NDLI: Tert-butylhydroquinone induces mitochondrial oxidative stress causing Nrf2 activation

Content Provider	Springer Nature Link
Author	Imhoff, Barry R. Hansen, Jason M.
Copyright Year	2010
Abstract	Tert-butylhydroquinone (tBHQ), the major metabolite of butylated hydroxyanisole, induces an antioxidant response through the redox-sensitive transcription factor, nuclear factor-E2-related factor-2 (Nrf2). However, the mechanism by which tBHQ induces Nrf2 activity is not entirely understood. Here, we show that tBHQ preferentially alters the redox status in the mitochondrial compartment in HeLa cells. HeLa cells treated with tBHQ showed a preferential oxidation of mitochondrial thioredoxin-2 (Trx2), while cellular glutathione and cytosolic thioredoxin-1 were not affected. Preferential mitochondrial oxidation by tBHQ was supported by detection of reactive oxygen species (ROS) specific to this compartment. To determine the role of Trx2 in regulating downstream effects of tBHQ, HeLa cells were transiently transfected with an empty, Trx2, or C93S (Cys93Ser) Trx2 dominant-negative mutant expression vector. Overexpression of Trx2 decreased basal mitochondrial ROS production, whereas expression of C93S Trx2 enhanced it. In addition, under untreated conditions, expression of C93S Trx2 led to an increase in the basal activities of Nrf2. With tBHQ treatments, Trx2 overexpression suppressed Nrf2 accumulation and activity, whereas expression of C93S Trx2 had no effect on the degree of inducibility or Nrf2 accumulation but did increase the overall activity of Nrf2. Quantitative polymerase chain reaction analysis of Nrf2-regulated gene expression corroborate Trx2 control of tBHQ-mediated Nrf2 activation. These data show a compartment-specific effect where tBHQ-induced Nrf2 signaling is mediated by Trx2 and suggest that antioxidant status in various compartments would provide different levels of control of redox signaling.
Starting Page	541
Ending Page	551
Page Count	11
File Format	PDF
ISSN	07422091
Journal	Cell Biology and Toxicology
Volume Number	26
Issue Number	6
e-ISSN	15736822
Language	English
Publisher	Springer Netherlands
Publisher Date	2010-04-29
Publisher Place	Dordrecht
Access Restriction	Subscribed
Subject Keyword	Mitochondria Nrf2 Oxidative stress Tert-butylhyrdroquinone Thioredoxin Biochemistry Pharmacology/Toxicology Cell Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Health, Toxicology and Mutagenesis Toxicology

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

Acetaldehyde-induced mitochondrial dysfunction sensitizes hepatocytes to oxidative damage

Adriamycin-induced oxidative mitochondrial cardiotoxicity

PM2.5 induces Nrf2-mediated defense mechanisms against oxidative stress by activating PIK3/AKT signaling pathway in human lung alveolar epithelial A549 cells

Mitochondrial perturbation attenuates bile acid-induced cytotoxicity

FK506 affects mitochondrial protein synthesis and oxygen consumption in human cells

Tert-butylhydroquinone mitigates Carbon Tetrachloride induced Hepatic Injury in mice.

Xylene Induces Oxidative Stress and Mitochondria Damage in Isolated Human Lymphocytes.

Cadmium induces mitochondria-dependent apoptosis of normal human hepatocytes

L-carnitine modulates blood platelet oxidative stress

Tert-butylhydroquinone induces mitochondrial oxidative stress causing Nrf2 activation

Similar Documents

Acetaldehyde-induced mitochondrial dysfunction sensitizes hepatocytes to oxidative damage

Adriamycin-induced oxidative mitochondrial cardiotoxicity

PM2.5 induces Nrf2-mediated defense mechanisms against oxidative stress by activating PIK3/AKT signaling pathway in human lung alveolar epithelial A549 cells

Mitochondrial perturbation attenuates bile acid-induced cytotoxicity

FK506 affects mitochondrial protein synthesis and oxygen consumption in human cells

Tert-butylhydroquinone mitigates Carbon Tetrachloride induced Hepatic Injury in mice.

Xylene Induces Oxidative Stress and Mitochondria Damage in Isolated Human Lymphocytes.

Cadmium induces mitochondria-dependent apoptosis of normal human hepatocytes

L-carnitine modulates blood platelet oxidative stress

Tert-butylhydroquinone induces mitochondrial oxidative stress causing Nrf2 activation