Ricin is a protein toxin derived from the seeds of the castor oil plant, Ricinus communis. This substance is naturally produced during the processing of castor beans, which are grown globally for the production of castor oil. Ricin is categorized as a Type 2 Ribosome-Inactivating Protein (RIP). Because of its toxicity, it is classified as a potential bioterrorism agent. The toxin can be manufactured into a powder, mist, or liquid, and even a small amount can cause severe harm.
The Sensory Profile of Ricin
Purified ricin presents as a fine, white, or off-white powder. When isolated from the castor bean mash, the toxin is odorless and tasteless. This lack of sensory warning signals makes it particularly dangerous when used in contaminated food, water, or aerosol form.
The raw castor bean may possess a faint taste, but the purified protein toxin does not impart any noticeable flavor or scent to materials it is mixed with. A person would not be aware of exposure until the onset of symptoms begins. This undetectability is a primary factor in the substance’s appeal as a covert weapon.
How Ricin Attacks the Body
Ricin is a heterodimeric molecule composed of two polypeptide chains, A and B, linked by a disulfide bond. The B-chain (RTB) binds to galactose-containing receptors on the surface of eukaryotic cells, facilitating the toxin’s entry. This binding allows the entire toxin complex to be internalized by the cell through endocytosis.
Once inside, the toxin undergoes retrograde transport, moving through the Golgi apparatus and into the endoplasmic reticulum. The disulfide bond linking the chains is cleaved, releasing the catalytically active A-chain (RTA) into the cell’s cytosol. The RTA acts as an RNA N-glycosidase enzyme, which is the mechanism of cellular destruction.
The RTA irreversibly removes a specific adenine nucleotide (A4324) within the 28S ribosomal RNA. This location is part of the Sarcin/Ricin Loop (SRL) on the 60S subunit of the ribosome. Removing this adenine destroys the ribosome’s ability to interact with elongation factors necessary for protein synthesis. By inactivating the protein-making machinery, the cell can no longer produce necessary proteins, leading rapidly to cell death, tissue necrosis, and multi-organ failure.
Ingestion Versus Inhalation: Different Paths of Exposure
The symptoms of ricin poisoning and the time until they appear depend on the route of exposure. When ricin is swallowed in contaminated food or water, the gastrointestinal tract is the first and most damaged area. Initial symptoms, appearing within six to ten hours, include nausea, vomiting, abdominal pain, and bloody diarrhea.
Damage to the gastrointestinal lining leads to internal bleeding and dehydration, which can rapidly cause hypovolemic shock. The absorbed toxin can damage distant organs, including the liver, spleen, and kidneys, often resulting in death from multi-organ failure within several days. The oral route is generally less toxic compared to other pathways because digestive enzymes degrade some of the protein toxin.
Exposure through inhalation, typically by breathing in a mist or powder, targets the respiratory system, with symptoms appearing within four to eight hours. Initial signs are flu-like, including fever, a cough, and chest tightness, which quickly progress to difficulty breathing. The toxin causes inflammation and damage to the lung tissue, leading to pulmonary edema, where fluid builds up in the lungs. This fluid accumulation prevents oxygen from entering the bloodstream, causing the victim’s skin to turn blue, and death results from respiratory failure.