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Renal Mitochondrial Lipid Peroxidation during Sepsis.

Singh P, Parajuli N, Mayeux PR, MacMillan-Crow LA - J Kidney (2016)

Bottom Line: However, few studies have attempted to dissect specific renal targets and/or types of oxidative injury using the cecal ligation and puncture (CLP) murine model of sepsis.Our results show that CLP induced increased 4-hydroxy-nonenal protein adduction (marker of lipid peroxidation) in renal homogenates and mitochondrial fractions.This supports our prior report showing renal complex III inactivation following CLP.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, AR, USA.

ABSTRACT

Sepsis can provoke kidney injury, which increases mortality. Human and animal studies have documented increased renal oxidative injury and mitochondrial damage during sepsis. However, few studies have attempted to dissect specific renal targets and/or types of oxidative injury using the cecal ligation and puncture (CLP) murine model of sepsis. The purpose of this short communication is to examine the extent of lipid peroxidation within renal mitochondria using CLP and blue native gel electrophoresis which separates intact mitochondrial respiratory complexes. Our results show that CLP induced increased 4-hydroxy-nonenal protein adduction (marker of lipid peroxidation) in renal homogenates and mitochondrial fractions. Blue native gel electrophoresis revealed that respiratory complex III was selectively targeted within mitochondrial fractions. This supports our prior report showing renal complex III inactivation following CLP. Future studies will identify specific renal proteins within complex III that are modified during sepsis to provide mechanistic insight on how mitochondrial respiration is inhibited during sepsis.

No MeSH data available.


Related in: MedlinePlus

Sepsis increased renal 4-HNE protein adduction. Representative 4-HNE western blot from mice subjected to CLP (sepsis) or sham surgery. Actin was used as a loading control. Densitometry showing band intensity 4-HNE/actin. Mice subjected to CLP (18 hr) showed increased 4-HNE compared to sham animals. *P<0.05 vs. sham; n = 4/group.
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Figure 1: Sepsis increased renal 4-HNE protein adduction. Representative 4-HNE western blot from mice subjected to CLP (sepsis) or sham surgery. Actin was used as a loading control. Densitometry showing band intensity 4-HNE/actin. Mice subjected to CLP (18 hr) showed increased 4-HNE compared to sham animals. *P<0.05 vs. sham; n = 4/group.

Mentions: We first sought to determine whether sepsis induces endogenous 4-HNE production within the kidney. A representative western blot showing 4-HNE levels in total renal homogenates in the CLP group compared to the Sham group are presented in Figure 1. Densitometry revealed significant increases in 4-HNE protein adduction in CLP compared to Sham. Actin was used as a loading control. To our knowledge, this is the first report showing increased endogenous renal 4-HNE protein adduction during sepsis. Hussain et al. showed increased 4-HNE adduction within the diaphragm after administration of lipopolysaccharide, a model of endotoxemia [21].


Renal Mitochondrial Lipid Peroxidation during Sepsis.

Singh P, Parajuli N, Mayeux PR, MacMillan-Crow LA - J Kidney (2016)

Sepsis increased renal 4-HNE protein adduction. Representative 4-HNE western blot from mice subjected to CLP (sepsis) or sham surgery. Actin was used as a loading control. Densitometry showing band intensity 4-HNE/actin. Mice subjected to CLP (18 hr) showed increased 4-HNE compared to sham animals. *P<0.05 vs. sham; n = 4/group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4836864&req=5

Figure 1: Sepsis increased renal 4-HNE protein adduction. Representative 4-HNE western blot from mice subjected to CLP (sepsis) or sham surgery. Actin was used as a loading control. Densitometry showing band intensity 4-HNE/actin. Mice subjected to CLP (18 hr) showed increased 4-HNE compared to sham animals. *P<0.05 vs. sham; n = 4/group.
Mentions: We first sought to determine whether sepsis induces endogenous 4-HNE production within the kidney. A representative western blot showing 4-HNE levels in total renal homogenates in the CLP group compared to the Sham group are presented in Figure 1. Densitometry revealed significant increases in 4-HNE protein adduction in CLP compared to Sham. Actin was used as a loading control. To our knowledge, this is the first report showing increased endogenous renal 4-HNE protein adduction during sepsis. Hussain et al. showed increased 4-HNE adduction within the diaphragm after administration of lipopolysaccharide, a model of endotoxemia [21].

Bottom Line: However, few studies have attempted to dissect specific renal targets and/or types of oxidative injury using the cecal ligation and puncture (CLP) murine model of sepsis.Our results show that CLP induced increased 4-hydroxy-nonenal protein adduction (marker of lipid peroxidation) in renal homogenates and mitochondrial fractions.This supports our prior report showing renal complex III inactivation following CLP.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, AR, USA.

ABSTRACT

Sepsis can provoke kidney injury, which increases mortality. Human and animal studies have documented increased renal oxidative injury and mitochondrial damage during sepsis. However, few studies have attempted to dissect specific renal targets and/or types of oxidative injury using the cecal ligation and puncture (CLP) murine model of sepsis. The purpose of this short communication is to examine the extent of lipid peroxidation within renal mitochondria using CLP and blue native gel electrophoresis which separates intact mitochondrial respiratory complexes. Our results show that CLP induced increased 4-hydroxy-nonenal protein adduction (marker of lipid peroxidation) in renal homogenates and mitochondrial fractions. Blue native gel electrophoresis revealed that respiratory complex III was selectively targeted within mitochondrial fractions. This supports our prior report showing renal complex III inactivation following CLP. Future studies will identify specific renal proteins within complex III that are modified during sepsis to provide mechanistic insight on how mitochondrial respiration is inhibited during sepsis.

No MeSH data available.


Related in: MedlinePlus