Metal pollutants are a global health risk due to their ability to contribute to a variety of diseases. Aluminum (Al), a ubiquitous environmental contaminant is implicated in anemia, osteomalacia, hepatic disorder, and neurological disorder. In this review, we outline how this intracellular generator of reactive oxygen species (ROS) triggers a metabolic shift towards lipogenesis in astrocytes and hepatocytes. This Al-evoked phenomenon is coupled to diminished mitochondrial activity, anerobiosis, and the channeling of α-ketoacids towards anti-oxidant defense. The resulting metabolic reconfiguration leads to fat accumulation and a reduction in ATP synthesis, characteristics that are common to numerous medical disorders. Hence, the ability of Al toxicity to create an oxidative environment promotes dysfunctional metabolic processes in astrocytes and hepatocytes. These molecular events triggered by Al-induced ROS production are the potential mediators of brain and liver disorders.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s10565-013-9239-0 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
All Blood Brain Barrier Cell Types Demonstrate Capability to Influence Differential Tenofovir and Emtricitabine Metabolism and Transport in the Brain.
ACS Pharmacol Transl Sci
November 2024
Department of Pharmacology and Chemical Biology, Emory University School of Medicine, Atlanta, Georgia 30322, United States.
The blood brain barrier (BBB) represents a significant obstacle in brain drug penetration that challenges efforts in the treatment of neurological disorders. Therapeutically targeting the brain requires interactions with each BBB cell type, including endothelial cells, pericytes, and astrocytes. Yet, the relative contribution of these BBB cell types to the mechanisms that facilitate brain drug disposition is not well characterized.
View Article and Find Full Text PDFMANF serves as a novel hepatocyte factor to promote liver regeneration after 2/3 partial hepatectomy via doubly targeting Wnt/β-catenin signaling.
Cell Death Dis
September 2024
School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China.
Liver regeneration is an intricate pathophysiological process that has been a subject of great interest to the scientific community for many years. The capacity of liver regeneration is very critical for patients with liver diseases. Therefore, exploring the mechanisms of liver regeneration and finding good ways to improve it are very meaningful.
View Article and Find Full Text PDFDrug Metabolism and Transport Capacity of Endothelial Cells, Pericytes, and Astrocytes: Implications for CNS Drug Disposition.
bioRxiv
August 2024
Department of Pharmacology and Chemical Biology, Emory University School of Medicine, Atlanta, GA, USA.
Therapeutically targeting the brain requires interactions with endothelial cells, pericytes, and astrocytes at the blood brain barrier (BBB). We evaluated regional and cell-type specific drug metabolism and transport mechanisms using rhesus macaques and treatment of primary human cells. Here, we report heterogenous distribution of representative drugs, tenofovir (TFV), emtricitabine (FTC), and their active metabolites, which cerebrospinal fluid measures could not reflect.
View Article and Find Full Text PDFExpression of SDF-1/CXCR4 and related inflammatory factors in sodium fluoride-treated hepatocytes.
PLoS One
June 2024
Department of Endemic Disease Prevention and Control, Qinghai Institute for Endemic Disease Prevention and Control, Xi'ning, China.
Article Synopsis
- The impact of excess fluoride on liver health remains unclear, but studies suggest it can cause inflammation and damage to the hepatic system.
- This study explores the SDF-1/CXCR4 signaling pathway's role in this process by conducting in vitro experiments on human liver cells (LX-2) exposed to sodium fluoride.
- Results indicated that higher levels of SDF-1/CXCR4 and inflammatory factors such as NF-κB, IL-6, TNF-α, and IL-1β were significantly expressed in the fluoride-treated group, indicating that fluoride may activate inflammatory responses through this signaling pathway.
Insights into the roles of Apolipoprotein E in adipocyte biology and obesity.
Int J Obes (Lond)
September 2024
Department of Biochemical Science and Technology, National Taiwan University, Taipei, Taiwan.
Apolipoprotein E (APOE) is a multifunctional protein expressed by various cell types, including hepatocytes, adipocytes, immune cells of the myeloid lineage, vascular smooth muscle cells, astrocytes, etc. Initially, APOE was discovered as an arginine-rich peptide within very-low-density lipoprotein, but it was subsequently found in triglyceride-rich lipoproteins in humans and other animals, where its presence facilitates the clearance of these lipoproteins from circulation. Recent epidemiolocal studies and experimental research in mice suggest a link between ApoE and obesity.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!