CHOLERA TOXIN Chemical Properties

storage temp. 

0-6°C

solubility 

H2O: soluble10mg/mL

form 

lyophilized powder

Safety Information

Hazard Codes 

T

Risk Statements 

24/25-52/53

Safety Statements 

36/37-45-61

RIDADR 

3172

WGK Germany 

2

RTECS 

LF3100000

HazardClass 

6.1

PackingGroup 

I

Toxicity

cholera toxin is secreted by the gram-negative bacterium Vibrio cholerae. It is a gastrointestinal toxin that increases adenylate cyclase activity of mucosa of the small intestine, thereby increasing cyclic AMP within these cells. Cyclic AMP stimulates active transport of ions by these epithelial cells, resulting in a large efflux of Na+ and water into the gut. The toxin enters cells by interacting with a GM1 ganglioside on the cell surface. After entry, the A1 subunit catalyzes the transfer of an ADP-ribose unit from NAD+ to an arginine side chain of the adenylate cyclase regulatory G protein, blocking its GTPase activity. Thus the adenylate cyclase deactivation mechanism is destroyed, and cyclic AMP is continually produced. The major sign of cholera poisoning is severe diarrhea; several liters of body water may be lost within a few hours, leading to shock and death if fluid is not replaced. Treatment involves physiological support (including i.v. fluids) and antibiotics.

CHOLERA TOXIN Usage And Synthesis

Uses

Cholera Toxin from Vibrio cholerae has been used as a positive control in cAMP (cyclic AMP) assay for enterotoxins. It has been added as a supplement in cell culture media of primary tumors and epithelial cells.

Biochem/physiol Actions

Toxin consisting of an A subunit (27 kDa) surrounded by five B subunits (approximately 12 kDa each), which attach the toxin to ganglioside GM1 on the cell surface. The A subunit catalyzes ADP-ribosylation of the α-subunit of the stimulatory G protein (Gαs), reducing GTPase activity and activating the α-subunit. This activation of Gαs leads to an increase in the activity of adenylyl cyclase, resulting in increased levels of cAMP. Also ADP-ribosylates transducin in the eye rod outer segments, inactivating its GTPase activity. Cholera toxin has also been reported to ADP-ribosylate tubulin. Shown to be a potent mucosal vaccine adjuvant, inducing T helper cell type 2 responses by inhibiting the production of interleukin-12.

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