Castor

 Ricinus Communis (Castor Bean, Castor-Oil-Plant, Palma Christi).

Kinetics:

• Ricin a tozxalbumin is the principal toxin.
• Toxalbumins are very toxic proteinaceous compounds of plant origin.
• Ricin is 100 times less toxic orally than parenterally; the difference is apparently not a result of the effects of trypsin or pepsin.
• Toxicosis is not only associated with plant, but most often with seed and seed products.
• Orally, ricin is readily absorbed from the stomach and intestine.
• Ricin is water soluble and not present in castor oil.
• Being a protein, and a fairly large molecule, ricin is heat labile. In castor bean cake, meal, etc. the ricin is generally inactivated by heating.

Mechainsm of action:  Exact mechanism is still unknown but is is believed that:

It consists of an enzymic polypeptide that catalyzes the N-glycosidic cleavage of a specific adenine residue from 28S ribosomal RNA, joined by a single disulfide bond to a galactose (cell)-binding lectin.

 The enzymatic activity renders ribosomes containing depurinated 28S RNA incapable of protein synthesis.

The bipartite molecular structure of ricin allows it to bind to the mammalian cell surface, enter via endocytic uptake, and deliver the catalytically active polypeptide into the cell cytosol where it irreversibly inhibits protein synthesis causing cell death.

Clinical Signs:

• Signs appear after a characteristic lag period of a few hours to days, usually onset is between 12 hours and 48 hours.
• Nausea, gastrointestinal irritation, abdominal pain, diarrhea which is often bloody, tenesmus, dehydration and at postmortem severe inflammation of the stomach and intestine.
• Anorexia, cessation of rumination.
• Excessive thirst.
• Weakness, muscle twitching.
• Dullness of vision, convulsions, dyspnea, opisthotonus, coma and death.
• Sometimes clonic convulsions and decreased tendon reflexes are described.
• After convulsions, death may result from paralysis of the respiratory center – artificial respiration may not preserve life for long because of rapid onset of concurrent vasomotor paralysis.
• Clotting time may be prolonged, possible hypoprothrombinemia.
• Cyanosis.

Treatment :

• Early – Use of emetics in appropriate species followed by activated charcoal and a saline cathartic unless contraindicated (as in marked diarrhea) is useful.
• A gastrointestinal tract protectant such as kaolin-pectin and fluid therapy are useful. Appropriate fluid and electrolyte therapy can greatly increase chances of survival.
• Judicious use of anticonvulsants if necessary.
• Maintain (or establish) respiration, fluid, and electrolyte balance.
• Oral antacids to alleviate local irritation.
• Ascorbic acid increases survival rates.
• Forced alkaline diuresis has been suggested to prevent nephrosis.