Reduced and oxidized glutathione and pyridine coenzymes, glutathione-related enzymes and Cu,Zn-superoxide dismutase (Cu,Zn-SOD) were investigated in the RBC of patients with chronic renal failure (CRF) and in age- and sex-matched controls. The effects of hemodialysis (HD) were also studied. A defective RBC redox state was shown in the CRF group based on a decreased GSH/GSSG ratio and NADPH levels. Increased activities of glutathione transferase (GSH-S-T) and Cu,Zn-SOD were observed before HD. Dialysis apparently restores the levels of antioxidant enzymes and at the same time strongly affects the redox state. Thus we can speculate that HD can generate severe redox impairment inducing damage in RBC and plasma antioxidant enzymes. Increased erythrocyte GSSG and GSM-S-T levels coupled with a reduced hexose monophosphate shunt (HMPS) function may be useful indexes of oxidative stress in uremic anemia.

Download full-text PDF

Source
http://dx.doi.org/10.1159/000204332DOI Listing

Publication Analysis

Top Keywords

redox state
12
uremic anemia
8
effects hemodialysis
8
antioxidant enzymes
8
erythrocyte redox
4
state uremic
4
anemia effects
4
hemodialysis relevance
4
relevance glutathione
4
glutathione metabolism
4

Similar Publications

Background: Osteoporosis (OP) is a systemic disease characterized by low bone mass. New progress has been made in the study of OP, such as lipid peroxidation. However, the role of lipid peroxides in osteoclast differentiation is still unclear.

View Article and Find Full Text PDF

Versatile nitrate-respiring heterotrophs are previously concealed contributors to sulfur cycle.

Nat Commun

January 2025

State Key Laboratory of Urban Water Resource and Environment, School of Environment, Harbin Institute of Technology, Harbin, 150090, PR China.

Heterotrophic denitrifiers play crucial roles in global carbon and nitrogen cycling. However, their inability to oxidize sulfide renders them vulnerable to this toxic molecule, which inhibits the key enzymatic reaction responsible for reducing nitrous oxide (NO), thereby raising greenhouse gas emissions. Here, we applied microcosm incubations, community-isotope-corrected DNA stable-isotope probing, and metagenomics to characterize a cohort of heterotrophic denitrifiers in estuarine sediments that thrive by coupling sulfur oxidation with denitrification through chemolithoheterotrophic metabolism.

View Article and Find Full Text PDF

A cost-effective strategy is reported utilizing ionic liquid (IL), 1-hexyl-3-methylimidazolium bisulfate ([HMIM] HSO), to delaminate TiC MXene, thereby enhancing its efficiency in electrocatalyzing tryptophan (Trp) oxidation. The positively charged IL effectively intercalates within the negatively charged MXene layers, fostering structural stability through π-π stacking and electrostatic interactions. Consequently, the resulting IL-TiC composite not only maintained the inherent electronic conductivity of TiC but also significantly augmented its electrocatalytic prowess.

View Article and Find Full Text PDF

SERCA2 dysfunction accelerates angiotensin II-induced aortic aneurysm and atherosclerosis by induction of oxidative stress in aortic smooth muscle cells.

J Mol Cell Cardiol

January 2025

School of Pharmaceutical Sciences, Chongqing University, Chongqing 401331, China; State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Harbin Medical University, China; Chongqing Key Laboratory of New Drug Delivery System, Chongqing 400038, China. Electronic address:

Background And Aim: Our previous research indicates that sarcoplasmic/endoplasmic reticulum calcium ATPase 2 (SERCA2) dysfunction facilitates the phenotypic transformation of aortic smooth muscle cells (ASMCs) and intensifies aortic aneurysm through the regulation of calcium-dependent pathways and endoplasmic reticulum stress. Our hypothesis is that additional mechanisms are involved in aortic aneurysm and atherosclerosis induced by SERCA2 dysfunction from the perspective of ASMC phenotypic transformation.

Methods & Results: In SERCA2 dysfunctional mice and their control littermates, ASMCs were isolated to analyze protein expression and cell functions, and angiotensin II was infused into these mice that were backcrossed into LDL receptor deficient background to induce aortic aneurysm and atherosclerosis.

View Article and Find Full Text PDF

Pharmacological ascorbate combined with rucosopasem selectively radio-chemo-sensitizes NSCLC via generation of HO.

Redox Biol

January 2025

Free Radical and Radiation Biology Program, Department of Radiation Oncology, Holden Comprehensive Cancer Center, The University of Iowa College of Medicine, Iowa City, IA 52242, USA; Interdisciplinary Graduate Program in Human Toxicology, The University of Iowa, Iowa City, IA, 52242, USA.

Differences in cancer and normal cell oxidative metabolism provide a unique therapeutic opportunity for developing combined modality approaches with redox-active small molecules as radio-chemosensitizers that are well-tolerated by normal tissues. Pentaazamacrocyclic Mn (II)-containing (MnPAM) superoxide dismutase (SOD) mimetics and pharmacological ascorbate given IV to achieve [mM] plasma levels (pharmacological ascorbate: P-AscH‾) have been shown to act individually as cancer cell radio- and chemosensitizers via the generation of HOin vivo. The current study shows that the combination of newly developed MnPAM dismutase mimetic, rucosopasem manganese (RUC) with P-AscH‾ radio-sensitizes non-small cell lung cancer cells (NSCLC) and increases steady state levels of intracellular HO with no additional toxicity to normal human bronchial epithelial cells (HBECs).

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!