Archives of Biochemistry and Biophysics, Journal Year: 2023, Volume and Issue: 738, P. 109558 - 109558
Published: March 5, 2023
Language: Английский
Archives of Biochemistry and Biophysics, Journal Year: 2023, Volume and Issue: 738, P. 109558 - 109558
Published: March 5, 2023
Language: Английский
Redox Biology, Journal Year: 2022, Volume and Issue: 59, P. 102569 - 102569
Published: Dec. 5, 2022
The metabolic associated fatty liver disease (MAFLD) is a public health challenge, leading to global increase in chronic disease. respiratory exposure of silica nanoparticles (SiNPs) has revealed induce hepatotoxicity. However, its role the pathogenesis and progression MAFLD was severely under-studied. In this context, hepatic impacts SiNPs were investigated vivo vitro through using ApoE-/- mice free acid (FFA)-treated L02 hepatocytes. Histopathological examinations biochemical analysis showed via intratracheal instillation aggravated steatosis, lipid vacuolation, inflammatory infiltration even collagen deposition mice, companied with increased ALT, AST LDH levels. enhanced synthesis inhibited β-oxidation efflux may account for TC/TG by SiNPs. Consistently, induced elevated TC FFA-treated cells. Further, activation oxidative stress detected vitro, as evidenced ROS accumulation, MDA, declined GSH/GSSG down-regulated Nrf2 signaling. Endoplasmic reticulum (ER) also triggered response SiNPs-induced reflecting remarkable ER expansion BIP expression. More importantly, an UPLC-MS-based metabolomics that disturbed profile prominently on amino acids metabolisms. particular, identified differential metabolites strongly correlated ensuing accumulation injuries, contributing diseases. Taken together, our study promoted steatosis damage, resulting aggravation progression. metabolisms-mediated key contributor phenomenon from perspective.
Language: Английский
Citations
79Redox Biology, Journal Year: 2023, Volume and Issue: 63, P. 102739 - 102739
Published: May 10, 2023
Silver nanoparticles (AgNPs) have widely used in industrial and medical applications for their excellent antibacterial activities. AgNPs can penetrate into the brain cause neuronal death, but limited evidence focused on toxic effects mechanic study hippocampal neuron. This aimed to investigate molecular mechanisms of mitochondrial damage apoptosis mouse HT22 cells further explore role reactive oxygen species (ROS) GTPase dynamin-related protein 1 (Drp1) AgNPs-induced neurotoxicity. Our results showed that acute exposure at low doses (2-8 μg/mL) increased ROS generation, decreased membrane potential (MMP) ATP synthesis cells. In addition, promoted fragmentation mitochondria-dependent via excessive fission/fusion by 8 μg/mL treatment 24 h. The mechanism was involved expression Drp1, fission (Fis1), mitofusin 1/2 (Mfn1/2) inhibited optic atrophy (OPA1), mainly mediated phosphorylation Drp1 Ser616. impairment due particle-specific effect rather than silver ions release. Furthermore Drp1-mediated contributed induced AgNPs, all aforementioned changes were significantly rescued N-acetyl-l-cysteine (NAC) Mdivi-1 except OPA1 expression. Hence, our provide a novel neurotoxic neurotoxicity revealed activation ROS-Drp1-mitochondrial axis. These findings deepen current evidences neurotoxicological evaluation aid guiding proper different areas, especially biomedical use.
Language: Английский
Citations
53Journal of Hazardous Materials, Journal Year: 2020, Volume and Issue: 406, P. 124626 - 124626
Published: Nov. 24, 2020
Language: Английский
Citations
75Chemosphere, Journal Year: 2021, Volume and Issue: 275, P. 129969 - 129969
Published: Feb. 16, 2021
Language: Английский
Citations
71Journal of Nanobiotechnology, Journal Year: 2022, Volume and Issue: 20(1)
Published: March 19, 2022
Abstract Copper oxide nanoparticles (CuONPs) are widely used metal NPs owing to their excellent physical–chemical properties. Circulation translocation of CuONPs after inhalation leads vascular endothelial injury. Mitochondria, an important regulatory hub for maintaining cell functions, signaling organelles in responses NPs-induced However, how mitochondrial dynamics (fission and fusion) mitophagy (an autophagy process degrade damaged mitochondria) elaborately orchestrated maintain homeostasis CuONPs-induced injury is still unclear. In this study, we demonstrated that exposure disturbed through oxidative stress-dependent manner cells, as evidenced by the increase fission accumulation fragmented mitochondria. Inhibition with Mdivi-1 aggravated mtROS production death. Furthermore, found led activation PINK1-mediated mitophagy, pharmacological inhibition wortmannin, chloroquine or genetical siRNA-mediated knockdown PINK1 profoundly repressed suggesting protective role toxicity. Intriguingly, identified TAX1BP1 was primary receptor link ubiquitinated mitochondria autophagosomes, since elevated production, decreased clearance cells More importantly, verified urolithin A, a activator, promoted removal induced both vitro vivo. Overall, our findings indicated modulating may be therapeutic strategy pathological caused exposure. Graphical
Language: Английский
Citations
44Journal of Hazardous Materials, Journal Year: 2022, Volume and Issue: 434, P. 128820 - 128820
Published: April 1, 2022
Language: Английский
Citations
39Biotechnology Advances, Journal Year: 2023, Volume and Issue: 69, P. 108277 - 108277
Published: Nov. 3, 2023
Language: Английский
Citations
23Journal of Environmental Sciences, Journal Year: 2024, Volume and Issue: 151, P. 200 - 210
Published: March 19, 2024
Language: Английский
Citations
12World Journal of Hepatology, Journal Year: 2024, Volume and Issue: 16(4), P. 566 - 600
Published: April 24, 2024
The unique physicochemical properties inherent to nanoscale materials have unveiled numerous potential applications, spanning beyond the pharmaceutical and medical sectors into various consumer industries like food cosmetics. Consequently, humans encounter nanomaterials through diverse exposure routes, giving rise health considerations. Noteworthy among these are silica specific metallic nanoparticles, extensively utilized in products, which garnered substantial attention due their propensity accumulate induce adverse effects liver. This review paper aims provide an exhaustive examination of molecular mechanisms underpinning nanomaterial-induced hepatotoxicity, drawing insights from both vitro vivo studies. Primarily, most frequently observed manifestations toxicity following cells or animal models involve initiation oxidative stress inflammation. Additionally, we delve existing employed for evaluating hepatotoxic nanomaterials, emphasizing persistent endeavors advance bolster reliability nanotoxicology research.
Language: Английский
Citations
11Environmental Science Nano, Journal Year: 2021, Volume and Issue: 8(5), P. 1177 - 1195
Published: Jan. 1, 2021
The toxicity and ecotoxicity effects, handling disposal of synthetic amorphous silica nanoparticles aerogels are reviewed discussed.
Language: Английский
Citations
38