Abstract
3-Nitropropionic acid as well as 3-nitro-1-propanol and its beta-D-glucopyranoside (miserotoxin) are the plant and fungal toxins reported to interrupt mitochondrial electron transport resulting in cellular energy deficit. These nitrotoxins induce neurological degeneration in ruminants and humans. 3-Nitropropionic acid-intoxicated rats serve as the animal model for Huntington's disease.
Highlights
The nitrotoxins, 3-nitropropionic acid, 3-nitro-1-propanol and 3-nitro-1-propyl-β-D-glucopyranoside called miserotoxin, were found in many leguminous plants. These compounds are toxic principle of various milk vetches (Astragalus spp.) that are distributed worldwide. These poisonous plants are often a reason of intoxication of cattle, sheep, and horses in the United States and Canada [33,49,50]. 3-Nitropropionic acid is sometimes produced on moldy crops as for example sugarcane or peanuts in amounts sufficient to cause severe neurological disorders when consumed by humans [45,39]. 3-Nitropropionic acid is produced by the fungus Arthrinium spp
3-nitro-1-propanal, as well as 3-nitro-1-propanol and some of its ethers. 3-Nitro-1-propanol has been obtained by borane-dimethylsulfide reduction of both 3-nitro-1-propanal and 3-nitropropionic acid
That in some species of Astragalus, for example Astragalus bisulcatus or A. lentiginosus, whose growth in Canada, other very toxic chemical, indolizidine alkaloid swainsonine (II) was observed, which cause locoism in cattle, horse, and sheep [40] and it is not challenged that biological effects of nitrotoxins and swainsonine may be cumulated
Summary
Summary: 3-Nitropropionic acid as well as 3-nitro-1-propanol and its β-D-glucopyranoside (miserotoxin) are the plant and fungal toxins reported to interrupt mitochondrial electron transport resulting in cellular energy deficit. These nitrotoxins induce neurological degeneration in ruminants and humans. 3-Nitropropionic acid-intoxicated rats serve as the animal model for Huntington’s disease
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