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"Poisonous" does not mean deadly. Some manifestations of toxicity are subtle. The dose, as always, determines if a plant is safe source of nutrients or a toxic hazard.

Miserotoxin and its substituent Nitro- compounds

Structures of miserotoxin

Miserotoxin is a 3-nitro-1-propanol beta-D-glucoside which is found in many species of Astragalus. In order for it to cause poisoning, however, it must be hydrolyzed to release the nitropropanol moiety. This hydrolysis occurs by the action of beta-glucosidase, implying that animals with low beta-gluc activities are unaffected. This is born out on the case of rats who were unaffected by miserotoxin dosage but died from nitropropanol ingestion (Majak, Cheng, Muir, Pass 1984) . However, the case of ruminants is different, the microbes of the rumen often having substantial beta-gluc activity. While the rumen does afford some protection against the nitro- compounds by microbial metabolism,there are cases in which it is less effective. Certain Astragalus species have higher toxicity than others because they carry the nitropropanol glucoside whereas other species carry a nitropropionic acid glucoside. The nitropropanol aglycone is degraded by rumen microbesabout half as quickly as nitropropionic acid is. This gives a greater opportunity for absorption and subsequent poisoning.

McDiarmid et al. (1992) hypothesized, based on evidence presented in a number of studies, that miserotoxin poisoning of ruminants followed this metabolic course:

  1. the glycoside is hydrolyzed by microbial enzymes in the rumen
  2. nitropropanol is rapidly absorbed and oxidized into nitropropionic acid (an inhibitor of succinate dehydrogenase, a key enzyme for the krebs cycle).This is the major cause of poisoning.
    • -some of the nitropropanol is degraded to nitrite, elevating serum levels of methemoglobin. (McDiarmid, Pass, Benn, Majak 1992)

By reducing cellular ATP levels through krebs cycle inhibition, certain homeostatic mechanisms of the cell are compromised, in particular, the ATP driven sodium pumps. Without sodium pump action, the cells cannot maintain Na+ levels and begin to swell prior to lysis and/or cell death. This action is particularly notable in neural cells where cell death has drastic effects on the whole animal. (Pass 1994)

Miserotoxin Poisoning
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