The intact muscle lipid composition of bulls: an investigation by MALDI-TOF MS and 31P NMR

Dannenberger, Dirk; Süß, Rosmarie; Teuber, Kristin; Fuchs, Beate; Nuernberg, Karin; Schiller, Jürgen

doi:10.1016/j.chemphyslip.2009.10.011

Cited by 23 publications

(19 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our DHB/CHCA binary matrix‐based tissue MALDI‐MS analysis is optimized for charged lipids, not for neutral lipids such as TAG . TAG has been analyzed using MALDI‐MS with DHB as a matrix, after extraction and solubilization . Clinical tissue samples in patients with RCC may contain only small nests of scattered tumor cells, which poses a technical challenge for molecular research.…”

Section: Discussionmentioning

confidence: 99%

Low C24‐OH and C22‐OH sulfatides in human renal cell carcinoma

et al. 2014

View full text Add to dashboard Cite

Histopathologic diagnosis of renal cell carcinoma (RCC) may sometimes be difficult with small biopsy samples. We applied histology-directed matrix-assisted laser desorption/ionization mass spectrometry to RCC samples to evaluate whether and how lipid profiles are different between RCC and normal tissue. We evaluated 59 RCC samples and 24 adjacent normal tissue samples collected from patients who underwent surgery. Five peaks were significantly differently expressed (p < 10(-7)) between RCCs and adjacent normal tissue samples. C24-OH sulfatide (ST-OH {18:1/24:0}[M-H](-); m/z 906.7 in the negative ion mode) and C22-OH sulfatide (ST-OH {18:1/22:0}[M-H](-); m/z 878.6 in the negative ion mode) were most significantly underexpressed in RCC samples, compared with adjacent normal tissue samples. With 100 random training-to-test partitions within these samples, the median prediction accuracy (RCC vs. normal) ranged from 96.3% to 100% at p cutoff values for feature selection ranging from 0.001 to 10(-7). Two oncocytoma samples were predicted as normal tissue by five lipids that were differentially expressed between RCC and normal tissue at p < 10(-7). Clear-cell, papillary, and chromophobe RCCs were different in lipid profiles. Permutation p- values for 0.632+ bootstrap cross-validated misclassification rates were less than 0.05 for all the classifiers. Thus, lipid profiles differentiate RCC from normal tissue and may possibly classify the histology of RCC.

show abstract

Section: Discussionmentioning

confidence: 99%

Low C24‐OH and C22‐OH sulfatides in human renal cell carcinoma

et al. 2014

View full text Add to dashboard Cite

show abstract

“…12, 13 In this study we demonstrate that bystander effects induced by E. faecalis are associated with increased production of 4-HNE by infected macrophages. This aldehyde is a breakdown product of lipid peroxidation 16 and acts as a diffusible clastogen 19 that causes γH2AX deposition due to DNA double-strand breaks. It also induces G 2 M cell cycle arrest and damages the mitotic spindle.…”

Section: Discussionmentioning

confidence: 99%

“…In the presence of transition metals, superoxide causes lipid peroxidation and can form highly reactive electrophiles such as 4-hydroxy-2-nonenal (4-HNE), malondialdehyde, and 4-oxo-2-nonenal. 16 These α, β-unsaturated aldehydes are diffusible, can covalently modify proteins, and are known to form mutagenic DNA adducts. 17–19 Among these, 4-HNE has been the most intensively studied and may additionally contribute to carcinogenesis by inhibiting DNA repair, inducing COX-2, and modulating MAPK and NF-κB signaling.…”

Section: Introductionmentioning

confidence: 99%

4-Hydroxy-2-Nonenal Mediates Genotoxicity and Bystander Effects Caused by Enterococcus faecalis–Infected Macrophages

et al. 2012

View full text Add to dashboard Cite

BACKGROUND & AIMS Enterococcus faecalis is a human intestinal commensal that produces extracellular superoxide and promotes chromosome instability via macrophage-induced bystander effects. We investigated the ability of 4-hydroxy-2-nonenal (4-HNE)—a diffusible breakdown product of ω-6 polyunsaturated fatty acids—to mediate these effects. METHODS 4-HNE was purified from E faecalis-infected macrophages; its genotoxicity was assessed in human colon cancer (HCT116) and primary murine colon epithelial (YAMC) cell lines. RESULTS 4-HNE induced G2M cell cycle arrest, led to formation γH2AX foci, and disrupted the mitotic spindle in both cell lines. Binucleate tetraploid cells that formed following incubation with 4-HNE were associated with the activation of stathmin and microtubule catastrophe. Silencing glutathione S-transferase α-4, a scavenger of 4-HNE, increased susceptibility of epithelial cells to 4-HNE-induced genotoxicity. Interleukin-10 knockout mice colonized with superoxide-producing E faecalis developed inflammation and colorectal cancer, whereas colonization with a superoxide-deficient strain resulted in inflammation but not cancer. 4-HNE-protein adducts were found in the lamina propria and macrophages in areas of colorectal inflammation. CONCLUSIONS 4-HNE can act as an autochthonous mitotic spindle poison in normal colonic epithelial and colon cancer cells. This finding links the macrophage-induced bystander effects to colorectal carcinogenesis.

show abstract

“…The two dichloromethane fractions were pooled and the solvent evaporated. The lipid fraction was analyzed by positive-ion MALDI-TOF MS and 31 P NMR spectroscopy as described by Dannenberger et al 41 Shortly, the lipid extract was mixed 1:1 (v/v) with the matrix solution (0.5 M 2,5-dihdyroxybenzoic acid in methanol), and 1 μ l of this mixture was directly applied onto the MALDI target. All MALDI-TOF mass spectra were acquired on an Autoflex I mass spectrometer (Bruker Daltonics, Bremen, Germany) with ion reflector.…”

Section: Methodsmentioning

confidence: 99%

Functional consequences of sphingomyelinase-induced changes in erythrocyte membrane structure

et al. 2012

View full text Add to dashboard Cite

Inflammation enhances the secretion of sphingomyelinases (SMases). SMases catalyze the hydrolysis of sphingomyelin into phosphocholine and ceramide. In erythrocytes, ceramide formation leads to exposure of the removal signal phosphatidylserine (PS), creating a potential link between SMase activity and anemia of inflammation. Therefore, we studied the effects of SMase on various pathophysiologically relevant parameters of erythrocyte homeostasis. Time-lapse confocal microscopy revealed a SMase-induced transition from the discoid to a spherical shape, followed by PS exposure, and finally loss of cytoplasmic content. Also, SMase treatment resulted in ceramide-associated alterations in membrane–cytoskeleton interactions and membrane organization, including microdomain formation. Furthermore, we observed increases in membrane fragility, vesiculation and invagination, and large protein clusters. These changes were associated with enhanced erythrocyte retention in a spleen-mimicking model. Erythrocyte storage under blood bank conditions and during physiological aging increased the sensitivity to SMase. A low SMase activity already induced morphological and structural changes, demonstrating the potential of SMase to disturb erythrocyte homeostasis. Our analyses provide a comprehensive picture in which ceramide-induced changes in membrane microdomain organization disrupt the membrane–cytoskeleton interaction and membrane integrity, leading to vesiculation, reduced deformability, and finally loss of erythrocyte content. Understanding these processes is highly relevant for understanding anemia during chronic inflammation, especially in critically ill patients receiving blood transfusions.

show abstract

The intact muscle lipid composition of bulls: an investigation by MALDI-TOF MS and 31P NMR

Cited by 23 publications

References 38 publications

Low C24‐OH and C22‐OH sulfatides in human renal cell carcinoma

Low C24‐OH and C22‐OH sulfatides in human renal cell carcinoma

4-Hydroxy-2-Nonenal Mediates Genotoxicity and Bystander Effects Caused by Enterococcus faecalis–Infected Macrophages

Functional consequences of sphingomyelinase-induced changes in erythrocyte membrane structure

Contact Info

Product

Resources

About