Sialic acid binding lectin (SBL) isolated from Rana catesbeiana oocytes is a multifunctional protein which has lectin activity, ribonuclease activity and antitumor activity. However, the mechanism of antitumor effects of SBL is unclear to date and the validity for human leukemia cells has not been fully studied. We report here that SBL shows cytotoxicity for some human leukemia cell lines including multidrug-resistant (MDR) cells. The precise mechanisms of SBL-induced apoptotic signals were analyzed by combinational usage of specific caspase inhibitors and the mitochondrial membrane depolarization detector JC-1. It was demonstrated that SBL causes mitochondrial perturbation and the apoptotic signal is amplified by caspases and cell death is executed in a caspase-dependent manner. The efficacy of this combinational usage was shown for the first time, to distinguish the apoptotic pathway in detail. SBL selectively kills tumor cells, is able to exhibit cytotoxicity regardless of P-glycoprotein expression and has potential as an alternative to conventional DNA-damaging anticancer drugs.
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http://dx.doi.org/10.3892/ijo.2013.2092 | DOI Listing |
Physiol Res
December 2024
Institute of Physiology, Biomedical Centre, Charles University, Faculty of Medicine in Plzen, Plzen, Czech Republic.
Mitochondria represent pivotal cellular organelles endowed with multifaceted functionalities encompassing cellular respiration, metabolic processes, calcium turnover, and the regulation of apoptosis, primarily through the generation of reactive oxygen species (ROS). Perturbations in mitochondrial dynamics have been intricately linked to the etiology of numerous cardiovascular pathologies, such as heart failure, ischemic heart disease, and various cardiomyopathies. Notably, recent attention has been directed towards the detrimental impact of micro- and nanoplastic pollution on mitochondrial integrity, an area underscored by a paucity of comprehensive investigations.
View Article and Find Full Text PDFNeurobiol Dis
January 2025
Center for Translational Research in Neurodegenerative Disease, College of Medicine, University of Florida, Gainesville, FL, USA; Department of Neuroscience, College of Medicine, University of Florida, Gainesville, FL, USA; McKnight Brain Institute, University of Florida, Gainesville, FL, USA; Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD, USA; Norman Fixel Institute for Neurological Diseases, University of Florida, Gainesville, FL, USA. Electronic address:
Parkinson's Disease (PD) is a multisystem disorder in which dysregulated neuroimmune crosstalk and inflammatory relay via the gut-blood-brain axis have been implicated in PD pathogenesis. Although alterations in circulating inflammatory cytokines and reactive oxygen species (ROS) have been associated with PD, no biomarkers have been identified that predict clinical progression or disease outcome. Gastrointestinal (GI) dysfunction, which involves perturbation of the underlying immune system, is an early and often-overlooked symptom that affects up to 80 % of individuals living with PD.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, BC V6T 1Z3, Canada.
An impact of legalization and decriminalization of marijuana is the gradual increase in the use of cannabis for recreational purposes, which poses a potential threat to society and healthcare systems worldwide. However, the discovery of receptor subtypes, endogenous endocannabinoids, and enzymes involved in synthesis and degradation, as well as pharmacological characterization of receptors, has led to exploration of the use of cannabis in multiple peripheral and central pathological conditions. The role of cannabis in the modulation of crucial events involving perturbed physiological functions and disease progression, including apoptosis, inflammation, oxidative stress, perturbed mitochondrial function, and the impaired immune system, indicates medicinal values.
View Article and Find Full Text PDFAm J Physiol Endocrinol Metab
January 2025
Knight Cardiovascular Institute, Oregon Health & Science University, Portland, OR, 97239.
Maternal obesity puts the offspring at high risk of developing obesity and cardio-metabolic diseases in adulthood. Here, we utilized a mouse model of maternal high-fat diet (HFD)-induced obesity that recapitulates metabolic perturbations seen in humans. We show increased adiposity in the offspring of HFD-fed mothers (Off-HFD) when compared to the offspring regular diet-fed mothers (Off-RD).
View Article and Find Full Text PDFCells
January 2025
Groupe de Recherche en Signalisation Cellulaire (GRSC), Département de Biologie Médicale, Université du Québec à Trois-Rivières, 3351 Boulevard des Forges, Trois-Rivières, QC G8Z 4M3, Canada.
Elevated glucose levels at the fetal-maternal interface are associated with placental trophoblast dysfunction and increased incidence of pregnancy complications. Trophoblast cells predominantly utilize glucose as an energy source, metabolizing it through glycolysis in the cytoplasm and oxidative respiration in the mitochondria to produce ATP. The TGFβ1/SMAD2 signaling pathway and the transcription factors PPARγ, HIF1α, and AMPK are key regulators of cell metabolism and are known to play critical roles in extravillous trophoblast cell differentiation and function.
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