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Sialidases/neuraminidases remove terminal sialic acid residues from glycoproteins, glycolipids, and oligosaccharides. Our previous research has revealed the distribution of sialidase in non-clinical fungal isolates from different ecological niches, including Antarctica. Fungi adapted to extremely low temperatures possess defense mechanisms necessary for their survival such as the response against oxidative stress. The relationship between oxidative stress and sialidase synthesis has been studied extremely sparsely. The aim of the present study was to investigate the involvement of sialidase in the cell response of the Antarctic strain P29 against oxidative stress induced by long- and short-term exposure to low temperatures. The changes in growth temperatures for 120 h (long-term stress) affected biomass accumulation, glucose consumption, sialidase synthesis, and the activity of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). The short-term temperature downshift (6 h) caused oxidative stress, evidenced by changes in the levels of biomarkers, including lipid peroxidation, oxidatively damaged proteins, and the accumulation of reserve carbohydrates. Simultaneously, a sharp increase in SOD and CAT activity was found, which coincided with a significant increase in sialidase activity. This study marks the first demonstration of increased sialidase activity in filamentous fungi isolated from extreme cold environments as a response to oxidative stress.
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http://dx.doi.org/10.3390/life15060926 | DOI Listing |
Biochim Biophys Acta Biomembr
September 2025
Instituto de Física, Universidade Federal de Goiás, Goiânia, GO, Brazil. Electronic address:
Three antileishmanial compounds incorporating a butylated hydroxytoluene (BHT) moiety and an acrylate-based Michael acceptor scaffold were rationally designed from the lead structures LQFM064 and LQFM332, which feature a chalcone-derived core. Their activities against Leishmania (L.) amazonensis were evaluated.
View Article and Find Full Text PDFChem Biodivers
September 2025
School of Pharmaceutical Science, Yunnan Key Laboratory of Pharmacology for Natural Products/College of Modern Biomedical Industry, NHC Key Laboratory of Drug Addiction Medicine, Kunming Medical University, Kunming, P. R. China.
20(R)-ginsenoside Rg3 can reduce the effects of oxidative stress and cell death in cerebral ischemia‒reperfusion injury (CIRI). Neuroinflammation is crucial post-CIRI, but how 20(R)-Rg3 affects ischemia‒reperfusion-induced neuroinflammation is unclear. To study 20(R)-Rg3's effects on neuroinflammation and neuronal preservation in stroke models and explore toll-like receptor 4/myeloid differentiation factor-88/nuclear factor kappa B (TLR4/MyD88/NF-κB) pathway mechanisms.
View Article and Find Full Text PDFJ Agric Food Chem
September 2025
Department of Food Science and Engineering, Ningbo University, Ningbo 315211, P.R. China.
Sleep deprivation (SD) is a major contributor to cognitive impairment, often accompanied by central neuroinflammation and gut microbiota dysbiosis. The tryptophan (TRP) pathway, activated via indoleamine 2,3-dioxygenase (IDO), serves as a critical link between immune activation and neuronal damage. Umbelliferone (UMB), a naturally occurring coumarin compound, possesses anti-inflammatory, antioxidant, and microbiota-modulating properties.
View Article and Find Full Text PDFElife
September 2025
Department of Biology, University of Copenhagen, Copenhagen, Denmark.
Sickness-induced sleep is a behavior conserved across species that promotes recovery from illness, yet the underlying mechanisms are poorly understood. Here, we show that interleukin-6-like cytokine signaling from the gut to brain glial cells regulates sleep. Under healthy conditions, this pathway promotes wakefulness.
View Article and Find Full Text PDFPLoS One
September 2025
Department of Emergency, The People's Hospital of Guangxi Zhuang Autonomous Region and Research Center of Medical Sciences, Guangxi Academy of Medical Sciences, Nanning, Guangxi, China.
Radiotherapy, a prevalent and effective treatment for various malignancies, often causes collateral damage to normal skin and soft tissues in the irradiated area. To address this, we developed a novel approach combining SVFG-modified adipose-derived high-activity matrix cell clusters (HAMCC) with concentrated growth factors (CGF) to enhance regeneration and repair of radiation-induced skin and soft tissue injuries. Our study included cellular assays, wound healing evaluations, and histological analyses.
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