A four-fold increase in the iron content of normal subjects was detected in plasma after 5 hours of iron administration. Iron supplementation had a surprisingly erratic effect on four patients with hepatomegaly secondary to heart insufficiency, since the increase in the iron content in the plasma after iron-dextran administration was either within the control range or significantly lower, independently of the initial values. Thiobarbituric acid reactive substances (TBARS) content was 2.5 +/- 0.2 and 4.3 +/- 0.4 microM for control and hepatomegalic subjects, respectively. The TBARS basal level was increased by iron supplementation. The difference between TBARS content in hepatomegalic and control subjects, after 5 hours of iron administration, was increased by 50% as compared to the difference in the basal content of TBARS. alpha-Tocopherol (alpha-T) content in plasma from subjects with hepatomegaly showed a significant decrease (-41%) as compared to control subjects. No significant difference over the basal level of alpha-T was measured after 5 hours of iron administration in any subject. The data presented here suggest that abnormal liver condition affects iron-dependent oxidative stress in plasma. Moreover, alpha-T does not seem to be the main antioxidant to control iron-dependent oxidative stress in plasma.
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http://dx.doi.org/10.1191/0960327103ht372oa | DOI Listing |
Cell Death Differ
January 2025
Translational Research Centre of Orthopedics, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
Ferroptosis is one of the cell death programs occurring after spinal cord injury (SCI) and is driven by iron-dependent phospholipid peroxidation. However, little is known about its underlying regulation mechanism. The present study demonstrated that lipid peroxidation was promoted in patients with SCI.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Gynecology, Handan Central Hospital, Handan, China.
Background: Ferroptosis, a recently discovered iron-dependent cell death, is linked to various diseases but its role in endometriosis is still not fully understood.
Methods: In this study, we integrated microarray data of endometriosis from the GEO database and ferroptosis-related genes (FRGs) from the FerrDb database to further investigate the regulation of ferroptosis in endometriosis and its impact on the immune microenvironment. WGCNA identified ferroptosis-related modules, annotated by GO & KEGG.
Front Pharmacol
January 2025
Department of Oncology, Shengjing Hospital of China Medical University, Shenyang, China.
Breast cancer is the most commonly diagnosed cancer worldwide. Metal metabolism is pivotal for regulating cell fate and drug sensitivity in breast cancer. Iron and copper are essential metal ions critical for maintaining cellular function.
View Article and Find Full Text PDFTissue Cell
December 2024
Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea. Electronic address:
Urolithin A (URA), a product of the gut microflora from foods rich in ellagitannins found in berries and nuts, has demonstrated anti-inflammatory and antioxidative stress properties in various disease models. Ferroptosis, an iron-dependent form of cell death, is considered a pathogenic cause of tendinopathy. However, the effects of URA on hyperlipidemic tenocytes and the related molecular mechanisms for the treatment of tendinopathy have not been elucidated.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
January 2025
The First College of Clinical Medical Science, China Three Gorges University, 443000 Yichang, Hubei, China.
Multiple sclerosis (MS) is a chronic autoimmune disorder marked by neuroinflammation, demyelination, and neuronal damage. Recent advancements highlight a novel interaction between iron-dependent cell death, known as ferroptosis, and gut microbiota, which may significantly influences the pathophysiology of MS. Ferroptosis, driven by lipid peroxidation and tightly linked to iron metabolism, is a pivotal contributor to the oxidative stress observed in MS.
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