PMID: 16636303Apr 26, 2006Paper

Marginal zinc deficiency increased the susceptibility to acute lipopolysaccharide-induced liver injury in rats

Experimental Biology and Medicine
Melissa Shea-BudgellZhaoming Xu

Abstract

Lipopolysaccharide (LPS) triggers a global activation of inflammatory responses leading to liver injury in humans. Zinc pretreatment has been shown to prevent LPS-induced hepatic necrosis. In North America, suboptimal zinc status is more common than once realized. However, the effect of inadequate zinc nutrition on the host's susceptibility to LPS-induced liver injury is not known. The objective of this study was to determine whether marginal zinc deficiency would render rats more susceptible to LPS-induced liver injury. Weanling Sprague-Dawley rats were assigned to one of three dietary treatment groups: marginally low zinc ad libitum (Z3; 3 mg zinc/kg diet), adequate zinc ad libitum (Z30; 30 mg zinc/kg diet), or adequate zinc pair-fed (Z30P) group. After 6 weeks, each dietary treatment group was further divided into LPS-control (saline) groups (C-Z3, C-Z30P, C-Z30) and LPS-treatment (1 mg/kg body weight, intraperitoneal, 8 hrs) groups (LPS-Z3, LPS-Z30P, LPS-Z30). LPS reduced the serum zinc concentration and increased the liver zinc concentration regardless of dietary zinc intake. Serum alanine aminotransferase level was higher in the LPS-Z3 rats than in the LPS-Z30P and LPS-Z30 rats. LPS also induced hepatocyte necrosis and ne...Continue Reading

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Citations

Nov 23, 2010·Current Gastroenterology Reports·Juliane I BeierCraig J McClain
Dec 21, 2013·Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract·Abby K GeletzkeDavid I Soybel
May 5, 2020·Biological Trace Element Research·Robert A DiSilvestroElizabeth Joseph
Feb 27, 2009·Critical Care Medicine·Daren L KnoellElliott D Crouser
Mar 9, 2010·American Journal of Physiology. Lung Cellular and Molecular Physiology·Shengying BaoDaren L Knoell
Sep 28, 2010·Biological Chemistry·Juliane I Beier, Craig J McClain

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