Background: The production of free radicals is increased in inflammatory bowel disease, and trace elements are crucial components of several antioxidants. Trace elements deficiency may therefore compromise the defense against oxidative damage. The aims of this study were to measure plasma and tissue concentration of trace elements and antioxidants and to relate this to disease activity.
Methods: A 10-ml blood sample and six colonic biopsy specimens were obtained from 24 patients with either active ulcerative colitis or in remission and 10 patients with irritable bowel syndrome for measurement of trace elements and trace element-dependent enzymes.
Results: Patients with moderately active disease had significantly lower plasma iron, selenium, and glutathione peroxidase levels than patients in remission and controls, whereas no significant differences were found between the zinc and copper values of patients and controls. Mucosal concentrations of zinc and metallothionein were reduced, whereas iron and glutathione peroxidase concentrations were increased in patients with endoscopically active disease as compared with controls and patients in remission.
Conclusions: Patients with ulcerative colitis have altered plasma and tissue levels of trace elements and antioxidant-related enzymes. The resulting reduced protection against free radicals may contribute to the inflammatory process.
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http://dx.doi.org/10.1080/00365529850171936 | DOI Listing |
BMC Med Imaging
January 2025
Department of Radiology, Shenzhen Children's Hospital, Shantou University Medical College, 7019 Yitian Road, Futian District, Shenzhen, 518038, China.
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Sci Rep
January 2025
Praxis Dr.Carmine, Etzelstrasse 21, Pfaeffikon SZ, 8808, Switzerland.
Spot-urinary biomarkers are crucial in medical, epidemiological, and environmental studies, but their variability due to hydration levels requires precise dilution adjustments. Traditional methods, like conventional creatinine correction (CCRC), are limited in compensating for variations in urine concentration, causing substantial inconsistencies, particularly at the extremes of the diuresis spectrum. While restricting the creatinine (CRN) range to 0.
View Article and Find Full Text PDFGeroscience
January 2025
Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Nuthetal, Germany.
Research in aging often refers to animal models, particularly C57BL/6J (B6J) mice, considered gold standard. However, B6J mice are distributed by different suppliers, which results in divers substrains exhibiting notable phenotypic differences. To ensure a suitable phenotype of cardiac aging, we performed heart analyses of young (5 months) and old B6J mice (24 months) from two substrains: B6JRj (Janvier) and B6JCrl mice (Charles River).
View Article and Find Full Text PDFThe human () gene encodes a plasma membrane protein SLC39A8 (ZIP8) that mediates the specific uptake of the metals Cd, Mn, Zn, Fe, Co, and Se Pathogenic variants within are associated with congenital disorder of glycosylation type 2 (CDG type II) or Leigh-like syndrome. However, numerous mutations of uncertain significance are also linked to different conditions or benign traits. Our study characterized 21 variants and measured their impact on protein localization and intracellular levels of Cd, Zn, and Mn We identified four variants that disrupt protein expression, five variants with high retention in the endoplasmic reticulum, and 12 variants with localization to the plasma membrane.
View Article and Find Full Text PDFDrug Metab Dispos
January 2025
Department of Pharmacology and Experimental Therapeutics, Louisiana State University Health Science Center, New Orleans, Louisiana; The Stanley S. Scott Cancer Center, Louisiana State University Health Science Center, New Orleans, Louisiana. Electronic address:
Environmentally persistent free radicals (EPFRs) are a recently recognized component of particulate matter that cause respiratory and cardiovascular toxicity. The mechanism of EPFR toxicity appears to be related to their ability to generate reactive oxygen species (ROS), causing oxidative damage. EPFRs were shown to affect cytochrome P450 (P450) function, inducing the expression of some forms through the Ah receptor.
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