBS. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide MTT assay, lactate dehydrogenase assay, morphology and cleaved caspase 9 protein, and microtubule-associated protein 1 light chain 3 were all used to measure cell viability, necrosis, apoptosis and autophagy quantitation, respectively. Results showed that the WAF of oil-dispersant mixtures caused cell death in the lung epithelial cells, in a dose-dependent manner, with the major cellular pathways of necrosis and apoptosis involved. Autophagy also occurred in cells exposed to WAF mixtures at lower concentrations before any detectable cell death, indicating greater sensitivity to WAF exposure. The three types of cell behavior, namely necrosis, apoptosis and autophagy, may play different roles in oil spill-related respiratory disorders.
Copyright ? 2012 Elsevier B.V. All rights reserved.