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Key Documents

20-247

Sigma-Aldrich

Peroxynitrite, degraded

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About This Item

UNSPSC Code:
41116012
eCl@ss:
32160405
NACRES:
NA.42

form

liquid

Quality Level

manufacturer/tradename

Upstate®

technique(s)

nitration: suitable

shipped in

dry ice

Application

Research Category
Neuroscience
Research Sub Category
Neurodegenerative Diseases

Quality

Routinely evaluated by treatment of non-stimulated A431 cells with degraded peroxynitrite; subsequent lack of positive staining was detected with anti-nitrotyrosine antibody (06-284).

Physical form

Degraded peroxynitrite (50-100mM); solution containing approximately 255mM H2O2, 0.18M NaOH, 0.23M NaCl, 23mM NaNO3 and 20mM NaNO2.

Storage and Stability

1 year at -70°C

Legal Information

UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

Pictograms

Corrosion

Signal Word

Warning

Hazard Statements

Hazard Classifications

Eye Irrit. 2 - Met. Corr. 1 - Skin Irrit. 2

Storage Class Code

5.1B - Oxidizing hazardous materials

WGK

WGK 2

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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Oxidative chemistry of peroxynitrite.
Beckman, J S, et al.
Test, 233, 229-240 (1994)
Pathological implications of nitric oxide, superoxide and peroxynitrite formation.
Beckman, J S and Crow, J P
Biochemical Society Transactions, 21, 330-334 (1993)
James Murray et al.
The Journal of biological chemistry, 278(39), 37223-37230 (2003-07-15)
There is growing evidence that oxidative phosphorylation (OXPHOS) generates reactive oxygen and nitrogen species within mitochondria as unwanted byproducts that can damage OXPHOS enzymes with subsequent enhancement of free radical production. The accumulation of this oxidative damage to mitochondria in

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