Abrin is a potent toxin that has been isolated from the seeds of Abrus precatorius (or Rosary pea). Its use as a tool for research was described in 1972 by Sharon and Lis. Abrin exists in two forms, abrin a and abrin b. Both are composed of two chains, an A-chain and a B-chain. A disulfide bond between Cys247 of the A-chain and Cys8 of the B-chain links the A and B chains. The A-chain is 251 residues and is divided into 3 folding domains. The A-chain catalytically inactivates 60S ribosomal subunits by removing adenine from positions 4 and 324 of 28S rRNA therefore inhibiting protein synthesis. The B-chain is a galactose specific lectin that facilitates the binding of abrin to cell membranes. The B-chain of both forms of abrin consist of 268 amino acid residues and share 256 identical residues. Comparison of their sequences with that of the ricin's B-chain shows that 60% of the residues of abrin's B-chain are identical to those of the ricin's B-chain and that two saccharide-binding sites in ricin B-chain identified by a crystallographic study are highly conserved in abrin B-chain. The mechanism of toxic action of abrin is identical to that of ricin, but the toxicity of abrin in mice is 75 times that of ricin (0.04 µg/kg for abrin compared to3 µg/kg for ricin.) The diagnosis, clinical features, treatment, protection, prophylaxis and so on is also the same for both abrin and ricin intoxications.

The clinical picture, clinical signs, symptoms, and pathological manifestations in intoxicated victims depends on the route of exposure. When inhaled as a small particle aerosol, ricin produces symptoms within 8 hours. Respiratory distress, fever, cough, dyspnea, nausea, and chest tightness are followed by profuse sweating, the development of pulmonary edema, cyanosis, hypotension, and finally respiratory failure and circulatory collapse. Time to death ranges from 36-72 hours, depending on the dose received. Ingestion of ricin causes gastrointestinal signs and gastrointestinal hemorrhage with necrosis of liver, spleen, and kidneys; intramuscular intoxication causes severe localized pain, muscle and regional lymph node necrosis, and moderate involvement of visceral organs. Transient leukocytosis appears to be a constant feature in humans, whether intoxication is via injection or oral ingestion. Leukocyte counts are 2- to 5-fold higher than the normal value. Children are more sensitive than adults to fluid loss, due to vomiting and diarrhea, and can quickly become severely dehydrated and die. If death has not occurred in 3-5 days, the victim usually recovers.