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Search Results (4)

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Keywords = 2,3,7,8-tetrachlorodibenzodioxin

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16 pages, 2846 KiB  
Article
Dioxin-Induced PAI-1 Expression: A Novel Pathway to Pancreatic β-Cell Failure in Type 2 Diabetes
by Suyeol Im, Sora Kang, Woo Jung Son, Minuk Son, Seung Jun Oh, Hye Ji Yoon and Youngmi Kim Pak
Int. J. Mol. Sci. 2024, 25(22), 11974; https://doi.org/10.3390/ijms252211974 - 7 Nov 2024
Viewed by 1542
Abstract
Exposure to environment-polluting chemicals (EPCs), which are ligands of the aryl hydrocarbon receptor (AhR), is associated with the development of type 2 diabetes (T2D). This study explores the mechanisms by which AhR ligands contribute to β-cell failure in T2D. Incubation of RINm5F rat [...] Read more.
Exposure to environment-polluting chemicals (EPCs), which are ligands of the aryl hydrocarbon receptor (AhR), is associated with the development of type 2 diabetes (T2D). This study explores the mechanisms by which AhR ligands contribute to β-cell failure in T2D. Incubation of RINm5F rat pancreatic β-cells with low-dose 2,3,7,8-tetrachlorodibenzodioxin (TCDD), the most potent AhR ligand, inhibited glucose-stimulated insulin secretion (GSIS). A single injection of TCDD in wild type mice reduced the size of Langerhans islets, but not in AhR liver knock-out mice (AhR-LKO). RNA-seq database analysis identified Serpine1, encoding for plasminogen activator inhibitor type-1 (PAI-1) as a TCDD-mediated secretory protein that is synthesized in an AhR-dependent manner in the liver. Elevated PAI-1 levels were shown to induce Caspase-3/7-dependent apoptosis in RINm5F cells, suggesting a novel pathway through which EPCs exacerbate T2D. These findings support the hypothesis that chronic exposure to AhR ligands may directly inhibit GSIS in pancreatic β-cells and indirectly induce β-cell apoptosis through increased PAI-1. This study provides new insights into the EPC-PAI-1 axis as a missing link between pancreatic β-cell failure and the progression of T2D and offers a potential target for therapeutic intervention. Full article
(This article belongs to the Special Issue New Advances in Type 2 Diabetes and Its Complications)
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22 pages, 4070 KiB  
Article
Low-Dose Dioxin Reduced Glucose Uptake in C2C12 Myocytes: The Role of Mitochondrial Oxidative Stress and Insulin-Dependent Calcium Mobilization
by Suyeol Im, Sora Kang, Ji Hwan Kim, Seung Jun Oh and Youngmi Kim Pak
Antioxidants 2022, 11(11), 2109; https://doi.org/10.3390/antiox11112109 - 26 Oct 2022
Cited by 7 | Viewed by 3487
Abstract
Chronic exposure to some environmental polluting chemicals (EPCs) is strongly associated with metabolic syndrome, and insulin resistance is a major biochemical abnormality in the skeletal muscle in patients with metabolic syndrome. However, the causal relationship is inconsistent and little is known about how [...] Read more.
Chronic exposure to some environmental polluting chemicals (EPCs) is strongly associated with metabolic syndrome, and insulin resistance is a major biochemical abnormality in the skeletal muscle in patients with metabolic syndrome. However, the causal relationship is inconsistent and little is known about how EPCs affect the insulin signaling cascade in skeletal muscle. Here, we investigated whether exposure to 100 pM of 2,3,7,8-tetrachlorodibenzodioxin (TCDD) as a low dose of dioxin induces insulin resistance in C2C12 myocytes. The treatment with TCDD inhibited the insulin-stimulated glucose uptake and translocation of glucose transporter 4 (GLUT4). The low-dose TCDD reduced the expression of insulin receptor β (IRβ) and insulin receptor substrate (IRS)-1 without affecting the phosphorylation of Akt. The TCDD impaired mitochondrial activities, leading to reactive oxygen species (ROS) production and the blockage of insulin-induced Ca2+ release. All TCDD-mediated effects related to insulin resistance were still observed in aryl hydrocarbon receptor (AhR)-deficient myocytes and prevented by MitoTEMPO, a mitochondria-targeting ROS scavenger. These results suggest that low-dose TCDD stress may induce muscle insulin resistance AhR-independently and that mitochondrial oxidative stress is a novel therapeutic target for dioxin-induced insulin resistance. Full article
(This article belongs to the Special Issue Oxidative Stress in Diabetes and Complications)
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12 pages, 1271 KiB  
Communication
Studies towards the Synthesis of Novel 3-Aminopropoxy-Substituted Dioxins Suitable for the Development of Aptamers for Photonic Biosensor Applications
by Stefania Kalantzi, Sofia Leonardi, Eleanna Vachlioti, Eleni G. Kaliatsi, Κοnstantina Papachristopoulou, Constantinos Stathopoulos, Nikolaos Vainos and Dionissios Papaioannou
Materials 2021, 14(16), 4727; https://doi.org/10.3390/ma14164727 - 21 Aug 2021
Viewed by 2599
Abstract
Hydroxy-substituted tetrachlorodibenzo[b,e][1,4]dioxin and tetrachlorodibenzo[b,d]furans have been synthesized using 3,4-dichloroanisole, 2,3,6-trichlorophenol and 4,5-dichlorocatechol as starting materials and electrophilic and/or nucleophilic aromatic substitution reactions for the assembly of the dibenzo[b,e][1,4]dioxin and dibenzo[b,d]furan systems. The thus-obtained phenolic compounds [...] Read more.
Hydroxy-substituted tetrachlorodibenzo[b,e][1,4]dioxin and tetrachlorodibenzo[b,d]furans have been synthesized using 3,4-dichloroanisole, 2,3,6-trichlorophenol and 4,5-dichlorocatechol as starting materials and electrophilic and/or nucleophilic aromatic substitution reactions for the assembly of the dibenzo[b,e][1,4]dioxin and dibenzo[b,d]furan systems. The thus-obtained phenolic compounds were then alkylated with N-1-(4,4-dimethyl-2,6-dioxocyclohexylidene)ethyl (Dde)-protected 3-bromopropan-1-amine to give the corresponding N-Dde protected 3-aminopropoxy-substituted tetrachlorodibenzo[b,e][1,4]dioxin and tetrachlorodibenzo[b,d]furans, respectively. Hydrazinolysis-mediated Dde removal from the former compound provided the corresponding amino-substituted dioxin, which was coupled to carboxy-substituted magnetic beads affording magnetic beads coated by the amino-substituted dioxin. The latter is an attractive intermediate for the development of selective single-standard DNA (ssDNA) aptamers, which constitute molecular recognition elements in photonic biosensors with potential application to the monitoring of the dangerous environmental pollutants, dioxins having serious implications in human health. Full article
(This article belongs to the Special Issue Materials Light Life)
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10 pages, 226 KiB  
Article
Synthesis of a Molecularly Imprinted Polymer for Dioxin
by Cosimino Malitesta, Rosaria Anna Picca, Giuseppe Ciccarella, Vito Sgobba and Magda Brattoli
Sensors 2006, 6(8), 915-924; https://doi.org/10.3390/s6080915 - 24 Aug 2006
Cited by 8 | Viewed by 12076
Abstract
A molecularly imprinted polymer for recognising selectively 2,3,7,8-tetrachlorodibenzodioxin (TCDD) was made by a new non-covalent method employing a“dummy” template. The proposed way represents a simplification of a synthetic schemeproposed by Lübke et al.[1] for covalent imprinting. Comparison of extraction yields of thenovel polymer, [...] Read more.
A molecularly imprinted polymer for recognising selectively 2,3,7,8-tetrachlorodibenzodioxin (TCDD) was made by a new non-covalent method employing a“dummy” template. The proposed way represents a simplification of a synthetic schemeproposed by Lübke et al.[1] for covalent imprinting. Comparison of extraction yields of thenovel polymer, a non imprinted polymer and an imprinting polymer, prepared by theoriginal procedure demonstrates the binding capacity of the proposed polymer, which is inprinciple applicable to solid phase extraction (SPE) of dioxin. Full article
(This article belongs to the Special Issue Supramolecular Sensors)
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