Trimethyltin-induced apoptosis is associated with upregulation of inducible nitric oxide synthase and Bax in a hippocampal cell line

Zhang, L; Li, L; Prabhakaran, Krishnan; Borowitz, Joseph L.; Isom, Gary E.

doi:10.1016/j.taap.2006.05.004

Cited by 52 publications

(31 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The TUNEL assay was performed on paraformaldehyde (4% in PBS) fixed cells using the Apoptag ™ in situ apoptosis detection kit (Oncor, Gaithersburg, MD) as described previously [23].…”

Section: Cell Death Assaymentioning

confidence: 99%

“…The 2′,7′-dichlorofluorescin-diacetate (DCF-DA) assay was used to measure cellular generation of ROS [23]. Cells were loaded with 30 μM DCF-DA (Molecular Probes, Eugene, OR) for 30 min at 37°C in the dark and then washed with PBS to remove free DCF-DA.…”

Section: Measurement Of Ros Generationmentioning

confidence: 99%

“…Changes in ΔΨ m were estimated using the cationic fluorescent dye (JC-1) as described previously [23]. JC-1 is a dual-emission potential-sensitive probe that measures ΔΨ m since the ratio of green to red fluorescence of JC-1 is dependent on the mitochondrial membrane potential.…”

Section: Mitochondrial Membrane Potential (δψ M )mentioning

confidence: 99%

See 2 more Smart Citations

HIF-1α activation by a redox-sensitive pathway mediates cyanide-induced BNIP3 upregulation and mitochondrial-dependent cell death

Zhang

Liu

et al. 2007

Free Radical Biology and Medicine

View full text Add to dashboard Cite

Cyanide produces degeneration of the nervous system in which different modes of cell death are activated in the vulnerable brain areas. In brain, the mechanism underlying the cell death is not clear. In this study, an immortalized dopaminergic cell line was used to characterize the cell death signaling cascade activated by cyanide. Cyanide-treated cells exhibited a time-and concentration-dependent apoptosis that was caspase-independent. Cyanide induced a rapid surge of intracellular reactive oxygen species (ROS) generation, followed by p38 mitogen-activated protein kinase (MAPK) activation and nuclear accumulation of hypoxia-inducible factor-1α (HIF-1α). Activation of p38 MAPK and HIF-1α accumulation were attenuated by N-acetyl-L-cysteine (antioxidant), catalase (hydrogen peroxide scavenger) or a selective p38 MAPK inhibitor (SB203580). Cyanide activated the hypoxia response element (HRE) promoter, which was also blocked by the antioxidants and SB203580. HRE activation was followed by increased BNIP3 gene transcription, as reflected by elevated BNIP3 mRNA and protein levels. BNIP3 upregulation was reduced by selective RNAi knockdown of HIF-1α. Overexpression of BNIP3 produced mitochondrial dysfunction (reduced membrane potential), caspase-independent apoptosis, and sensitization of the cells to cyanideinduced toxicity. Expression of a dominant negative mutant or RNAi knockdown of BNIP3 protected the cells from cyanide. It was concluded that cyanide activated the HIF-1α-mediated pathway of BNIP3 induction through a redox-sensitive process. Increased BNIP3 expression then served as an initiator of mitochondrial-mediated death.

show abstract

“…The TUNEL assay was performed on paraformaldehyde (4% in PBS) fixed cells using the Apoptag ™ in situ apoptosis detection kit (Oncor, Gaithersburg, MD) as described previously [23].…”

Section: Cell Death Assaymentioning

confidence: 99%

Section: Measurement Of Ros Generationmentioning

confidence: 99%

See 1 more Smart Citation

HIF-1α activation by a redox-sensitive pathway mediates cyanide-induced BNIP3 upregulation and mitochondrial-dependent cell death

Zhang

Liu

et al. 2007

Free Radical Biology and Medicine

View full text Add to dashboard Cite

show abstract

“…In fact, Bid and Bax have been shown to promote mPTP opening Zamzami et al 2000), whereas anti-apoptotic members of the Bcl-2 family (e.g., Bcl-2 and Bcl-x L ) exert an inhibitory effect . Opening of the mPTP is provoked by several factors, including elevated levels of oxidative (Rajesh et al 2003) and nitrosative stress (Marriott et al 2004;Zhang et al 2006). Furthermore, it has been shown that enhanced production of reactive oxygen (ROS) and nitrogen species (RNS) may induce a proapoptotic shift of the pattern of expression of Bcl-2 proteins (e.g., increased Bax to Bcl-2 ratio) (Savory et al 1999;Mishra et al 2006;Qin et al 2006).…”

Section: Introductionmentioning

confidence: 99%

“…Among the reactive aldehydes stemming from lipid peroxidation, 4-hydroxy-2-nonenal (HNE) has been shown to interfere with mitochondrial function (Chen et al 2001) and to promote mPTP opening (Vieira et al 2001). ROS can also elicit RNS production (Zhang, Li, Prabhakaran, Borowitz, and Isom 2006), via up-regulation of the inducible isoform of nitric oxide synthase (iNOS) (Zhen et al 2008). Chronic overproduction of RNS can lead to irreversible nitration of proteins, with an apparent selectivity for those of mitochondrial origin (Aulak et al 2001), and to enhanced production of ROS (Poderoso et al 1996).…”

Section: Introductionmentioning

confidence: 99%

Age-related activation of mitochondrial caspase-independent apoptotic signaling in rat gastrocnemius muscle

Marzetti

Wohlgemuth

Lees

et al. 2008

Mechanisms of Ageing and Development

156

149

View full text Add to dashboard Cite

Mitochondria-mediated apoptosis represents a central process driving age-related muscle loss. However, the temporal relation between mitochondrial apoptotic signaling and sarcopenia as well as the regulation of release of pro-apoptotic factors from the mitochondria has not been elucidated. In this study, we investigated mitochondrial apoptotic signaling in skeletal muscle of rats across a wide age range. We also investigated whether mitochondrial-driven apoptosis was accompanied by changes in the expression of Bcl-2 proteins and components of the mitochondrial permeability transition pore (mPTP). Analyses were performed on gastrocnemius muscle of 8-, 18-, 29-and 37-month-old male Fischer 344 ×Brown Norway rats (9 per group). Muscle weight declined progressively with advancing age, concomitant with increased apoptotic DNA fragmentation. Cytosolic and nuclear levels of apoptosis inducing factor (AIF) and endonuclease G (EndoG) increased in old and senescent animals. In contrast, cytosolic levels of cytochrome c were unchanged with age. Mitochondrial Bcl-2, Bax and Bid increased dramatically in 37-month-old rats, with no changes in the Bax/Bcl-2 ratio in any of the age groups. Finally, expression of cyclophilin D was enhanced at very old age. Our findings indicate that the mitochondrial caspase-independent apoptotic pathway may play a more prominent role in skeletal muscle loss than caspase-mediated apoptosis.

show abstract

Methylzinnverbindungen [MAK Value Documentation in German language, 2014]

2014

The MAK‐Collection for Occupational Health and Safety

View full text Add to dashboard Cite

Trimethyltin-induced apoptosis is associated with upregulation of inducible nitric oxide synthase and Bax in a hippocampal cell line

Cited by 52 publications

References 50 publications

HIF-1α activation by a redox-sensitive pathway mediates cyanide-induced BNIP3 upregulation and mitochondrial-dependent cell death

HIF-1α activation by a redox-sensitive pathway mediates cyanide-induced BNIP3 upregulation and mitochondrial-dependent cell death

Age-related activation of mitochondrial caspase-independent apoptotic signaling in rat gastrocnemius muscle

Methylzinnverbindungen [MAK Value Documentation in German language, 2014]

Contact Info

Product

Resources

About