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Ageratina Altissima

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Stephen T. Lee – One of the best experts on this subject based on the ideXlab platform.

  • Effect of grinding and long-term storage on the toxicity of white snakeroot (Ageratina Altissima) in goats
    Research in veterinary science, 2018
    Co-Authors: T. Zane Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Carol G. Chitko-mckown
    Abstract:

    Abstract White snakeroot (Ageratina Altissima) contains the putative toxin tremetone and can produce a disease called “trembles” or “milk sickness”. However the toxicity of tremetone has not been demonstrated in vivo. It has been reported that the plant is less toxic after drying and grinding. The objectives of these studies were to determine: 1) the toxic effect of grinding white snakeroot 4 months prior to dosing and, 2) the toxic effect of storing white snakeroot at ambient temperature for 5 years. Dried white snakeroot, ground 1 day, 1 month, and 4 months prior to dosing, was orally gavaged to goats at 2% of their body weight for up to 28 days or until they were minimally poisoned (minimal muscular weakness and increased serum creatine kinase (CK) activities). All four goats dosed with white snakeroot that had been ground 4 months previously and stored at room temperature were poisoned, became exercise intolerant, and had increased serum CK activities (>5600 U/ L). White snakeroot stored for 5 years was toxic as 3 of 5 dosed goats developed clinical disease within only 6 days of dosing even though approximately 80% of the tremetone in the plant had disappeared during the 5-year storage period. The results from this study demonstrate that previous grinding and extended storage did not significantly alter white snakeroot toxicity. The results also indicate that tremetone concentration is not the singular indicator of toxicity and that other white snakeroot toxins or toxic tremetone degradation products remain in dried, stored white snakeroot.

  • Toxicity of Compounds Isolated from White Snakeroot (Ageratina Altissima) to Adult and Larval Yellow Fever Mosquitoes (Aedes aegypti).
    Natural product communications, 2016
    Co-Authors: Alden S. Estep, James J. Becnel, Stephen T. Lee
    Abstract:

    Botanicals have been the source for several classes of pesticides for mosquitoes. However, increasing resistance to these products and reduced numbers of choices necessitate the search for new active ingredients. Ageratina Altissima (L.) King & H. Rob. or white snakeroot, is found throughout the eastern United States and contains known toxic compounds. We examine chromenes (benzopyrans) and benzofurans isolated fiom this plant for larvicidal and adulticidal activity against the dengue vector Aedes aegypti L. Initial activity identified several compounds that were effective against either larvae or adults. Interestingly, only two compounds were effective against both larva and adults. Dose curves were constructed from further testing of these active compounds to allow. comparative ranking of efficacy. We identified dehydrotremetone as the most effective larvicide (0.03 ± 0.001 ng/μL) and 6-acetyl-7-methoxy-2,2- dimethylchromene as the most effective adulticide (1.17 ± 0.31 μg/org) although other compounds were also active. This study provides additional useful data for evaluation of chromenes and benzofurans as possible mosquiticidal agents.

  • Toxicity of white snakeroot (Ageratina Altissima) and chemical extracts of white snakeroot in goats.
    Journal of agricultural and food chemistry, 2015
    Co-Authors: T. Zane Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Mark G. Collett, Steven R Buck, James A. Pfister
    Abstract:

    White snakeroot (Ageratina Altissima) is a sporadically toxic plant that causes trembles in livestock and milk sickness in humans that drink tainted milk. The putative toxin in white snakeroot is tremetone and possibly other benzofuran ketones, even though it has not been demonstrated in vivo. Toxic white snakeroot was dosed to goats, and they developed clinical signs of poisoning, exercise intolerance, significant increases in serum enzyme activities, and histological changes. Tremetone and the other benzofuran ketones were extracted with hexane; the extracts and residues were analyzed for tremetone and dosed to goats at tremetone and benzofuran ketone concentrations similar to the original plant material. However, none of the dosed goats developed the disease. The results demonstrate for the first time that white snakeroot is a potent myotoxin in goats and that other compound(s), which may be lost or modified during the extraction process, could be involved in causing trembles and milk sickness.

Bryan L. Stegelmeier – One of the best experts on this subject based on the ideXlab platform.

  • Effect of grinding and long-term storage on the toxicity of white snakeroot (Ageratina Altissima) in goats
    Research in veterinary science, 2018
    Co-Authors: T. Zane Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Carol G. Chitko-mckown
    Abstract:

    Abstract White snakeroot (Ageratina Altissima) contains the putative toxin tremetone and can produce a disease called “trembles” or “milk sickness”. However the toxicity of tremetone has not been demonstrated in vivo. It has been reported that the plant is less toxic after drying and grinding. The objectives of these studies were to determine: 1) the toxic effect of grinding white snakeroot 4 months prior to dosing and, 2) the toxic effect of storing white snakeroot at ambient temperature for 5 years. Dried white snakeroot, ground 1 day, 1 month, and 4 months prior to dosing, was orally gavaged to goats at 2% of their body weight for up to 28 days or until they were minimally poisoned (minimal muscular weakness and increased serum creatine kinase (CK) activities). All four goats dosed with white snakeroot that had been ground 4 months previously and stored at room temperature were poisoned, became exercise intolerant, and had increased serum CK activities (>5600 U/ L). White snakeroot stored for 5 years was toxic as 3 of 5 dosed goats developed clinical disease within only 6 days of dosing even though approximately 80% of the tremetone in the plant had disappeared during the 5-year storage period. The results from this study demonstrate that previous grinding and extended storage did not significantly alter white snakeroot toxicity. The results also indicate that tremetone concentration is not the singular indicator of toxicity and that other white snakeroot toxins or toxic tremetone degradation products remain in dried, stored white snakeroot.

  • Toxicity of white snakeroot (Ageratina Altissima) and chemical extracts of white snakeroot in goats.
    Journal of agricultural and food chemistry, 2015
    Co-Authors: T. Zane Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Mark G. Collett, Steven R Buck, James A. Pfister
    Abstract:

    White snakeroot (Ageratina Altissima) is a sporadically toxic plant that causes trembles in livestock and milk sickness in humans that drink tainted milk. The putative toxin in white snakeroot is tremetone and possibly other benzofuran ketones, even though it has not been demonstrated in vivo. Toxic white snakeroot was dosed to goats, and they developed clinical signs of poisoning, exercise intolerance, significant increases in serum enzyme activities, and histological changes. Tremetone and the other benzofuran ketones were extracted with hexane; the extracts and residues were analyzed for tremetone and dosed to goats at tremetone and benzofuran ketone concentrations similar to the original plant material. However, none of the dosed goats developed the disease. The results demonstrate for the first time that white snakeroot is a potent myotoxin in goats and that other compound(s), which may be lost or modified during the extraction process, could be involved in causing trembles and milk sickness.

  • Toxicity of White Snakeroot (Ageratina Altissima) and Chemical Extracts of White Snakeroot in Goats
    , 2015
    Co-Authors: Zane T Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Mark G. Collett, Steven R Buck, James A. Pfister
    Abstract:

    White snakeroot (Ageratina Altissima) is a sporadically toxic plant that causes trembles in livestock and milk sickness in humans that drink tainted milk. The putative toxin in white snakeroot is tremetone and possibly other benzofuran ketones, even though it has not been demonstrated in vivo. Toxic white snakeroot was dosed to goats, and they developed clinical signs of poisoning, exercise intolerance, significant increases in serum enzyme activities, and histological changes. Tremetone and the other benzofuran ketones were extracted with hexane; the extracts and residues were analyzed for tremetone and dosed to goats at tremetone and benzofuran ketone concentrations similar to the original plant material. However, none of the dosed goats developed the disease. The results demonstrate for the first time that white snakeroot is a potent myotoxin in goats and that other compound(s), which may be lost or modified during the extraction process, could be involved in causing trembles and milk sickness

T. Zane Davis – One of the best experts on this subject based on the ideXlab platform.

  • Effect of grinding and long-term storage on the toxicity of white snakeroot (Ageratina Altissima) in goats
    Research in veterinary science, 2018
    Co-Authors: T. Zane Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Carol G. Chitko-mckown
    Abstract:

    Abstract White snakeroot (Ageratina Altissima) contains the putative toxin tremetone and can produce a disease called “trembles” or “milk sickness”. However the toxicity of tremetone has not been demonstrated in vivo. It has been reported that the plant is less toxic after drying and grinding. The objectives of these studies were to determine: 1) the toxic effect of grinding white snakeroot 4 months prior to dosing and, 2) the toxic effect of storing white snakeroot at ambient temperature for 5 years. Dried white snakeroot, ground 1 day, 1 month, and 4 months prior to dosing, was orally gavaged to goats at 2% of their body weight for up to 28 days or until they were minimally poisoned (minimal muscular weakness and increased serum creatine kinase (CK) activities). All four goats dosed with white snakeroot that had been ground 4 months previously and stored at room temperature were poisoned, became exercise intolerant, and had increased serum CK activities (>5600 U/ L). White snakeroot stored for 5 years was toxic as 3 of 5 dosed goats developed clinical disease within only 6 days of dosing even though approximately 80% of the tremetone in the plant had disappeared during the 5-year storage period. The results from this study demonstrate that previous grinding and extended storage did not significantly alter white snakeroot toxicity. The results also indicate that tremetone concentration is not the singular indicator of toxicity and that other white snakeroot toxins or toxic tremetone degradation products remain in dried, stored white snakeroot.

  • Toxicity of white snakeroot (Ageratina Altissima) and chemical extracts of white snakeroot in goats.
    Journal of agricultural and food chemistry, 2015
    Co-Authors: T. Zane Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Mark G. Collett, Steven R Buck, James A. Pfister
    Abstract:

    White snakeroot (Ageratina Altissima) is a sporadically toxic plant that causes trembles in livestock and milk sickness in humans that drink tainted milk. The putative toxin in white snakeroot is tremetone and possibly other benzofuran ketones, even though it has not been demonstrated in vivo. Toxic white snakeroot was dosed to goats, and they developed clinical signs of poisoning, exercise intolerance, significant increases in serum enzyme activities, and histological changes. Tremetone and the other benzofuran ketones were extracted with hexane; the extracts and residues were analyzed for tremetone and dosed to goats at tremetone and benzofuran ketone concentrations similar to the original plant material. However, none of the dosed goats developed the disease. The results demonstrate for the first time that white snakeroot is a potent myotoxin in goats and that other compound(s), which may be lost or modified during the extraction process, could be involved in causing trembles and milk sickness.

  • Evaluation of Drying Methods and Toxicity of Rayless Goldenrod (Isocoma pluriflora) and White Snakeroot (Ageratina Altissima) in Goats
    Journal of agricultural and food chemistry, 2012
    Co-Authors: Stephen T. Lee, T. Zane Davis, Daniel Cook, Bryan L. Stegelmeier
    Abstract:

    White snakeroot and rayless goldenrod cause “trembles” and “milk sickness” in livestock and humans, respectively. The toxin in white snakeroot and rayless goldenrod was identified in 1927 and 1930, respectively, as tremetol. It was reported that the toxin in white snakeroot disappears as it is dried and that completely dried plants were incapable of producing trembles or milk sickness. Conversely, it has been reported that the rayless goldenrod toxin was not destroyed by drying and that the plant is toxic either fresh or dry. In this study the concentrations of tremetone, dehydrotremetone, and structurally similar compounds were determined in white snakeroot and rayless goldenrod before and after various drying conditions. Tremetone, dehydrotremetone, and structurally similar compounds in rayless goldenrod and white snakeroot are most stable upon freeze-drying, followed by air-drying, and least stable upon oven-drying (60 °C). Also demonstrated is that tremetone is stable and that dried white snakeroot an…

Wendi D. Roe – One of the best experts on this subject based on the ideXlab platform.

  • Untargeted metabolic profiling of dogs with a suspected toxic mitochondrial myopathy using liquid chromatography-mass spectrometry.
    Toxicon : official journal of the International Society on Toxinology, 2019
    Co-Authors: H. Hunt, Karl Fraser, Nicholas J. Cave, Brett D. Gartrell, Ja Petersen, Wendi D. Roe
    Abstract:

    ‘Go Slow myopathy‘ (GSM) is a suspected toxic myopmyopathy in dogs that primarily occurs in the North Island of New Zealand, and affected dogs usually have a history of consuming meat, offal or bones from wild pigs (including previously frozen and/or cooked meat). Previous epidemiological and pathological studies on GSM have demonstrated that changes in mitochondrial structure and function are most likely caused by an environmental toxin that dogs are exposed to through the ingestion of wild pig. The disease has clinical, histological and biochemical similarities to poisoning in people and animals from the plant Ageratina Altissima (white snakeroot). Aqueous and lipid extracts were prepared from liver samples of 24 clinically normal dogs and 15 dogs with GSM for untargeted liquid chrochromatography-mass spectrometry. Group-wise comparisons of mass spectral data revealed 38 features that were significantly different (FDR

  • untargeted metabolic profiling of dogs with a suspected toxic mitochondrial myopathy using liquid chromatography mass spectrometry
    Toxicon, 2019
    Co-Authors: H. Hunt, Karl Fraser, Nicholas J. Cave, Brett D. Gartrell, Ja Petersen, Wendi D. Roe
    Abstract:

    ‘Go Slow myopathy‘ (GSM) is a suspected toxic myopmyopathy in dogs that primarily occurs in the North Island of New Zealand, and affected dogs usually have a history of consuming meat, offal or bones from wild pigs (including previously frozen and/or cooked meat). Previous epidemiological and pathological studies on GSM have demonstrated that changes in mitochondrial structure and function are most likely caused by an environmental toxin that dogs are exposed to through the ingestion of wild pig. The disease has clinical, histological and biochemical similarities to poisoning in people and animals from the plant Ageratina Altissima (white snakeroot). Aqueous and lipid extracts were prepared from liver samples of 24 clinically normal dogs and 15 dogs with GSM for untargeted liquid chrochromatography-mass spectrometry. Group-wise comparisons of mass spectral data revealed 38 features that were significantly different (FDR<0.05) between normal dogs and those with GSM in aqueous extracts, and 316 significantly different features in lipid extracts. No definitive cause of the myopathy was identified, but alkaloids derived from several plant species were among the possible identities of features that were more abundant in liver samples from affected dogs compared to normal dogs. Mass spectral data also revealed that dogs with GSM have reduced hepatic phospholipid and sphingolipid concentrations relative to normal dogs. In addition, affected dogs had changes in the abundance of kynurenic acid, various dicarboxylic acids and N-acetylated branch chain amino acids, suggestive of mitochondrial dysfunction.

Tim J. Evans – One of the best experts on this subject based on the ideXlab platform.