POISONOUS PARTS
Whole plant.3
TOXICITY
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Toxic Constituents
Pyrrolizidine alkaloids such as monocrotaline and retrorsine.4,5
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Toxic Dose
Long-term consumption of 1 mg pyrrolizidine alkaloids per day can be toxic.6
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Mechanism
Pyrrolizidine alkaloids are converted into highly reactive metabolites after transformation in the liver by the cytochrome P450 system. These metabolites bind to proteins, DNA and RNA, and induce acute and chronic toxicities. Liver is the major organ affected, and veno-occlusive disease (Budd-Chiari syndrome) could occur. As liver metabolism is involved, toxicity is not strictly dose-dependent but shows individual variability.7,8
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Poisoning Features
Pyrrolizidine alkaloid poisoning has acute and chronic effects. Acute: abdominal pain, hepatomegaly, ascites, liver necrosis and even death. Chronic: hepatomegaly, recurrent ascites, hepatic vein occlusion (Budd-Chiari syndrome), cirrhosis, hepatocellular carcinoma, pulmonary hypertension and even death.6,7
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Poisoning Events
There were 2 main sources of pyrrolizidine alkaloid poisoning. The consumption of cereal grains contaminated by the toxic weeds had caused numerous poisoning in many countries. In Afghanistan alone, an estimated 8000 people were affected with more than 1600 deaths. The other source is the use of pyrrolizidine alkaloid-containing herbs for medicinal and dietary purposes, leading to poisoning in all parts of the world.6,7
CLINICAL MANAGEMENT
Supportive treatment. Early diagnosis and avoidance of further exposure to the toxins is important.8
IDENTIFICATION FEATURES
Erect herbs, 60–120 cm tall; branches striate, pubescent. Leaves simple, 3–8 × 1–3.5 cm, apex emarginate, slightly pubescent abaxially. Racemes terminal, about 5 cm long, 10–20-flowered. Calyx 2-lipped, sparsely pubescent. Corolla yellow, vexillum, wings and keel are nearly equal in length, keel long beaked. Pods 3–4 cm long, 10–20-seeded. Seeds about 2 mm long, elliptic, brown.9
LABORATORY ANALYSIS
Monocrotaline and retrorsine can be detected by GC-MS and LC-MS/MS.10–12