In this study, the effects of concentrations 0, 100, 250, 500, 750 and 1000 mg kg(-1) of nanoscale zero-valent iron (nZVI) on germination, seedlings growth, physiology and toxicity mechanisms were investigated. The results showed that nZVI had no effect on germination, but inhibited the rice seedlings growth in higher concentrations (>500 mg kg(-1) nZVI). The highest suppression rate of the length of roots and shoots reached 46.9% and 57.5%, respectively. The 1000mg kg(-1) nZVI caused the highest suppression rates for chlorophyll and carotenoids, at 91.6% and 85.2%, respectively. In addition, the activity of antioxidant enzymes was altered by the translocation of nanoparticles and changes in active iron content. Visible symptoms of iron deficiency were observed at higher concentrations, at which the active iron content decreased 61.02% in the shoots, but the active iron content not decreased in roots. Interestingly, the total and available amounts of iron in the soil were not less than those in the control. Therefore, the plants iron deficiency was not caused by (i) deficiency of available iron in the soil and (ii) restraint of the absorption that plant takes in the available iron, while induced by (ⅲ) the transport of active iron from the root to the shoot was blocked. The cortex tissues were seriously damaged by nZVI which was transported from soil to the root, these were proved by scanning electron microscopy (SEM), transmission electron microscopy (TEM) and energy dispersive spectroscopy (EDS). This current study shows that the mechanism of iron deficiency in rice seedling was due to transport of active iron from the root to the shoot blocked, which was caused by the uptake of nZVI.
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http://dx.doi.org/10.1016/j.envpol.2016.01.028 | DOI Listing |
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 PDFJ Transl Autoimmun
June 2025
Rheumatology Research Center, Tehran University of Medical Science, Tehran, Iran.
Iron is a crucial element for living organism in terms of oxygen transport, hematopoiesis, enzymatic activity, mitochondrial respiratory chain function and also immune system function. The human being has evolved a mechanism to regulate body iron. In some rheumatic diseases such as rheumatoid arthritis (RA), systemic lupus erythematous (SLE), systemic sclerosis (SSc), ankylosing spondylitis (AS), and gout, this balanced iron regulation is impaired.
View Article and Find Full Text PDFCureus
December 2024
Internal Medicine, National Hospital of Sri Lanka, Colombo, LKA.
Hereditary hemochromatosis occurs due to genetic mutations, namely, cysteine-to-tyrosine substitution at amino acid 282 (C282Y) and histidine-to-aspartic acid substitution at 63 (H63D) mutations. The role of H63D mutation in hemochromatosis is less clear, and its penetrance is low even in homozygotes. Therefore, iron overload in H63D heterozygotes is extremely rare and scarcely reported.
View Article and Find Full Text PDFSmall
January 2025
State Key Laboratory of High Performance Ceramics and Superfine Microstructure, Shanghai Institute of Ceramics, Chinese Academy of Sciences, Shanghai, 200050, China.
Emerging evidence demonstrates that inducing ferroptosis, a nonapoptotic programmed cell death mode, holds significant potential for tumor treatment. However, current ferroptosis strategies utilizing exogenous Fenton-type heavy metal species or introducing glutathione (GSH)/glutathione peroxidase 4 (GPX4) suppressants are hampered by latent adverse effects toward organisms, while utilizing endogenous iron may cause undesirable tumor angiogenesis through specific signaling pathways. Here, a ferric ion (Fe)-responsive and DNAzyme-delivered coordination nanosystem (ZDD) is developed to achieve a novel scheme of synergistic tumor-specific ferroptosis and gene therapy, which modulates and harnesses the endogenous iron in tumors for inducing ferroptosis while intercepting tumor angiogenesis to enhance therapeutic efficacy.
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.
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