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The toxic factor in white snakeroot: identity, analysis and prevention
1Veterinary Toxicology and Entomology Research Laboratory, US Department of Agriculture, College Station, TX 77840.
Veterinary and Human Toxicology
|January 1, 1990
Summary
White snakeroot poisoning remains a threat to livestock and humans, causing trembles and milk sickness. Identifying the toxic compounds and their mechanisms is crucial for understanding toxicity thresholds.
Area of Science:
- Toxicology
- Veterinary Medicine
- Environmental Health
Background:
- White snakeroot (Eupatorium rugosum) has historical significance for causing trembles and milk sickness in animals and humans since the American Revolution.
- Livestock production resurgence and raw milk consumption increase the risk of milk sickness from white snakeroot exposure.
- Horses and goats exhibit particular sensitivity to white snakeroot poisoning.
Observation:
- The toxic principles of white snakeroot remain unidentified, hindering toxicity threshold assessments in most animals and humans.
- Metabolic studies in chicks suggest a specific metabolic enzyme may be the target of the toxic principle.
- Components toxic after microsomal activation by Cytochrome P-450 have been isolated from white snakeroot.
Findings:
- Cytochrome P-450 mediates the activation of toxic components in white snakeroot.
- In vitro activation can be completely inhibited by 1-aminobenzotriazole, a specific inhibitor of Cytochrome P-450.
- The precise mechanism of action for white snakeroot toxins in animals and humans is currently unknown.
Implications:
- Further research is essential to identify the specific toxicants in white snakeroot.
- Understanding the mechanism of action and toxicity thresholds is critical for mitigating poisoning risks.
- Expeditious studies are needed to address the ongoing public health and veterinary concerns posed by white snakeroot.
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