CASTOR bEan ricinUs COMMUNIS Department of Clinical toxicology Loghman Poison Center Mithra Rahimi MD

are glycoproteins that are classified according to their binding affinity for specific carbohydrate ligands, particularly galactosamines, and by the number of chains linked by disulfide bonds.  Toxalbumins such as and are lectins that are such potent cytotoxins that they are used as biologic weapons. Ricin, extracted from the castor bean exerts its cytotoxicity by 2 separate mechanisms.  The compound is a large molecule that consists of two polypeptide chains bound by disulfide bonds.  It must enter the cell to exert its toxic effect.  The B chain binds to the terminal galactose of cell surfacglycolipids and glycoproteins.  The bound then undergoes endocytosis and is transported via endosomes to the Golgi apparatus and the endoplasmic reticulum.  There the A chain is translocated  to the cytosol, where it stops protein synthesis by inhibiting the 28S subunit of the 60S ribosome.  In addition to the GI manifestations of  vomiting, diarrhea, and dehydration,  Ricin can cause cardiac, hematologic,  hepatic, and renal toxicity.

 Just how lethal are ingestions of the ornamental seeds?  The highest concentration of xenobiotic is in the hard, brown-mottled seeds.  Despite the obvious toxicity of this compound, death probably can be prevented by early and aggressive fluid and electrolyte replacement after oral ingestion.  (but not injection or inhalation)  These seeds are both tempting and available, even to children in the USA, because they are attractive enough to be used to make jewelry, and their parent plants are showy enough to have been exported for horticultural purposes outside of their native India.  (including to the USA).  Although mastication of one seed by a child liberates enough ricin to produce death, this outcome (or even serious toxicity) is uncommon, even if the seeds are chewed, probably because GI absorption of the xenobiotic is poor and supportive care is effective. Activated charcoal should be administered promptly!

HADDAD & WINCHESTER  Severe toxic GE with hemorrhage is a hallmark of toxicity from toxalbumin-containing seeds such as:  1)castor oil plant seeds (Ricinus communis) ,  2)Jatropha spp seeds,  3)rosary peas ()  Abdominal pain, vomiting, and frequent heme-positive stools with tenesmus can occur as early as 1 to 3 hours postingestion  or can be delayed for several days.

 GI symptoms progress over 4 to 36 hours to dehydration and cardiac, renal, and hepatic toxicity in severe poisoning.  Pathophysiology involves toxalbumin  inhibition of the 60S ribosomal subunit, which arrests protein synthesis and causes: cell death.

 The reticuloendothelial and highly proliferative intestinal cells are particularly vulnerable to the effects of ricin.

 While one masticated castor bean or rosary pea(containing up to 10 mg ricin) is potentially fatal to a toddler.  The frequently cited human fatal oral dose of 1 mg/kg is unconfirmed. TINTINALLI  Ricin is a potent toxalbumin that inhibits protein synthesis and causes severe cytotoxic effects on multiple organ systems.  It may be one of the most poisonous naturally occurring substances known.  Although present in all parts of the castor  bean Plant, ricin is concentrated mostly  in the bean.  Only 1% to 5% of the bean is ricin.  Castor beans are covered by a hard, relatively impervious outer shell that must be chewed or in some way broken in order for the ricin to cause toxicity.  Symptoms develop 6 to 8 hours after exposure!

Symptoms include GE, which may be severe and hemorrhagic, followed by delirium, seizures, coma, and death.  Beans are particularly antigenic and  may cause severe hpersensitivity and coetaneous and systemic allergic reactions.  Whole-bowel irrigation has been  Advocated to ensure rapid and completed contamination of the GI tract.  Beans should be counted to ensure complete recovery