Salicylate- and Aspirin-Induced Uncoupling of Oxidative Phosphorylation in Mitochondria Isolated from the Mucosal Membrane of the Stomach

Jörgensen, T. Glarborg; Weis-Fogh, Ulla Sivertsen; Nielsen, H. H.; Olesen, H. P.

doi:10.1080/00365517609054490

Cited by 52 publications

(11 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The impact of SA on mitochondrial function is not a cucumber-specific phenomenon. Similar uncoupling and inhibitory effects have also been reported in tobacco [67], soybean [68], Arabidopsis [69], and even in mammalian cells [70]. In Arabidopsis, SA directly acted on mitochondrial respiratory complex III and inhibited its activity [69].…”

Section: Discussionsupporting

confidence: 58%

Quantitative Proteomic Profiling of Early and Late Responses to Salicylic Acid in Cucumber Leaves

Dong

Cao

et al. 2016

PLoS ONE

View full text Add to dashboard Cite

Salicylic acid (SA) is an important phytohormone that plays vital regulatory roles in plant growth, development, and stress responses. However, studies on the molecular mechanism of SA, especially during the early SA responses, are lagging behind. In this study, we initiated a comprehensive isobaric tag for relative and absolute quantitation (iTRAQ)-based proteomic analysis to explore the early and late SA-responsive proteins in leaves of cucumber (Cucumis sativus L.) seedlings. Upon SA application through the roots, endogenous SA accumulated in cucumber leaves. By assaying the changes in marker gene expression and photosynthetic rate, we collected samples at 12 h and 72 h post treatment (hpt) to profile the early and late SA responsiveness, respectively. The iTRAQ assay followed by tandem mass spectrometry revealed 135 differentially expressed proteins (DEPs) at 12 hpt and 301 DEPs at 72 hpt. The functional categories for these SA-responsive proteins included in a variety of biochemical processes, including photosynthesis, redox homeostasis, carbohydrate and energy metabolism, lipid metabolism, transport, protein folding and modification, proteolysis, cell wall organization, and the secondary phenylpropanoid pathway. Conclusively, based on the abundant changes of these DEPs, together with their putative functions, we proposed a possible SA-responsive protein network. It appears that SA could elicit reactive oxygen species (ROS) production via enhancing the photosynthetic electron transferring, and then confer some growth-promoting and stress-priming effects on cells during the late phase, including enhanced photosynthesis and ROS scavenging, altered carbon metabolic flux for the biosynthesis of amino acids and nucleotides, and cell wall reorganization. Overall, the present iTRAQ assay provides higher proteome coverage and deepened our understanding of the molecular basis of SA-responses.

show abstract

Section: Discussionsupporting

confidence: 58%

Quantitative Proteomic Profiling of Early and Late Responses to Salicylic Acid in Cucumber Leaves

Dong

Cao

et al. 2016

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…(24,25) The ATP deficiency and the accumulation of adenosine diphosphate (ADP) and adenosine monophosphate (AMP) stimulate glycolysis in enterocytes. (26) The maximally stimulated glycolysis induced the production of lactate rather than acelyl CoA, because pyruvate dehydrogenase activities are low in enterocytes.…”

Section: The Pathophysiology Of Nsaid-induced Small Intestinal Injuriesmentioning

confidence: 99%

The pathophysiology of non-steroidal anti-inflammatory drug (NSAID)-induced mucosal injuries in stomach and small intestine

Matsui

Shimokawa

Kaneko

et al. 2011

J. Clin. Biochem. Nutr.

226

182

View full text Add to dashboard Cite

Non-steroidal anti-inflammatory drugs are the most commonly prescribed drugs for arthritis, inflammation, and cardiovascular protection. However, they cause gastrointestinal complications. The pathophysiology of these complications has mostly been ascribed to non-steroidal anti-inflammatory drugs’ action on the cyclooxygenase inhibition and the subsequent prostaglandin deficiency. However, recent clinical demonstrated the prevalence of non-steroidal anti-inflammatory drugs-induced small intestinal mucosal injury is more often than previously expected. In this review, we discuss the defense mechanisms of stomach, and the pathophysiology of non-steroidal anti-inflammatory drugs-induced injury of stomach and small intestine, especially focused on non-steroidal anti-inflammatory drugs’ action on mitochondria.

show abstract

“…Other studies also demonstrated importance of mitochondrial disorders by NSAIDs on their intestinal toxicity. (20,21) …”

Section: Nsaids-induced Small Bowel Injury and Mitochondrial Disordersmentioning

confidence: 99%

Mitochondrial disorders in NSAIDs-induced small bowel injury

Watanabe¹,

Tanigawa²,

Nadatani³

et al. 2011

J. Clin. Biochem. Nutr.

View full text Add to dashboard Cite

Recent studies using small bowel endoscopy revealed that non-steroidal anti-inflammatory drugs including low-dose aspirin, can often induce small bowel injury. Non-steroidal anti-inflammatory drugs-induced small bowel mucosal injury involves various factors such as enterobacteria, cytokines, and bile. Experimental studies demonstrate that both mitochondrial disorders and inhibition of cyclooxygenases are required for development of non-steroidal anti-inflammatory drugs-induced small bowel injury. Mitochondrion is an organelle playing a central role in energy production in organisms. Many non-steroidal anti-inflammatory drugs directly cause mitochondrial disorders, which are attributable to uncoupling of oxidative phosphorylation induced by opening of the mega channel called mitochondrial permeability transition pore on the mitochondrial membrane by non-steroidal anti-inflammatory drugs. Bile acids and tumor necrosis factor-α also can open the permeability transition pore. The permeability transition pore opening induces the release of cytochrome c from mitochondrial matrix into the cytosol, which triggers a cascade of events that will lead to cell death. Therefore these mitochondrial disorders may cause disturbance of the mucosal barrier function and elevation of the small bowel permeability, and play particularly important roles in early processes of non-steroidal anti-inflammatory drugs-induced small bowel injury. Although no valid means of preventing or treating non-steroidal anti-inflammatory drugs-induced small bowel injury has been established, advances in mitochondrial studies may bring about innovation in the prevention and treatment of this kind of injury.

show abstract

Salicylate- and Aspirin-Induced Uncoupling of Oxidative Phosphorylation in Mitochondria Isolated from the Mucosal Membrane of the Stomach

Cited by 52 publications

References 21 publications

Quantitative Proteomic Profiling of Early and Late Responses to Salicylic Acid in Cucumber Leaves

Quantitative Proteomic Profiling of Early and Late Responses to Salicylic Acid in Cucumber Leaves

The pathophysiology of non-steroidal anti-inflammatory drug (NSAID)-induced mucosal injuries in stomach and small intestine

Mitochondrial disorders in NSAIDs-induced small bowel injury

Contact Info

Product

Resources

About