Reactive nitrogen species have been implicated in the pathogenesis of over 40 human diseases, including inflammation. Evidences suggest that reactive nitrogen species such as nitrite/nitrate and halogenated oxidant-HOCl accumulate at the site of inflammation. At physiologically attainable concentrations, HOCl was found to significantly damage the antiproteolytic potential of human alpha(2)M and induce subtle changes in conformation as judged by fluorescence analysis. Our studies further suggest that at physiological concentrations, nitrite offered significant protection against HOCl induced alpha(2)M inactivation. Our studies suggest that nitrite may act as an antioxidant at physiological concentrations by removing HOCl at sites where both NO(2) and HOCl are formed.
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http://dx.doi.org/10.1007/s10930-010-9249-1 | DOI Listing |
Ecology
January 2025
Department of Biology, Baylor University, Waco, Texas, USA.
Ecosystem-scale primary production may be proximately limited by nitrogen (N) but ultimately limited by phosphorus (P) because N fixation contributes new N that accumulates relative to P at ecosystem scales. However, the duration needed to transition between proximate N limitation and ultimate P limitation remains unknown for most ecosystems, including lakes. Here we present the results of a fully replicated, multi-annual lake mesocosm experiment that permitted full air-water-sediment interactions that mimicked lake ecosystem ecology.
View Article and Find Full Text PDFNephrology (Carlton)
February 2025
Department of Quality Management, Tianjin Blood Center, Tianjin, China.
Aim: To study the effect and elucidate the underlying mechanisms of VDAC1-ΔC on autophagy in renal tubular epithelial cells injured by hypoxia/reoxygenation.
Methods: C57/BL6 mice were randomly divided into groups: sham operation group, IRI 1d group and IRI 2d group. The inner canthal blood of mice was collected to detect the levels of serum creatinine and urea nitrogen and kidney tissues were sampled, and sections were stained with Periodic acid-Schiff for morphological evaluation.
J Occup Health
January 2025
Department of Environmental Health, University of Fukui School of Medical Science, Eiheiji, Fukui, Japan.
Objectives: Many chemicals have been used for industrial purposes, and some of them are carcinogenic to humans. However, their molecular mechanisms have not been well understood. Reactive oxygen species are generated from industrial chemicals and contribute to carcinogenesis.
View Article and Find Full Text PDFMetabolites
December 2024
Laboratory of Quality & Safety Risk Assessment for Aquatic Products (Harbin), Heilongjiang River Fisheries Research Institute of Chinese Academy of Fishery Sciences, Ministry of Agriculture and Rural Areas, Harbin 150070, China.
: Owing to the progressive rise in saline waters globally, resulting in detrimental impacts on freshwater aquaculture, the underlying molecular distinctions governing the response to alkaline stress between diploid and triploid crucian carp remain unknown. : This investigation explores the effects of 20 and 60 mmol NaHCO stress over 30 days on the gills of diploid and triploid crucian carp, employing histological, biochemical, and multi-omic analyses. : Findings reveal structural damage to gill lamellas in the examined tissue.
View Article and Find Full Text PDFMater Today Bio
February 2025
Research Center of Nanomedicine Technology, The Second Affiliated Hospital of Guangxi Medical University, Nanning, 530000, PR China.
Nanozymes with specific catalytic activity inhibit inflammation and promote wound healing efficiently and safely. In this work, multifunctional manganese-based nanozymes (MnGA) with antioxidant properties were successfully constructed via a simple coordination reaction in which manganese chloride was used as the manganese source and gallic acid (GA) was used as the ligand solution. MnGA possesses both catalase-like (CAT-like) and superoxide dismutase-like (SOD-like) activities and a reactive nitrogen species (RNS) scavenging capacity, which enables it to efficiently inhibit the inflammatory response.
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