Apoptosis is a cell suicide mechanism that enables organisms to control cell number and eliminate cells that threaten survival (1). Apoptosis is also an important phenomenon in cytotoxicity induced by anticancer drugs (2). Knowing the ability of a compound to induce or inhibit apoptosis is critical to making decisions about its drug-ability in the drug discovery process. Caspases, a group of cysteine proteases, play a central role as executioners in the apoptotic cell death process (3,4). For instance, caspase-2 is an upstream initiator of mitochondrial permeabilization (5). Cathepsins are apoptosis markers associated with tumors and Alzheimer’s disease (6).

Caspases are involved not only in apoptosis but also in cytokine maturation and cell growth and differentiation. Among them, caspase-1 is primarily involved in the process of pro-inflammatory cytokines. Caspase-3 and caspase-9 are essential for apoptosis during brain development. Caspase-8 is required for the development of heart muscle, cell proliferation in the hematopoietic lineage and death-receptor-mediated apoptosis (3,7).

Apoptosis and cytotoxicity can be quantitated by measuring active caspases, cathepsins, serine proteases, cholinesterase, and mitochondrial functionality in live cells with our new FLICA™, Magic Red™, MitoPT™, FLISP™, Cholinesterase, and Cytotoxicity kits.

These kits offer the following advantages:

Easy to use:
Potent caspase inhibitors are cell-permeable and non-cytotoxic.
No lysis, no permeabilization or antibodies, no radioisotopes are required.

Early detaction:
Quantitate apoptosis earlier than Annexin V and Tunnel assays

Sensitive & Accurate results:
Only cells with active enzymes fluoresce
No interference from pro-caspases

References:

1. Hajra KM, Liu JR. Apoptosis. 9(6):691-704 (2004).
2. Kim R, Tanabe K, et al. Cancer Chemother Pharmacol. 50(5):343-52 (2002).
3. Salvesen, G.S., and Dixit, V.M. Cell. 91:443-446 (1997).
4. Jin Wang and Michael J. Lenardo. Journal of Cell Science. 113:753-757 (2000).
5. Troy CM, Shelanski ML. Cell Death Differ. 10(1):101-7 (2003).
6. Motyckova, G., et al. Proc Natl Acad Sci. 98:5798-5803 (2001).
7. Kim Newton, and Andreas Strasser. Genes & Development. 17(7):819-825 (2003).