The present study was designed to evaluate the lipid peroxidation and non-enzymatic antioxidants in pregnancyinduced hypertension (PIH) compared with healthy normal pregnant and non-pregnant as controls. 75 cases were studied of which 25 were normal healthy controls (Group A), 25 healthy pregnant women (Group B) of third trimester and 25 were PIH (Group C) of the same trimester. In PIH, malondialdehyde a lipid peroxidation product was significantly increased as compared to normal pregnant and non-pregnant controls. The nonenzymatic antioxidants like reduced glutathione, Vitamin-E, Vitamin-C and Vitamin-A were significantly decreased in normal pregnants as compared to controls. A further significant decrease was noticed in PIH compared to normal pregnants. A significant negative correlation was detected between lipid peroxidation and non-enzymatic antioxidant levels. Our study clearly indicates a relationship between elevated lipid peroxidation, decreased non-enzymatic antioxidant in PIH. The measurement of non-enzymatic antioxidants in plasma may be useful predictor of the likely development of PIH.
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http://dx.doi.org/10.1007/s12291-008-0011-9 | DOI Listing |
Immune Netw
February 2025
College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Korea.
Ferroptosis, an iron-dependent form of regulated cell death, is driven by lipid peroxidation and shaped by metabolic and antioxidant pathways. In immune cells, ferroptosis susceptibility varies by cell types, lipid composition, and metabolic demands, influencing immune responses in cancer, infections, and autoimmune diseases. Therapeutically, targeting ferroptosis holds promise in cancer immunotherapy by enhancing antitumor immunity or inhibiting immunosuppressive cells.
View Article and Find Full Text PDFFront Cell Dev Biol
February 2025
Geriatric Health Research Center, Birjand University of Medical Sciences, Birjand, Iran.
Lung cancer (LC) is a highly prevalent and deadly type of cancer characterized by intricate molecular pathways that drive tumor development, metastasis, and resistance to conventional treatments. Recently, ferroptosis, a controlled mechanism of cell death instigated by iron-dependent lipid peroxidation, has gained attention for its role in LC progression and treatment. Noncoding RNAs (ncRNAs), such as microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), are emerging as key modulators of ferroptosis, significantly influencing LC biology.
View Article and Find Full Text PDFNutrients
February 2025
Postgraduate Program in Neuroscience and Cell Biology, Federal University of Pará/UFPA, Rua Augusto Corrêa 01, Bairro Guamá, Belém 66075-110, PA, Brazil.
Chronic treatment with dapsone (DDS) has been linked to adverse reactions involving all organ systems, such as dapsone hypersensitivity syndrome, methemoglobinemia and hemolytic anemia, besides neuroinflammation and neurodegeneration due to iron accumulation and oxidative stress. These effects probably occur due to the presence of its toxic metabolite DDS-NOH, which can generate reactive oxygen species (ROS) and iron overload. In this sense, antioxidant compounds with chelating properties, such as alpha-lipoic acid (ALA), may be an interesting adjuvant therapy strategy in treating or preventing these effects.
View Article and Find Full Text PDFNutrients
February 2025
Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.
Background/objective: Ferroptosis is an iron-dependent form of programmed cell death characterized by lipid peroxidation products (LPOs). A chemotherapeutic drug, 5-fluorouracil (5-FU), can induce epithelial mucositis and favor drug synergism with erastin in ferroptosis. tea saponin extract (TS) is known to exert antioxidative properties.
View Article and Find Full Text PDFInt J Mol Sci
March 2025
Institute of Genomics, School of Medicine, Huaqiao University, 668 Jimei Road, Xiamen 361021, China.
Oxidative stress-induced photoreceptor cell death is closely associated with the etiology of age-related macular degeneration (AMD), and sodium iodate (SI) has been widely used as an oxidant stimulus in AMD models to induce retinal pigment epithelium (RPE) and photoreceptor cell death. However, the mechanism underlying SI-induced photoreceptor cell death remains controversial and unclear. In this study, we elucidate that ferroptosis is a critical form of cell death induced by SI in photoreceptor-derived 661W cells.
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