NDLI: Reactive oxygen species induce apoptosis in bronchial epithelial BEAS-2B cells by inhibiting the antiglycation glyoxalase I defence: involvement of superoxide anion, hydrogen peroxide and NF-κB

Please wait, while we are loading the content...

The apoptosis of peripheral blood lymphocytes promoted by hyperbaric oxygen treatment contributes to attenuate the severity of early stage acute pancreatitis in rats

The MEK/ERK pathway is the primary conduit for Borrelia burgdorferi-induced inflammation and P53-mediated apoptosis in oligodendrocytes

Involvement of poly(ADP-ribose) polymerase in paraptotic cell death of D. discoideum

Reactive oxygen species induce apoptosis in bronchial epithelial BEAS-2B cells by inhibiting the antiglycation glyoxalase I defence: involvement of superoxide anion, hydrogen peroxide and NF-κB

Glutathione depletion regulates both extrinsic and intrinsic apoptotic signaling cascades independent from multidrug resistance protein 1

Superoxide activates mTOR–eIF4E–Bax route to induce enhanced apoptosis in leukemic cells

Mahanine synergistically enhances cytotoxicity of 5-fluorouracil through ROS-mediated activation of PTEN and p53/p73 in colon carcinoma

(E)-2,4-Bis(p-hydroxyphenyl)-2-butenal inhibits tumor growth via suppression of NF-κB and induction of death receptor 6

NSC126188 induces apoptosis of prostate cancer PC-3 cells through inhibition of Akt membrane translocation, FoxO3a activation, and RhoB transcription

Valproic acid enhances fludarabine-induced apoptosis mediated by ROS and involving decreased AKT and ATM activation in B-cell-lymphoid neoplastic cells

The putative BH3 mimetic S1 sensitizes leukemia to ABT-737 by increasing reactive oxygen species, inducing endoplasmic reticulum stress, and upregulating the BH3-only protein NOXA

Blocking autophagy enhances the apoptosis effect of bufalin on human hepatocellular carcinoma cells through endoplasmic reticulum stress and JNK activation

Prometaphase arrest-dependent phosphorylation of Bcl-2 and Bim reduces the association of Bcl-2 with Bak or Bim, provoking Bak activation and mitochondrial apoptosis in nocodazole-treated Jurkat T cells

Targeting elongation factor-2 kinase (eEF-2K) induces apoptosis in human pancreatic cancer cells

Perturbation of apoptosis upon binding of tRNA to the heme domain of cytochrome c

A high-throughput image-based screen for the identification of Bax/Bak-independent caspase activators against drug-resistant cancer cells

Apoptosis : Volume 18

Apoptosis : Volume 17

Apoptosis : Volume 16

Apoptosis : Volume 15

Apoptosis : Volume 14

Apoptosis : Volume 13

Apoptosis : Volume 12

Apoptosis : Volume 11

Apoptosis : Volume 10

Reactive oxygen species induce apoptosis in bronchial epithelial BEAS-2B cells by inhibiting the antiglycation glyoxalase I defence: involvement of superoxide anion, hydrogen peroxide and NF-κB

Content Provider	Springer Nature Link
Author	Antognelli, Cinzia Gambelunghe, Angela Talesa, Vincenzo Nicola Muzi, Giacomo
Copyright Year	2013
Abstract	Reactive oxygen species (ROS) are implicated in the regulation of apoptosis through a number of distinct mechanisms depending on cell type and stimulation conditions. Glyoxalase I (GI) metabolizes methylglyoxal (MG) and MG-derived advanced glycation end products (AGEs) known to cause apoptosis. This study examined the possible role of GI among the mechanisms of ROS-driven apoptosis in human bronchial epithelial BEAS-2B cells exposed to wood dust and signaling pathways by which these reactive species regulate GI expression. Our results showed that wood dust generated distinct ROS (superoxide anion, and hydrogen peroxide) by selectively inhibiting the enzymatic activity of superoxide dismutase or glutathione peroxidase and catalase enzymes. These ROS caused a dramatic inhibition of the antiglycation GI enzyme, leading to the intracellular accumulation of the pro-apoptotic AGE, argpyrimidine (AP) and programmed cell death via a mitochondrial pathway. Pre-treatment with N-acetyl-l-cysteine (NAC), a ROS scavenger, prevented these events. Hence, ROS-induced apoptosis in BEAS-2B cells occurred via a novel mechanism relying on GI inhibition and AP accumulation. We interestingly found that superoxide anion and hydrogen peroxide induced a diverse apoptosis level by differently inhibiting GI via NF-κB pathway. Since maintenance of an intact epithelium is a critically important determinant of normal respiratory function, the knowledge of the mechanisms underlying its disruption may provide insight into the genesis of a number of pathological conditions commonly occurring in wood dust occupational exposure. Our findings suggest that the antioxidant NAC may merit investigation as a potential preventive agent in wood dust exposure-induced respiratory diseases.
Starting Page	102
Ending Page	116
Page Count	15
File Format	PDF
ISSN	13608185
Journal	Apoptosis
Volume Number	19
Issue Number	1
e-ISSN	1573675X
Language	English
Publisher	Springer US
Publisher Date	2013-09-04
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	ROS Antioxidant enzymes Glyoxalase I Argpyrimidine Apoptosis NF-κB Cancer Research Cell Biology Oncology Biochemistry Virology
Content Type	Text
Resource Type	Article
Subject	Pharmaceutical Science Biochemistry (medical) Cell Biology Clinical Biochemistry Cancer Research Pharmacology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Glyoxalase I inhibition induces apoptosis in irradiated MCF-7 cells via a novel mechanism involving Hsp27, p53 and NF-κB.

Dimerized translationally controlled tumor protein increases interleukin-8 expression through MAPK and NF-κB pathways in a human bronchial epithelial cell line

Amygdalin Attenuates Airway Epithelium Apoptosis, Inflammation, and Epithelial-Mesenchymal Transition through Restraining the TLR4/NF-κB Signaling Pathway on LPS-Treated BEAS-2B Bronchial Epithelial Cells

Glyoxalase I drives epithelial-to-mesenchymal transition via argpyrimidine-modified Hsp70, miR-21 and SMAD signalling in human bronchial cells BEAS-2B chronically exposed to crystalline silica Min-U-Sil 5: Transformation into a neoplastic-like phenotype.

Epigallocatechin gallate protects BEAS-2B cells from lipopolysaccharide-induced apoptosis through upregulation of gastrin-releasing peptide

circ_0038467 promotes PM2.5-induced bronchial epithelial cell dysfunction

3-Methylindole-Induced Toxicity to Human Bronchial Epithelial Cell Lines

Fine particle matters induce DNA damage and G2/M cell cycle arrest in human bronchial epithelial BEAS-2B cells

Silver nanoparticles induce p53-mediated apoptosis in human bronchial epithelial (BEAS-2B) cells

Reactive oxygen species induce apoptosis in bronchial epithelial BEAS-2B cells by inhibiting the antiglycation glyoxalase I defence: involvement of superoxide anion, hydrogen peroxide and NF-κB

Similar Documents

Glyoxalase I inhibition induces apoptosis in irradiated MCF-7 cells via a novel mechanism involving Hsp27, p53 and NF-κB.

Dimerized translationally controlled tumor protein increases interleukin-8 expression through MAPK and NF-κB pathways in a human bronchial epithelial cell line

Amygdalin Attenuates Airway Epithelium Apoptosis, Inflammation, and Epithelial-Mesenchymal Transition through Restraining the TLR4/NF-κB Signaling Pathway on LPS-Treated BEAS-2B Bronchial Epithelial Cells

Glyoxalase I drives epithelial-to-mesenchymal transition via argpyrimidine-modified Hsp70, miR-21 and SMAD signalling in human bronchial cells BEAS-2B chronically exposed to crystalline silica Min-U-Sil 5: Transformation into a neoplastic-like phenotype.

Epigallocatechin gallate protects BEAS-2B cells from lipopolysaccharide-induced apoptosis through upregulation of gastrin-releasing peptide

circ_0038467 promotes PM2.5-induced bronchial epithelial cell dysfunction

3-Methylindole-Induced Toxicity to Human Bronchial Epithelial Cell Lines

Fine particle matters induce DNA damage and G2/M cell cycle arrest in human bronchial epithelial BEAS-2B cells

Silver nanoparticles induce p53-mediated apoptosis in human bronchial epithelial (BEAS-2B) cells

Reactive oxygen species induce apoptosis in bronchial epithelial BEAS-2B cells by inhibiting the antiglycation glyoxalase I defence: involvement of superoxide anion, hydrogen peroxide and NF-κB