Cell Injury Assay Kit                                                                                                                                                                                        Price

Product Description: The kinetic determination of the cellular enzyme lactate dehydrogenase (LDH) released upon cell damage or lysis is a
sensitive, precise, and convenient method for the studies of apoptosis and cytotoxicity reactions (J. Immunol. Methods 64:313,1983). The
inexpensive, non-radioactive colorimetric LDH assay provides a superb alternative to 51Cr release assays (Immunology 14:181,1968), which
often suffer from higher background levels. The Cell Injury Assay Kit is based on the reduction of the tetrazolium salt INT in a NADH-coupled
enzymatic reaction to formazan, which is water-soluble and exhibits an absorption maximum at 492 nm. Since the intensity of the red color formed
is proportional to the number of damaged or lysed cells, the assay has been widely used for the detection and quantification of apoptosis as well
as necrosis (Exp. Cell Res. 226:372, 1996) (see Cell Viability/Proliferation Assay Kit). The superior sensitivity of the non-radioactive assay kit
allows the assay to be completed within 30 min with minimal pipetting steps. Each kit is sufficient for approximately 200 assays using the 96-well
format. See related product Lactate Assay Kit. The method is adaptable to automation.

Kit Components:

LDH Assay Solution- 10 ml; store at -20°C

MSDS: DMSO, INT, acetic acid, Hepes

Related kits: Cell Viability Assay, Lipid Peroxidation Assay, Peroxide Assay, Nitric Oxide Assay, ATP Assay, Free Thiol Assay

Citation:
Lynch et al
Cell survival under stress is enhanced by a mitochondrial ATP-binding cassette transporter that regulates hemoproteins
Cancer Research 69:5560-5567, 2009
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Biomedical Research Service
& Clinical Application
Neonatal rat cardiomyocytes were
infected with LacZ and p53 adenovirus.
Cell injury/death was monitored by LDH
release after 24 and 48 hours. This study
shows overexpression of p53 causes
cardiomyocyte death.
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