Category: 2044-85-1

Zhao, Tingyi published the artcileDeficiency of Grx1 leads to high sensitivity of HeLaS3 cells to oxidative stress via excessive accumulation of intracellular oxidants including ROS, COA of Formula: C24H14Cl2O7, the main research area is Grx gene deficiency oxidative stress cells intracellular oxidant ROS; Glutaredoxin 1; oxidative stress; reactive oxygen species; redox homeostasis; γ-ray irradiation.

Oxidative stress is often initiated by excess reactive oxygen species (ROS) production, resulting in macromol. damage, which is implicated in many disease states. Glutaredoxin 1 (Grx1) is an antioxidant enzyme that plays an important role in redox signaling and redox homeostasis. In the present study, we generated HeLaS3 cell lines deficient in Grx1 by the CRISPR/CAS9 system to clarify how Grx1 affects the physiol. activities of HeLaS3 cells to respond to oxidative stress. First, the survival assay revealed that Grx1-deficient HeLaS3 cells were more sensitive to γ-ray irradiation, heat shock and H2O2 exposure than HeLaS3 wild-type cells. Next, the intracellular redox state was investigated using a fluorescent probe (2′-7’dichlorofluorescin diacetate), and the oxidized state of total proteins and a peroxidase Prx2 were measured by Western blot anal. Exposure to γ-ray irradiation, heat shock and H2O2 significantly induced more accumulation of intracellular oxidants including ROS and higher levels of oxidized proteins in Grx1-deficient HeLaS3 cells. Furthermore, MitoSox Red staining demonstrated that Grx1 deficiency causes a higher level of oxidants production in mitochondria. Moreover, Grx1-deficient HeLaS3 cells had a higher cytochrome c level and higher apoptosis rate (Annexin-V/FITC and EthD-III staining assay) upon oxidative stress. These results suggested that Grx1 deficiency lead to mitochondrial redox homeostasis disruption and apoptotic cell death upon oxidative stress. In addition, the results of proliferation assay and MitoTracker staining assay (multinuclear cell formation rate) suggested that oxidative stress exposure inhibits cell proliferation maybe by affecting cytoplasmic division in Grx1-deficient HeLaS3 cells.

Free Radical Research published new progress about Apoptosis. 2044-85-1 belongs to class esters-buliding-blocks, name is 2′,7′-Dichloro-3-oxo-3H-spiro[isobenzofuran-1,9′-xanthene]-3′,6′-diyl diacetate, and the molecular formula is C24H14Cl2O7, COA of Formula: C24H14Cl2O7.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Ahmmed, Bulbul published the artcileRg3 inhibits gemcitabine-induced lung cancer cell invasiveness through ROS-dependent, NF-κB- and HIF-1α-mediated downregulation of PTX3, Computed Properties of 2044-85-1, the main research area is Rg gemcitabine lung cancer cell ROS PTX HIF; gemcitabine; ginsenosides; hypoxia-inducible factor-1α (HIF-1α); nuclear factor kappa B (NF-κB); pentraxin-3; reactive oxygen species (ROS).

PTX3, a member of the long pentraxin subfamily, associated with innate immunity is indispensable for resistance to some cancer. Gemcitabine, an analog of cytosine arabinoside, has shown restrained benefits because of profound chemoresistance. The PTX3 expression on GEM in human lung cancer cells have not yet been clarified; the present study aimed to show reactive oxygen species (ROS) mediatory PTX3 expression through distinct mechanisms. Whereas ginsenoside Rg3 is a herbal medicine with strong antitumor activity. Furthermore, we tested the hypothesis; Rg3 abrogates GEM-induced production of ROS-mediated activation of Akt and extracellular signal-regulated kinase (ERK) pathways and inhibits nuclear piling-up of nuclear factor kappa B (NF-κB) and HIF-1α. On the basis of time and dose-dependent manner, our data demonstrated that GEM-induced PTX3 expression was dependent on ROS generation as it was abrogated by pretreatment of lung cancer cells with the free radical scavenger N-acetyl-L-cysteine. Increase in ROS expression in lung cancer cells on GEM treatment preceded the nuclear accumulation of NF-κB and HIF-1α and suppression of ROS diminished these effects. Our study findings reinforced the role regarding PTX3 signaling in GEM-induced resistance and pointed toward an unintended and undesired effect of chemotherapy and to get an active regimen; the synergy was associated with NF-κB downregulation in lung cancer.

Journal of Cellular Physiology published new progress about cDNA Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 2044-85-1 belongs to class esters-buliding-blocks, name is 2′,7′-Dichloro-3-oxo-3H-spiro[isobenzofuran-1,9′-xanthene]-3′,6′-diyl diacetate, and the molecular formula is C24H14Cl2O7, Computed Properties of 2044-85-1.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Haval, Gauri A. published the artcileExcess hydrogen peroxide inhibits head and foot regeneration in hydra by affecting DNA repair and expression of essential genes, Safety of 2′,7′-Dichloro-3-oxo-3H-spiro[isobenzofuran-1,9′-xanthene]-3′,6′-diyl diacetate, the main research area is foot hydrogen peroxide DNA repair; hydra; reactive oxygen species; regeneration.

ROS are necessary for various cellular processes. However, excess ROS cause damage to many biol. mols. and therefore must be tightly regulated in time and space. H2O2 is the most commonly used ROS as second messenger in the cell. It is a relatively long-lived freely diffusible signaling mol. during early events of injury. In the Cnidarian hydra, injury-induced ROS production is essential for regeneration to proceed. In the present study, we have examined influence of varying exposure to H2O2 on head and foot regeneration in the middlepieces of trisected hydra. We find that longer (4 h) exposure to 1 mM H2O2 inhibits both head and foot regeneration while shorter exposure (2 h) does not. Longer exposure to H2O2 resulted in extensive damage to DNA that could not be repaired, probably due to suboptimal induction of APE1, an enzyme necessary for base excision repair (BER). Concomitantly, genes involved in activation of Wnt pathway, necessary for head regeneration, were significantly downregulated. This appeared to be due to failure of both stabilization and transient nuclear localization of β-catenin. Similarly, genes involved in foot regeneration were also downregulated on longer exposure to H2O2. Thus, exposure to excess ROS inhibits regenerative processes in hydra through reduced expression of genes involved in regeneration and diminished DNA repair.

Journal of Biochemical and Molecular Toxicology published new progress about Animal gene Role: BSU (Biological Study, Unclassified), BIOL (Biological Study) (APE1). 2044-85-1 belongs to class esters-buliding-blocks, name is 2′,7′-Dichloro-3-oxo-3H-spiro[isobenzofuran-1,9′-xanthene]-3′,6′-diyl diacetate, and the molecular formula is C24H14Cl2O7, Safety of 2′,7′-Dichloro-3-oxo-3H-spiro[isobenzofuran-1,9′-xanthene]-3′,6′-diyl diacetate.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Hao, Jing published the artcileTea plant roots respond to aluminum-induced mineral nutrient imbalances by transcriptional regulation of multiple cation and anion transporters, SDS of cas: 2044-85-1, the main research area is aluminum mineral nutrient cation anion transporter tea plant root; Aluminum tolerance; Ion imbalance; Ionome; Metal transporter; Transcriptome.

Tea is one of the most popular non-alc. beverages in the world for its flavors and numerous health benefits. The tea tree (Camellia sinensis L.) is a well-known aluminum (Al) hyperaccumulator. However, it is not fully understood how tea plants have adapted to tolerate high concentrations of Al, which causes an imbalance of mineral nutrition in the roots. Here, we combined ionomic and transcriptomic profiling alongside biochem. characterization, to probe the changes of metal nutrients and Al responsive genes in tea roots grown under increasing concentrations of Al. It was found that a low level of Al (~0.4 mM) maintains proper nutrient balance, whereas a higher Al concentration (2.5 mM) compromised tea plants by altering micro- and macro-nutrient accumulation into roots, including a decrease in calcium (Ca), manganese (Mn), and magnesium (Mg) and an increase in iron (Fe), which corresponded with oxidative stress, cellular damage, and retarded root growth. Transcriptome anal. revealed more than 1000 transporter genes that were significantly changed in expression upon Al exposure compared to control (no Al) treatments. These included transporters related to Ca and Fe uptake and translocation, while genes required for N, P, and S nutrition in roots did not significantly alter. Transporters related to organic acid secretion, together with other putative Al-tolerance genes also significantly changed in response to Al. Two of these transporters, CsALMT1 and CsALS8, were functionally tested by yeast heterologous expression and confirmed to provide Al tolerance. This study shows that tea plant roots respond to high Al-induced mineral nutrient imbalances by transcriptional regulation of both cation and anion transporters, and therefore provides new insights into Al tolerance mechanism of tea plants. The altered transporter gene expression profiles partly explain the imbalanced metal ion accumulation that occurred in the Al-stressed roots, while increases to organic acid and Al tolerance gene expression partly explains the ability of tea plants to be able to grow in high Al containing soils. The improved transcriptomic understanding of Al exposure gained here has highlighted potential gene targets for breeding or genetic engineering approaches to develop safer tea products.

BMC Plant Biology published new progress about Anion transporters Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 2044-85-1 belongs to class esters-buliding-blocks, name is 2′,7′-Dichloro-3-oxo-3H-spiro[isobenzofuran-1,9′-xanthene]-3′,6′-diyl diacetate, and the molecular formula is C24H14Cl2O7, SDS of cas: 2044-85-1.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Gao, Libo published the artcileGeneral carbon dot-based platform for intracellular delivery of proteins, Application of 2′,7′-Dichloro-3-oxo-3H-spiro[isobenzofuran-1,9′-xanthene]-3′,6′-diyl diacetate, the main research area is carbon dot fluorescent protein intracellular delivery.

The shortcomings of proteins, such as poor stability in biol. environments, the impermeability of the membrane and the susceptibility to enzymolysis, restrict their potential applications. Therefore, constructing universal nanocarriers for intracellular delivery of a variety of proteins remains a great challenge. In this work, gallic acid (GA) and L-lysine were used as starting materials to synthesize carbon dots (CDs). The CDs were used as carriers to interact with bovine serum albumin (BSA), enhanced green fluorescent protein (EGFP) and glucose oxidase (GOx) via supramol. interaction to construct CDs-protein nanocomposites CDs-BSA, CDs-EGFP and CDs-GOx. Furthermore, CDs-EGFP and CDs-GOx can achieve intracellular protein delivery and maintain 89% of the biol. activity of GOx. In this work, the latency of CDs is projected as a universal platform for effective intracellular delivery of proteins.

Soft Matter published new progress about Carbon quantum dots. 2044-85-1 belongs to class esters-buliding-blocks, name is 2′,7′-Dichloro-3-oxo-3H-spiro[isobenzofuran-1,9′-xanthene]-3′,6′-diyl diacetate, and the molecular formula is C24H14Cl2O7, Application of 2′,7′-Dichloro-3-oxo-3H-spiro[isobenzofuran-1,9′-xanthene]-3′,6′-diyl diacetate.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Ham, Jiyeon published the artcileSilibinin-induced endoplasmic reticulum stress and mitochondrial dysfunction suppress growth of endometriotic lesions, Application In Synthesis of 2044-85-1, the main research area is silibinin endoplasmic reticulum stress mitochondrial dysfunction suppress growth; ROS; apoptosis; endometriosis; endoplasmic reticulum (ER) stress; silibinin.

Silibinin is a flavonolignan extracted from milk thistle, which has been used for treating liver disorders, various cancers, and gynecol. diseases. However, attempts for treating endometriosis with silibinin are lacking. In this study, we observed that silibinin exerts antiproliferative and apoptotic effects on human endometriotic cell lines VK2/E6E7 and End1/E6E7. We also identified that silibinin-induced oxidative stress and lipid peroxidation in human endometriotic cells. Moreover, we observed upregulation of calcium concentration in the cytosol and mitochondrial matrix, which resulted in mitochondrial dysfunction. Furthermore, induction of endoplasmic reticulum stress signals with rapid mitogen-activated protein kinase (MAPK) pathway signaling resulted in apoptosis of both cells. Using an animal model mimicking the retrograde menstruation hypothesis, we verified the effects of silibinin on reducing endometriotic lesions by inhibiting the expression of inflammatory cytokines in mice. Silibinin might be used as a novel therapeutic agent or supplement for inhibiting progression of endometriosis in vitro and in vivo.

Journal of Cellular Physiology published new progress about Cell culture. 2044-85-1 belongs to class esters-buliding-blocks, name is 2′,7′-Dichloro-3-oxo-3H-spiro[isobenzofuran-1,9′-xanthene]-3′,6′-diyl diacetate, and the molecular formula is C24H14Cl2O7, Application In Synthesis of 2044-85-1.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Wang, Yuting published the artcilePolybrominated diphenyl ethers quinone-induced intracellular protein oxidative damage triggers ubiquitin-proteasome and autophagy-lysosomal system activation in LO2 cells, SDS of cas: 2044-85-1, the main research area is polybrominated diphenyl ether quinone protein oxidative ubiquitin proteasome autophagy; Autophagy; Endoplasmic reticulum stress; PBDEQ; Protein oxidative damage; Ubiquitin-proteasome system.

Polybrominated di-Ph ethers (PBDEs), a kind of flame retardants, were widely used in the furniture, textile and electronics industries. Because of their lipophilic, persistent and bio-accumulative properties, PBDEs were listed on the Stockholm Convention as typical persistent organic pollutants (POPs). We have previously reported that a highly active, quinone-type metabolite of PBDEs (PBDEQ) causes DNA damage and subsequently triggers apoptosis. However, it is remaining unclear whether PBDEQ provokes protein damage and stimulates corresponding signaling cascade. Using human normal liver (LO2) cells as an in vitro model, we demonstrated that PBDEQ causes oxidative protein damage through excess reactive oxygen species (ROS). Consistently, we found PBDEQ exposure causes the depletion of protein thiol group, the appearance of carbonyl group and the accumulation of protein aggregates. Endoplasmic reticulum (ER) stress was involved in the repair of oxidized proteins. Under the scenario of severe damage, LO2 cells degrade oxidized proteins through ubiquitin-proteasome system (UPS) and autophagy. The blockage of these protein degradation pathways aggravates PBDEQ-induced cytotoxicity in LO2 cells, while antioxidant N-acetyl-cysteine (NAC) rescues PBDEQ-induced oxidative protein damage conversely. In summary, our current study first demonstrated PBDEQ-induced protein oxidative damage in LO2 cells, which offer a better understanding of the cytotoxicity of PBDEs and corresponding metabolites.

Chemosphere published new progress about Activating transcription factor 6α Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 2044-85-1 belongs to class esters-buliding-blocks, name is 2′,7′-Dichloro-3-oxo-3H-spiro[isobenzofuran-1,9′-xanthene]-3′,6′-diyl diacetate, and the molecular formula is C24H14Cl2O7, SDS of cas: 2044-85-1.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Zhang, Zhuhong published the artcileMechanistic study of silica nanoparticles on the size-dependent retinal toxicity in vitro and in vivo, Category: esters-buliding-blocks, the main research area is silica nanoparticles mechanistics retinal toxicity; Ganglion cell degeneration; Glial cell activation; Inflammation; ROS; Retinal toxicity; SiO2 NPs.

Silica nanoparticles (SiO2 NPs) are extensively applied in the biomedical field. The increasing medical application of SiO2 NPs has raised concerns about their safety. However, studies on SiO2 NP-induced retinal toxicity are lacking. We investigated the retinal toxicity of SiO2 NPs with different sizes (15 and 50 nm) in vitro and in vivo along with the underlying mechanisms. The cytotoxicity of SiO2 NPs with different sizes was assessed in R28 human retinal precursor cells by determining the ATP content and LDH release. The cell morphologies and nanoparticle distributions in the cells were analyzed by phase-contrast microscopy and transmission electron microscopy, resp. The mitochondrial membrane potential was examined by confocal laser scanning microscopy. The retinal toxicity induced by SiO2 NPs in vivo was examined by immunohistochem. anal. To further investigate the mechanism of retinal toxicity induced by SiO2 NPs, reactive oxygen species (ROS) generation, glial cell activation and inflammation were monitored. The 15-nm SiO2 NPs were found to have higher cytotoxicity than the larger NPs. Notably, the 15-nm SiO2 NPs induced retinal toxicity in vivo, as demonstrated by increased cell death in the retina, TUNEL-stained retinal cells, retinal ganglion cell degeneration, glial cell activation, and inflammation. In addition, The SiO2 NPs caused oxidative stress, as demonstrated by the increase in the ROS indicator H2DCF-DA. Furthermore, the pretreatment of R28 cells with N-acetylcysteine, an ROS scavenger, attenuated the ROS production and cytotoxicity induced by SiO2 NPs. These results provide evidence that SiO2 NPs induce size-dependent retinal toxicity and suggest that glial cell activation and ROS generation contribute to this toxicity.

Journal of Nanobiotechnology published new progress about Homo sapiens. 2044-85-1 belongs to class esters-buliding-blocks, name is 2′,7′-Dichloro-3-oxo-3H-spiro[isobenzofuran-1,9′-xanthene]-3′,6′-diyl diacetate, and the molecular formula is C24H14Cl2O7, Category: esters-buliding-blocks.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Yoon, Hyun Joong published the artcileNative low density lipoprotein increases the production of both nitric oxide and reactive oxygen species in the human umbilical vein endothelial cells, Formula: C24H14Cl2O7, the main research area is eNOS LDL ROS umbilical vein endothelial cell oxidative stress; Human umbilical vein endothelial cell; Inducible nitric oxide synthase; Native low density lipoprotein; Nitric oxide; Reactive oxygen species.

Background: Nitric oxide synthases (NOSs) are a unique family of enzymes that catalyze the production of nitric oxide (NO) from L-arginine. Atherogenic action of oxidized low-d. lipoproteins (oxLDL) may be mediated partly by the formation of NO in endothelial cells. Objective: The objective of this study was to identify sources of reactive oxygen species (ROS) causing native LDL (nLDL)-induced senescence of cultured human umbilical vein endothelial cells (HUVECs). Methods: HUVECs were treated with nLDL and NO production was assessed using Griess reagent as substrate and spectrophotometry in the absence or presence of specific inhibitors of endothelial NOS (eNOS) and inducible NOS (iNOS). In addition, expression levels of eNOS and iNOS were measured with ELISA and western blotting, and ROS was evaluated using 2′,7′-dichlorofluorescin diacetate (DCF-DA) and a fluorescence microplate reader. Results: NO formation in nLDL-treated HUVECs was significantly increased. Long-term treatment with nLDL up-regulated both eNOS and iNOS proteins. Such increase of NO production in HUVECs induced by nLDL was significantly suppressed by treatment with iNOS-selective inhibitor 1400 W, but not by the eNOS-selective inhibitor L-NIO. Native LDL treatment uncoupled Hsp90, the regulatory binding protein of eNOS, from the enzyme in HUVECs. Native LDL also significantly increased ROS production in HUVECs.

Genes & Genomics published new progress about Heat-shock protein HSP90 Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 2044-85-1 belongs to class esters-buliding-blocks, name is 2′,7′-Dichloro-3-oxo-3H-spiro[isobenzofuran-1,9′-xanthene]-3′,6′-diyl diacetate, and the molecular formula is C24H14Cl2O7, Formula: C24H14Cl2O7.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Amara, Ines published the artcileHericium Erinaceus Prevents DEHP-Induced Mitochondrial Dysfunction and Apoptosis in PC12 Cells, Computed Properties of 2044-85-1, the main research area is Hericium DEHP mitochondrial dysfunction apoptosis; Di (2-Ethylhexyl) pthalate; Hericium erinaceus; apoptosis; mitochondrial respiratory complexes; oxidative stress; vitagenes.

Hericium Erinaceus (HE) is a medicinal plant known to possess anticarcinogenic, antibiotic, and antioxidant activities. It has been shown to have a protective effect against ischemia-injury-induced neuronal cell death in rats. As an extending study, here we examined in pheochromocytoma 12 (PC12) cells, whether HE could exert a protective effect against oxidative stress and apoptosis induced by di(2-ethylhexyl)phthalate (DEHP), a plasticizer known to cause neurotoxicity. We demonstrated that pretreatment with HE significantly attenuated DEHP induced cell death. This protective effect may be attributed to its ability to reduce intracellular reactive oxygen species levels, preserving the activity of respiratory complexes and stabilizing the mitochondrial membrane potential. Addnl., HE pretreatment significantly modulated Nrf2 and Nrf2-dependent vitagenes expression, preventing the increase of pro-apoptotic and the decrease of anti-apoptotic markers. Collectively, our data provide evidence of new preventive nutritional strategy using HE against DEHP-induced apoptosis in PC12 cells.

International Journal of Molecular Sciences published new progress about Animal gene Role: BSU (Biological Study, Unclassified), BIOL (Biological Study) (Bax). 2044-85-1 belongs to class esters-buliding-blocks, name is 2′,7′-Dichloro-3-oxo-3H-spiro[isobenzofuran-1,9′-xanthene]-3′,6′-diyl diacetate, and the molecular formula is C24H14Cl2O7, Computed Properties of 2044-85-1.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics