Iron induced changes in growth, N2-fixation, CO2 fixation and photosynthetic activity were studied in a diazotrophic cyanobacterium Anabaena PCC 7120. Iron at 50 microM concentration supported the maximum growth, heterocyst frequency, CO2 fixation, photosystem I (PS I), photosystem II (PS II) and nitrogenase activities in the organism. Higher concentration of iron inhibited these processes. Chl a and PS II activities were more sensitive to iron than the protein and PS I activity.
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ACS Nano
January 2025
School of Chemistry and Chemical Engineering, Shanghai Jiao Tong University, Shanghai 200240, P. R. China.
Ferroptosis is a classic type of programmed cell death characterized by iron dependence, which is closely associated with many diseases such as cancer, intestinal ischemic diseases, and nervous system diseases. Transferrin (Tf) is responsible for ferric-ion delivery owing to its natural Fe binding ability and plays a crucial role in ferroptosis. However, Tf is not considered as a classic druggable target for ferroptosis-associated diseases since systemic perturbation of Tf would dramatically disrupt blood iron homeostasis.
View Article and Find Full Text PDFNeurochem Res
January 2025
Department of Radiology, the Second Affiliated Hospital of Kunming Medical University, No.374 Yunnan-Burma Road, Wuhua District, Kunming, Yunnan, 650101, PR China.
Objective: Post-resuscitation brain injury is a common sequela after cardiac arrest (CA). Increasing sirtuin1 (SIRT1) has been involved in neuroprotection in oxygen-glucose deprivation (OGD) neurons, and we investigated its mechanism in post-cardiopulmonary resuscitation (CPR) rat brain injury by mediating p65 deacetylation modification to mediate hippocampal neuronal ferroptosis.
Methods: Sprague-Dawley rat CA/CPR model was established and treated with Ad-SIRT1 and Ad-GFP adenovirus vectors, or Erastin.
Alzheimers Dement
December 2024
The University of Texas at San Antonio, San Antonio, TX, USA.
Background: Neurodegeneration is characterized by the progressive loss of neurons. However, the mechanisms by which neurons die in Alzheimer's disease (AD) remain elusive. Disrupted iron homeostasis is associated with accelerated cognitive decline, amyloid beta deposition, and AD progression, but its pathogenic relevance is poorly understood.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Australia, Melbourne, VIC, Australia.
Background: Allelic variation in apolipoprotein E (APOE) is by far the greatest contributor to Alzheimer's disease (AD) after age, but the mechanisms underlying how APOE impacts on the pathology of AD remain undefined. While most research is focusing on mechanisms associated with the presence of the APOE risk allele, several aspects of APOE biology remain poorly understood. In particular, the physiological relevance of APOE receptors and their impact on disease progression have been overlooked.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Rochester School of Medicine & Dentistry, Rochester, NY, USA.
Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by neuronal dysfunction leading to decreased memory and cognitive function. AD research has largely focused on the potential pathogenic role of two disease hallmarks: amyloid beta and phosphorylated tau. However, pharmacological interventions targeting these disease hallmarks have met with limited clinical trial success.
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