Document Detail


Role of lipase-generated free fatty acids in converting mesenteric lymph from a noncytotoxic to a cytotoxic fluid.
MedLine Citation:
PMID:  22899820     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Recent studies have shown that mesenteric lymph plays a very important role in the development of multiple-organ dysfunction syndrome under critical conditions. Great efforts have been made to identify the biologically active molecules in the lymph. We used a trauma-hemorrhagic shock (T/HS) model and the superior mesenteric artery occlusion (SMAO) model, representing a global and a localized intestinal ischemia-reperfusion insult, respectively, to investigate the role of free fatty acids (FFAs) in the cytotoxicity of mesenteric lymph in rats. Lymph was collected before, during, and after (post) shock or SMAO. The post-T/HS and SMAO lymph, but not the sham lymph, manifested cytotoxicity for human umbilical vein endothelial cells (HUVECs). HUVEC cytotoxicity was associated with increased FFAs, especially the FFA-to-protein ratio. Addition of albumin, especially delipidated albumin, reduced this cytotoxicity. Lipase treatment of trauma-sham shock (T/SS) lymph converted it from a noncytotoxic to a cytotoxic fluid, and its toxicity correlated with the FFA-to-protein ratio in a fashion similar to that of the T/HS lymph, further suggesting that FFAs were the key components leading to HUVEC cytotoxicity. Analysis of lymph by gas chromatography revealed that the main FFAs in the post-T/HS or lipase-treated T/SS lymph were palmitic, stearic, oleic, and linoleic acids. When added to the cell culture at levels comparable to those in T/HS lymph, all these FFAs were cytotoxic, with linoleic acid being the most potent. In conclusion, this study suggests that lipase-generated FFAs are the key components resulting in the cytotoxicity of T/HS and SMAO mesenteric lymph.
Authors:
Xiaofa Qin; Wei Dong; Susan M Sharpe; Sharvil U Sheth; David C Palange; Therese Rider; Ronald Jandacek; Patrick Tso; Edwin A Deitch
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-08-16
Journal Detail:
Title:  American journal of physiology. Gastrointestinal and liver physiology     Volume:  303     ISSN:  1522-1547     ISO Abbreviation:  Am. J. Physiol. Gastrointest. Liver Physiol.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-10-16     Completed Date:  2013-01-11     Revised Date:  2013-10-17    
Medline Journal Info:
Nlm Unique ID:  100901227     Medline TA:  Am J Physiol Gastrointest Liver Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  G969-78     Citation Subset:  IM    
Affiliation:
Department of Surgery, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, New Jersey 07103, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Endothelium, Vascular / physiopathology
Fatty Acids, Nonesterified / analysis*
Human Umbilical Vein Endothelial Cells
Humans
Lipase / analysis*
Lymph / chemistry*
Male
Mesenteric Artery, Superior / physiopathology
Mesenteric Vascular Occlusion / physiopathology*
Rats
Rats, Sprague-Dawley
Shock, Hemorrhagic / physiopathology*
Grant Support
ID/Acronym/Agency:
GM-59841/GM/NIGMS NIH HHS; R01 GM059841/GM/NIGMS NIH HHS; T32 069330//PHS HHS; T32 GM069330/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Fatty Acids, Nonesterified; EC 3.1.1.3/Lipase
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Birds of a Feather Stay Active Together: An Examination of an All-Male Older Adult Exercise Program.
Next Document:  Active cathepsins B, L, and S in murine and human pancreatitis.