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Studies on ferrous ion-induced lipid peroxidation of rat liver mitochondria. II. Relationship to incubation temperature.

Ferrous ion-induced lipid peroxidation in rat liver mitochondria has a lag in the induction period. The characteristics of the lag were investigated under various conditions. This lag period lengthened proportionally to increased temperature (4 degrees approximately 37 degrees C). In the presence of inorganic phosphate the lag period lengthened, reaching a maximum at about 20 degrees C, and then shortened with increased temperatute. Elongated lag periods were shown in heat-treated or protein digested mitochondria. Shortened lag periods were shown in snake venom-treated mitochondria. On the oth

When Powerhouses Fail and Rust Takes Over: Primary Mitochondrial and Lipid Metabolism Failure with Secondary Iron Accumulation and Lipid Peroxidation in Neurodegeneration with Brain Iron Accumulation.

Neurodegeneration with brain iron accumulation (NBIA) comprises a genetically heterogeneous group of rare movement disorders characterized by progressive neurodegeneration and selective basal ganglia iron deposition. Recent discoveries have fundamentally reshaped the understanding of NBIA, indicating that defects in coenzyme A metabolism, mitochondrial bioenergetics, lipid remodeling, autophagy-lysosomal pathways, and ferroptosis precede and promote secondary iron dyshomeostasis rather than resulting from primary abnormalities in iron metabolism. This review integrates recent mechanistic and t

ALOX15-Inhibitory Peptides Derived from Coffee Bean Protein Hydrolysates Confer Neuroprotection against Lipid Peroxidation.

Coffee beans are widely consumed worldwide and are known for their central nervous system-stimulating effects, mainly attributed to caffeine and other small molecules. However, the neuroprotective potential of coffee bean-derived peptides remains largely unexplored. In this study, coffee bean protein hydrolysates (CBPH) exhibited protective effects against RSL3- and 6-OHDA-induced neuronal injury. Virtual screening and molecular docking targeting 15-lipoxygenase (ALOX15), a key enzyme involved in oxidative neuronal damage, identified eight candidate inhibitory peptides. Among them, FAR and FPS

Colorectal Cancer Liver Metastasis-Associated Ferroptosis-Related Genes Modulate Lipid Peroxidation in Colorectal Cancer Cells.

Distant metastasis, predominantly to the liver, remains the leading cause of death in colorectal cancer (CRC), yet biomarkers that capture metastatic competence remain limited. Ferroptosis is an iron-dependent, lipid peroxidation-driven form of regulated cell death that can restrain tumor progression, but whether primary CRC from patients with liver metastasis shows ferroptosis-resistance-related features remains incompletely understood. In a small exploratory set of T-stage-matched primary CRC tumors with or without liver metastasis, we quantified glutathione redox and lipid peroxidation-rela

Glycemic status, antioxidant enzyme and lipid peroxidation among patients with diabetes mellitus in Buea Regional Hospital in Cameroon.

BACKGROUND: Oxidative stress has been suggested to play a role in the pathogenesis of type 2 diabetes mellitus (T2DM) and development of complications by altering antioxidant levels and inducing lipid peroxidation. Although patients with T2DM are reported to be under oxidative stress because of prolonged exposure to hyperglycemia, the influence of glycemic control in diabetes on enhanced free-radical activity is poorly understood. AIM: To evaluate the levels of malondialdehyde (MDA) - a marker of lipid peroxidation and catalase (CAT) - an antioxidant enzyme in patients with T2DM categorized b

TFPT Abundance Is Associated with Growth-Related Phenotypes and Cellular Features Linked to Lipid Peroxidation Defense in Hepatocellular Carcinoma.

TCF3 fusion partner (TFPT) remains insufficiently characterized in hepatocellular carcinoma (HCC), particularly in relation to tumor growth and cellular features linked to lipid peroxidation defense. We integrated public transcriptomic and clinical datasets and established stable TFPT-knockdown and TFPT-overexpression models in MHCC97-H and Huh-7 cells. TFPT expression was higher in HCC tissues and selected HCC cell lines. In TCGA-LIHC, higher TFPT expression was associated with shorter overall survival after multivariable adjustment (HR, 1.37; 95% CI, 1.06-1.77), although this association was

3-n-Butylphthalide Protects SH-SY5Y Cells from Ferroptosis by Inhibiting ACSL4-Mediated Lipid Peroxidation.

Parkinson's disease (PD) is the second most common neurodegenerative disorder, and its pathogenesis is closely associated with oxidative stress, mitochondrial dysfunction, and iron-dependent cell death. In our previous study, we showed that 3-n-butylphthalide (NBP) alleviates behavioral deficits in a PD mouse model. However, the underlying mechanisms remain unclear. Here, we found that NBP treatment significantly attenuated ferroptosis induced by Erastin or RSL3 in SH-SY5Y cells, as evidenced by improved cell viability, reduced reactive oxygen species (ROS) production, decreased mitochondrial

IFN𝛾 and IFN𝛾 mimetics prevent IFN-I-mediated TB susceptibility by regulating iron metabolism and lipid peroxidation.

Type I interferons (IFN-I) and IFNγ exert divergent effects during tuberculosis, but the mechanisms that determine whether macrophage activation promotes host defense or inflammatory pathology remain incompletely understood. Here, we dissect the interplay between IFN-I and IFNγ in macrophage activation using genetically susceptible B6.Sst1S macrophages. We show that, during tumor necrosis factor (TNF) stimulation, susceptible macrophages enter a persistent pathological activation state (pPAS) characterized by sustained lipid peroxidation and super-induction of IFN-I responses. This pathologica

LOX-1 mediated lipid peroxidation leads to dysfunction of tumor infiltrating CD8+ T cells in ovarian cancer.

Abnormal lipid accumulation in the tumor microenvironment (TME) promotes lipid peroxidation in tumor-infiltrating CD8+T cells (CD8+TILs), driving their dysfunction and impairing antitumor immunity in ovarian cancer (OC). To elucidate the underlying immunosuppressive mechanisms, we integrated clinical specimens, mouse models, and in-vitro validation. Notably, CD8+TILs from OC patients exhibited pronounced lipid peroxidation signatures. Elevated oxidized low-density lipoprotein (oxLDL) levels were detected in ovarian tumor interstitial fluid (TIF), tumor mass-derived supernatants, and tissue sec

Длиннокаменистые толстые кислоты как движущие факторы нейроинфламмации в нейродегенерации: механистические связи с липидом пероксидацией, Ферроптозом и митохондриальной дисфункцией.

Фон: Нейродегенеративные заболевания (НИ) рассматриваются главным образом как расстройства, характеризующиеся серьезным иммунометаболическим дисбалансом, характеризующимся текущей нейроинфламмацией и глиальной активацией. Хотя митохондриальная дисфункция и окислительный стресс являются хорошо известными особенностями, метаболические факторы в верхнем течении, связывающие эти патологические процессы, по-прежнему плохо понимаются. Методы: В ходе этого обзора мы изучили недавние доклинические и клинические исследования, в ходе которых были изучены связи между липидным метаболизмом, иммунометаболи

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… During these initial phases, lipid peroxidation is initiated under heightened oxidative stress, largely driven by an LCFA imbalance. Cells rely on specific localized defenses against lipid peroxidation. … The massive efflux of superoxide radicals drives lipid peroxidation of neuronal polyunsaturated fatty acids (LC-PUFAs). The existing iron imbalance and the unchecked accumulation of lipid peroxides act as the primary initiation signals for ferroptosis. 3.3. …

Dysregulation of mitochondrial α-ketoglutarate dehydrogenase leads to elevated lipid peroxidation in CHCHD2-linked Parkinson's disease models.

Dysregulation of mitochondrial function has been implicated in Parkinson's disease (PD), but the role of mitochondrial metabolism in disease pathogenesis remains to be elucidated. Using an unbiased metabolomic analysis of purified mitochondria, we identified alterations in α-ketoglutarate dehydrogenase (KGDH) pathway upon loss of PD-linked CHCHD2 protein. KGDH, a rate-limiting enzyme complex in the tricarboxylic acid cycle, was decreased in CHCHD2-deficient male mouse brains and human dopaminergic neurons. This deficiency of KGDH led to elevated α-ketoglutarate and increased lipid peroxidation

Nrf2 Alleviates Colistin-Induced Nephrotoxicity by Suppressing Ferroptosis via GPX4-Mediated Lipid Peroxidation and Mitochondrial Protection.

Colistin (CS)-induced nephrotoxicity remains a major clinical challenge, with its mechanisms not fully understood. This study aimed to investigate the involvement of ferroptosis and the nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant pathway in CS-induced kidney damage. In vivo, rats treated with CS exhibited kidney injury, marked by elevated serum blood urea nitrogen (BUN) and creatinine levels, increased biomarkers (kidney injury molecule-1 (Kim-1) and neutrophil gelatinase-associated lipocalin (NGAL)), and histopathological evidence of tubular damage. Oxidative stress was obs

Pharmacologic Ascorbate Radiosensitizes Pancreatic Cancer but Radioprotects Normal Tissue: The Role of Oxidative Stress-Induced Lipid Peroxidation.

The toxicity of ionizing radiation limits its effectiveness in the treatment of pancreatic ductal adenocarcinoma. Pharmacologic ascorbate (P-AscH-) has been shown to radiosensitize pancreatic cancer cells while simultaneously radioprotecting normal cells. We hypothesize that P-AscH- protects the small intestine while radiosensitizing pancreatic cancer cells partially through an oxidative stress mechanism. Duodenal samples from pancreaticoduodenectomy specimens of patients who underwent radio-chemotherapy ± P-AscH- and mouse tumor and jejunal samples treated with radiation ± P-AscH- were evalua

Oxidative Stress, Lipid Peroxidation and Ferroptosis Are Major Pathophysiological Signatures in the Placental Tissue of Women with Late-Onset Preeclampsia.

Preeclampsia, a serious and potentially life-threatening medical complication occurring during pregnancy, is characterized by hypertension and often accompanied by proteinuria and multiorgan dysfunction. It is classified into two subtypes based on the timing of diagnosis: early-onset (EO-PE) and late-onset preeclampsia (LO-PE). Despite being less severe and exhibiting distinct pathophysiological characteristics, LO-PE is more prevalent than EO-PE, although both conditions have a significant impact on placental health. Previous research indicates that different pathophysiological events within

Glycitein prevents reserpine-induced depression and associated comorbidities in mice: modulation of lipid peroxidation and TNF-α levels.

Depression is a debilitating mood disorder affecting millions worldwide and continues to pose a significant global health burden. Due to the multifaceted nature of depression, the current treatment regimens are not up to mark in terms of their multitargeting potential and least side effect profile. Molecules within the isoflavone class demonstrate promising potential in alleviating depression and associated conditions, offering a multifaceted approach to manage mental health concerns. Therefore, the current study was designed to explore the potential of glycitein, an isoflavone in managing res

Hyperglycemia-triggered lipid peroxidation destabilizes STAT4 and impairs anti-viral Th1 responses in type 2 diabetes.

Patients with type 2 diabetes (T2D) are more susceptible to severe respiratory viral infections, but the underlying mechanisms remain elusive. Here, we show that patients with T2D and coronavirus disease 2019 (COVID-19) infections, and influenza-infected T2D mice, exhibit defective T helper 1 (Th1) responses, which are an essential component of anti-viral immunity. This defect stems from intrinsic metabolic perturbations in CD4+ T cells driven by hyperglycemia. Mechanistically, hyperglycemia triggers mitochondrial dysfunction and excessive fatty acid synthesis, leading to elevated oxidative st

PUFAs add fuel to Crohn's disease-associated AIEC-induced enteritis by exacerbating intestinal epithelial lipid peroxidation.

Polyunsaturated fatty acids (PUFAs) have been shown to exacerbate Crohn's disease (CD) by promoting lipid peroxidation (LPO) of intestinal epithelial cells (IECs). Dysbiosis of the gut microbiota may play a crucial role in this process. CD patients often exhibit an increased abundance of Escherichia coli (E. coli) in the gut, and the colonization of adherent-invasive E. coli (AIEC) is implicated in the initiation of intestinal inflammation in CD. However, the impact of AIEC on LPO remains unclear. In this study, we observed that AIEC colonization in the terminal ileum of CD patients was associ

Microbiota-induced lipid peroxidation impairs obeticholic acid-mediated antifibrotic effect towards nonalcoholic steatohepatitis in mice.

Obeticholic acid (OCA) has been examined to treat non-alcoholic steatohepatitis (NASH), but has unsatisfactory antifibrotic effect and defic … s and phosphatidylethanolamines containing PUFA (PUFA-PEs), which are susceptible to be oxidized to lipid peroxides (notably arachidonic acid (ARA)-derived 12-HHTrE), inducing hepatocyte ferroptosis and activating hepatic stellate cells (HSCs). Inhibiting lipid peroxidation with pentoxifylline (PTX) rescues anti-fibrotic effect of OCA, suggesting combination of O …

Effects of albumin-bound nitrosyl iron complex with thiosulfate ligands on lipid peroxidation and activities of mitochondrial enzymes in vitro.

Nitric oxide (NO) mediates diverse physiological processes in living organisms. Small molecular NO donors usually lack stability and have a short half-life in human tissues, limiting the therapeutic application. The anionic tetranitrosyl iron complex with thiosulfate ligands (TNIC) is one of the most promising NO donors. This study shows that bovine serum albumin (BSA) can effectively stabilize the TNIC complex under aerobic (physiological) conditions, which contributes to its prolonged action as NO donor. Our results demonstrated that TNIC-BSA inhibits formation of TBARS - standard biomarker

Diminished Systemic Amino Acids Metabolome and Lipid Peroxidation in Ureteropelvic Junction Obstruction (UPJO) Infants Requiring Surgery.

Congenital anomalies of the urinary tract, and particularly of obstructive nephropathy such as ureteropelvic junction obstruction (UPJO) in infants, can later lead to chronic kidney disease and hypertension. Fundamental questions regarding underlying mechanisms remain unanswered. The aim of the present study was to quantitate the systemic amino acids metabolome in 21 UPJO infants requiring surgery (Group A) and 21 UPJO infants under conservative treatment (Group B). Nineteen healthy age-matched infants served as controls (Group C). Serum amino acids involved in several pathways and representat