Excess molybdenum (Mo) and cadmium (Cd) are harmful to animals, but neurotoxicity caused by Mo and Cd co-exposure in ducks is yet unknown. To assess joint impacts of Mo and Cd on autophagy via calcium homeostasis and unfolded protein response (UPR) in duck brain, 40 healthy 7-day-old ducks (Anas platyrhyncha) were assigned to 4 groups at random and fed diets supplemented with different doses of Mo or/and Cd for 16 weeks, respectively. Brain tissues were excised for experiment. Results exhibited that Mo or/and Cd disturbed calcium homeostasis by decreased ATPase activities and increased calcium (Ca) content, and upregulated calcium homeostasis-related factors Ca/CAM-dependent kinase IIɑ (CaMKIIɑ), calcineurin (CaN), inositol-1,4,5-trisphosphate receptor (IPR), and calreticulin (CRT) expression levels. Meanwhile, the upregulation of UPR-related factor expression levels indicated that Mo or/and Cd activated UPR. Moreover, Mo or/and Cd triggered autophagy through promoting the number of autophagosomes and LC3II immunofluorescence intensity and altering autophagy key factor expression levels. Correlation analysis showed that there were obvious connections among Ca homeostasis, endoplasmic reticulum (ER) stress, and autophagy induced by Mo or/and Cd. Thence, it can be speculated that autophagy initiated by Mo or/and Cd may be associated with interfering Ca homeostasis and triggering UPR.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s11356-022-18738-6 | DOI Listing |
Cell Mol Life Sci
January 2025
Univ. Lille, CNRS, UMR 8576 - UGSF - Unité de Glycobiologie Structurale Et Fonctionnelle, 59000, Lille, France.
Glycans are known to be fundamental for many cellular and physiological functions. Congenital disorders of glycosylation (CDG) currently encompassing over 160 subtypes, are characterized by glycan synthesis and/or processing defects. Despite the increasing number of CDG patients, therapeutic options remain very limited as our knowledge on glycan synthesis is fragmented.
View Article and Find Full Text PDFAdv Med Sci
January 2025
Department of Histology and Embryology, Faculty of Medicine, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, Toruń, Poland; Faculty of Medicine, Collegium Medicum, Mazovian Academy in Płock, Płock, Poland.
Purpose: Proper functioning of the endothelial barrier is crucial for cardiovascular system homeostasis. Oxidative stress can lead to endothelial dysfunction (ED), damaging lipids, proteins, and DNA. Reactive oxygen species also increase cytoplasmic Ca levels, activating transient receptor potential melastatin 2 (TRPM2), a membrane non-selective calcium channel.
View Article and Find Full Text PDFBull Exp Biol Med
January 2025
School of Basic Medicine, Gannan Medical University, Ganzhou, China.
Extracellular Ca is the first ligand that has been confirmed to function by activating the calcium-sensing receptor (CaSR), a member of G-protein coupled receptors. CaSR controls not only calcium homeostasis, but also plays a pivotal role in many cellular processes such as cell proliferation and apoptosis; moreover, it is implicated in the development of cardiovascular diseases. TGF-β/Smads signaling pathway is a classical pathway of renal fibrosis.
View Article and Find Full Text PDFFront Immunol
January 2025
Center for Translational Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Acute pancreatitis (AP) is an inflammatory disease of the pancreas and a complex process involving multiple factors, with mitochondrial damage playing a crucial role. Mitochondrial dysfunction is now considered a key driver in the development of AP. This dysfunction often presents as increased oxidative stress, altered membrane potential and permeability, and mitochondrial DNA damage and mutations.
View Article and Find Full Text PDFCurr Atheroscler Rep
January 2025
Department of Internal Medicine I, University Hospital Aachen, Pauwelsstraße, 30 52074, Aachen, Germany.
Purpose Of Review: This review explores the relationship between lipid-lowering therapies, particularly statins, and the risk of new-onset diabetes (NOD). It examines the underlying mechanisms and evaluates whether other lipid-lowering agents present similar risks.
Recent Findings: Recent meta-analyses further underscore a dose-dependent increase in NOD risk with statin therapy, particularly with high-intensity statins.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!