Heavy beef heart mitochondria depleted of phospholipids by treatment with phospholipase C followed by removal of the by products by lipase treatment or sonication in pentane were analyzed by electron microscopy, chemical analysis and assays of enzymatic activities. The results indicate that diglycerides are present after phospholipase C treatment and are inhibitors of NADH-cytochrome c reductase. After removal of diglycerides with lipase treatment, a phospholipid requirement for NADH-cytochrome c reductase could be demonstrated.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Structure-activity relationship expansion and microsomal stability assessment of the 2-morpholinobenzoic acid scaffold as antiproliferative phosphatidylcholine-specific phospholipase C inhibitors.
RSC Med Chem
January 2025
School of Chemical Sciences, University of Auckland Auckland 1010 New Zealand
Dysregulation of choline phospholipid metabolism and overexpression of phosphatidylcholine-specific phospholipase C (PC-PLC) is implicated in various cancers. Current known enzyme inhibitors include compounds based on a 2-morpholino-5--benzylamino benzoic acid, or hydroxamic acid, scaffold. In this work, 81 compounds were made by modifying this core structure to explore the pharmacophore.
View Article and Find Full Text PDFEfficacy of butylphthalein injection combined with alteplase thrombolysis in patients with acute cerebral infarction and its impact on Lp-PLA2 and CXCL16 levels.
Am J Transl Res
December 2024
Department of Neurology, Shandong Provincial Third Hospital, Shandong University Jinan 250031, Shandong, China.
Objective: To evaluate the efficacy of butylphthalein injection combined with alteplase thrombolysis in patients with acute cerebral infarction (ACI) and its effects on lipoprotein-associated phospholipase A2 (Lp-PLA2) and CXC chemokine ligand 16 (CXCL16) levels.
Methods: A total of 127 ACI patients admitted to Shandong Provincial Third Hospital between March 2020 and June 2023 were included and divided into a butylphthalein group (n = 67) and a control group (n = 60) based on their treatment regimen. All patients received basic treatment.
Effect of Fibrates on Lipoprotein-associated Phospholipase A2 Mass and Activity: A Systematic Review and Meta-analysis of Controlled Clinical Trials.
Curr Pharm Des
January 2025
Center for Global Health Research, Saveetha Medical College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, India.
Background: In vascular tissue, macrophages and inflammatory cells produce the enzyme lipoprotein- associated phospholipase A2 (Lp-PLA2). Treatment with fibrates decreases Lp-PLA2 levels in individuals with obesity and metabolic syndrome; however, these findings have not been fully clarified.
Objective: The goal of this study was to investigate the possible effects of fibrate therapy on Lp-PLA2 mass and activity through a meta-analysis of clinical trials.
Screening potential diagnostic biomarkers for PLA2R‑associated idiopathic membranous nephropathy by WGCNA analysis and LASSO algorithm.
Ren Fail
December 2025
Department of Nephrology, Xiamen Key Laboratory of Precision Diagnosis and Treatment of Chronic Kidney Disease, The Fifth Hospital of Xiamen, Xiamen, Fujian, China.
Adult nephrotic syndrome is primarily caused by membranous nephropathy (MN), with idiopathic membranous nephropathy (IMN) being a prominent subtype. The onset of phospholipase A2 receptor (PLA2R1)-associated IMN is critically linked to M-type PLA2R1 exposure, yet the mechanism underlying glomerular injury remains unclear. In this study, membranous nephropathy datasets (GSE115857, GSE200828) were retrieved from GEO.
View Article and Find Full Text PDFBioinformatic Analysis for Exploring Target Genes and Molecular Mechanisms of Cadmium-Induced Nonalcoholic Fatty Liver Disease and Targeted Drug Prediction.
J Appl Toxicol
January 2025
Department of Toxicology, School of Public Health, Jilin University, Changchun, China.
Cadmium (Cd) is a widely available metal that has been found to have a role in causing nonalcoholic fatty liver disease (NAFLD). However, the detailed toxicological targets and mechanisms by which Cd causes NAFLD are unknown. Therefore, the present work aims to reveal the main targets of action, cellular processes, and molecular pathways by which cadmium causes NAFLD.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!