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Stephen T. Lee - One of the best experts on this subject based on the ideXlab platform.
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Effect of grinding and long-term storage on the toxicity of white snakeroot (Ageratina Altissima) in goats
Research in veterinary science, 2018Co-Authors: T. Zane Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Carol G. Chitko-mckownAbstract: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.
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Toxicity of Compounds Isolated from White Snakeroot (Ageratina Altissima) to Adult and Larval Yellow Fever Mosquitoes (Aedes aegypti).
Natural product communications, 2016Co-Authors: Alden S. Estep, James J. Becnel, Stephen T. LeeAbstract: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.
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Toxicity of white snakeroot (Ageratina Altissima) and chemical extracts of white snakeroot in goats.
Journal of agricultural and food chemistry, 2015Co-Authors: T. Zane Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Mark G. Collett, Steven R Buck, James A. PfisterAbstract: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.
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Toxicity of White Snakeroot (Ageratina Altissima) and Chemical Extracts of White Snakeroot in Goats
2015Co-Authors: Zane T Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Mark G. Collett, Steven R Buck, James A. PfisterAbstract: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
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Experimental rayless goldenrod (Isocoma pluriflora) toxicosis in horses
Toxicon : official journal of the International Society on Toxinology, 2013Co-Authors: T.z. Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Jeffery O. HallAbstract:Rayless goldenrod (Isocoma pluriflora) sporadically poisons horses and other livestock in the southwestern United States. Similar to livestock poisoning by white snakeroot (Ageratina Altissima) in the midwestern United States, previous research suggests that benzofuran ketones (BFK: tremetone, dehydrotremetone, 6-hydroxytremetone, and 3-oxyangeloyl-tremetone) are responsible for the toxicity of rayless goldenrod. However, experimental reproduction of rayless goldenrod-induced disease and detailed descriptions of poisoning in horses with known concentrations of tremetone and other BFK has not been documented. In this study four horses were fed increasing amounts of rayless goldenrod to obtain doses of approximately 0, 10, 30, and 60 mg BFK/kg BW for 14 days. After seven days of dosing the horse dosed with 60 mg BFK/kg BW horse developed depression, reluctance to eat, dehydration, trembling, and muscle fatigue. Biochemical alterations including increases in the serum enzyme activities of CK, AST, ALT, and LDH, and increased cardiac troponin I concentration, were also identified. Physiologically the clinically poisoned horse had decreased endurance seen as reluctance to perform on the treadmill with increased resting heart rate and a prolonged recovery of heart rate following treadmill exercise. The condition of the horse continued to decline and it was euthanized and necropsied on day 10. At necropsy the myocardium was pale and soft and many of the appendicular and large apical muscles were pale and moist. Histologically, the myocardium had extensive myocardial degeneration and necrosis with extensive fibrosis and multifocal mineralization. Several of the large appendicular muscles in this horse also had small foci of skeletal muscle degeneration and necrosis. Less severe myocardial changes were also identified in the horse dosed with 30 mg BFK/kg BW after 14 days of dosing. No clinical, biochemical or histologic changes were identified in the control horse and the horse dosed with 10 mg BFK/kg BW. These results suggest that doses of 60 mg BFK/kg BW for seven days produce extensive myocardial lesions in horses. The horse dosed with 30 mg BFK/kg BW developed less severe, but similar myocardial lesions over a longer duration, this suggests that poisoning may be cumulative and lower doses of longer duration are also toxic. Horses seem to be uniquely sensitive to rayless goldenrod-induced myocardial disease, therefore cardiac troponin I may be a useful marker of rayless goldenrod poisoning in horses. More work is needed to determine which BFK produce myocardial toxicity and better determine the effects of dose and duration on poisoning in horses.
Bryan L. Stegelmeier - One of the best experts on this subject based on the ideXlab platform.
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Effect of grinding and long-term storage on the toxicity of white snakeroot (Ageratina Altissima) in goats
Research in veterinary science, 2018Co-Authors: T. Zane Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Carol G. Chitko-mckownAbstract: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.
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Toxicity of white snakeroot (Ageratina Altissima) and chemical extracts of white snakeroot in goats.
Journal of agricultural and food chemistry, 2015Co-Authors: T. Zane Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Mark G. Collett, Steven R Buck, James A. PfisterAbstract: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.
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Toxicity of White Snakeroot (Ageratina Altissima) and Chemical Extracts of White Snakeroot in Goats
2015Co-Authors: Zane T Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Mark G. Collett, Steven R Buck, James A. PfisterAbstract: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
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Experimental rayless goldenrod (Isocoma pluriflora) toxicosis in horses
Toxicon : official journal of the International Society on Toxinology, 2013Co-Authors: T.z. Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Jeffery O. HallAbstract:Rayless goldenrod (Isocoma pluriflora) sporadically poisons horses and other livestock in the southwestern United States. Similar to livestock poisoning by white snakeroot (Ageratina Altissima) in the midwestern United States, previous research suggests that benzofuran ketones (BFK: tremetone, dehydrotremetone, 6-hydroxytremetone, and 3-oxyangeloyl-tremetone) are responsible for the toxicity of rayless goldenrod. However, experimental reproduction of rayless goldenrod-induced disease and detailed descriptions of poisoning in horses with known concentrations of tremetone and other BFK has not been documented. In this study four horses were fed increasing amounts of rayless goldenrod to obtain doses of approximately 0, 10, 30, and 60 mg BFK/kg BW for 14 days. After seven days of dosing the horse dosed with 60 mg BFK/kg BW horse developed depression, reluctance to eat, dehydration, trembling, and muscle fatigue. Biochemical alterations including increases in the serum enzyme activities of CK, AST, ALT, and LDH, and increased cardiac troponin I concentration, were also identified. Physiologically the clinically poisoned horse had decreased endurance seen as reluctance to perform on the treadmill with increased resting heart rate and a prolonged recovery of heart rate following treadmill exercise. The condition of the horse continued to decline and it was euthanized and necropsied on day 10. At necropsy the myocardium was pale and soft and many of the appendicular and large apical muscles were pale and moist. Histologically, the myocardium had extensive myocardial degeneration and necrosis with extensive fibrosis and multifocal mineralization. Several of the large appendicular muscles in this horse also had small foci of skeletal muscle degeneration and necrosis. Less severe myocardial changes were also identified in the horse dosed with 30 mg BFK/kg BW after 14 days of dosing. No clinical, biochemical or histologic changes were identified in the control horse and the horse dosed with 10 mg BFK/kg BW. These results suggest that doses of 60 mg BFK/kg BW for seven days produce extensive myocardial lesions in horses. The horse dosed with 30 mg BFK/kg BW developed less severe, but similar myocardial lesions over a longer duration, this suggests that poisoning may be cumulative and lower doses of longer duration are also toxic. Horses seem to be uniquely sensitive to rayless goldenrod-induced myocardial disease, therefore cardiac troponin I may be a useful marker of rayless goldenrod poisoning in horses. More work is needed to determine which BFK produce myocardial toxicity and better determine the effects of dose and duration on poisoning in horses.
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Evaluation of Drying Methods and Toxicity of Rayless Goldenrod (Isocoma pluriflora) and White Snakeroot (Ageratina Altissima) in Goats
Journal of agricultural and food chemistry, 2012Co-Authors: Stephen T. Lee, T. Zane Davis, Daniel Cook, Bryan L. StegelmeierAbstract: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...
T. Zane Davis - One of the best experts on this subject based on the ideXlab platform.
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Effect of grinding and long-term storage on the toxicity of white snakeroot (Ageratina Altissima) in goats
Research in veterinary science, 2018Co-Authors: T. Zane Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Carol G. Chitko-mckownAbstract: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.
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Toxicity of white snakeroot (Ageratina Altissima) and chemical extracts of white snakeroot in goats.
Journal of agricultural and food chemistry, 2015Co-Authors: T. Zane Davis, Stephen T. Lee, Benedict T. Green, Bryan L. Stegelmeier, Mark G. Collett, Steven R Buck, James A. PfisterAbstract: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.
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Evaluation of Drying Methods and Toxicity of Rayless Goldenrod (Isocoma pluriflora) and White Snakeroot (Ageratina Altissima) in Goats
Journal of agricultural and food chemistry, 2012Co-Authors: Stephen T. Lee, T. Zane Davis, Daniel Cook, Bryan L. StegelmeierAbstract: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...
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Tremetone and structurally related compounds in white snakeroot ( Ageratina Altissima ): a plant associated with trembles and milk sickness.
Journal of Agricultural and Food Chemistry, 2010Co-Authors: Stephen T. Lee, T. Zane Davis, Dale R. Gardner, Steven M. Colegate, Daniel Cook, Benedict T. Green, Kimberly A. Meyerholtz, Christina R. Wilson, Bryan L. Stegelmeier, Tim J. EvansAbstract:Ingestion of white snakeroot (Ageratina Altissima) can cause trembles in livestock and milk sickness in humans. The toxicity has been associated with tremetol, a relatively crude, multicomponent lipophilic extract of the plant. In this study, 11 different compounds were isolated from white snakeroot-derived lipophilic extracts from 18 collections. Six of the isolated compounds have not been previously reported to be found in white snakeroot. High-performance liquid chromatography (HPLC) analysis indicated that there are three different chemotypes of white snakeroot from the plant samples analyzed. Elucidation of these chemotypes may explain the sporadic and unpredictable toxicity of white snakeroot to livestock and humans.
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Experimental Rayless Goldenrod (Isocoma pluriflora) Toxicosis in Goats
Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians Inc, 2010Co-Authors: Bryan L. Stegelmeier, Stephen T. Lee, T. Zane Davis, Benedict T. Green, Jeffery O. HallAbstract:Rayless goldenrod (Isocoma pluriflora) sporadically poisons livestock in the southwestern United States. Similarities with white snakeroot (Ageratina Altissima) poisoning and nearly identical chemical analyses led early researchers to conclude that tremetol, a mixture of benzofuran ketones, is the rayless goldenrod toxin. The toxicity of these ketone toxins have not been fully characterized nor are the pathogenesis and sequelae of poisoning completely understood. The objective of the current study was to characterize and describe the clinical and pathologic changes of rayless goldenrod toxicity in goats. Fifteen goats were gavaged with rayless goldenrod to obtain benzofuran ketone doses of 0, 10, 20, 40, and 60 mg/kg/day. After 7 treatment days, the goats were euthanized, necropsied, and tissues were processed for microscopic studies. After 5 or 6 days of treatment, the 40-mg/kg and 60-mg/kg goats were reluctant to move, stood with an erect stance, and became exercise intolerant. They had increased resting heart rate, prolonged recovery following exercise, and increased serum aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and creatinine kinase activities. All treated animals developed skeletal myopathy with dose-related distribution and severity. The goats dosed with 20 mg/kg and higher also developed myocardial degeneration and necrosis. Although skeletal myonecrosis was patchy and widely distributed, the quadriceps femoris was consistently damaged, even in low-dosed animals. Myocardial lesions were most severe in the papillary muscles of 60-mg/kg-dosed animals. This indicates that goats are highly susceptible to rayless goldenrod poisoning, and that the characteristic lesion of poisoning is skeletal and cardiac myonecrosis.
Wendi D. Roe - One of the best experts on this subject based on the ideXlab platform.
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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, 2019Co-Authors: H. Hunt, Karl Fraser, Nicholas J. Cave, Brett D. Gartrell, Ja Petersen, Wendi D. RoeAbstract:'Go Slow myopathy' (GSM) is a suspected toxic myopathy 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 chromatography-mass spectrometry. Group-wise comparisons of mass spectral data revealed 38 features that were significantly different (FDR
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untargeted metabolic profiling of dogs with a suspected toxic mitochondrial myopathy using liquid chromatography mass spectrometry
Toxicon, 2019Co-Authors: H. Hunt, Karl Fraser, Nicholas J. Cave, Brett D. Gartrell, Ja Petersen, Wendi D. RoeAbstract:'Go Slow myopathy' (GSM) is a suspected toxic myopathy 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 chromatography-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.
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Tremetone and structurally related compounds in white snakeroot ( Ageratina Altissima ): a plant associated with trembles and milk sickness.
Journal of Agricultural and Food Chemistry, 2010Co-Authors: Stephen T. Lee, T. Zane Davis, Dale R. Gardner, Steven M. Colegate, Daniel Cook, Benedict T. Green, Kimberly A. Meyerholtz, Christina R. Wilson, Bryan L. Stegelmeier, Tim J. EvansAbstract:Ingestion of white snakeroot (Ageratina Altissima) can cause trembles in livestock and milk sickness in humans. The toxicity has been associated with tremetol, a relatively crude, multicomponent lipophilic extract of the plant. In this study, 11 different compounds were isolated from white snakeroot-derived lipophilic extracts from 18 collections. Six of the isolated compounds have not been previously reported to be found in white snakeroot. High-performance liquid chromatography (HPLC) analysis indicated that there are three different chemotypes of white snakeroot from the plant samples analyzed. Elucidation of these chemotypes may explain the sporadic and unpredictable toxicity of white snakeroot to livestock and humans.
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quantitative method for the measurement of three benzofuran ketones in rayless goldenrod isocoma pluriflora and white snakeroot Ageratina Altissima by high performance liquid chromatography hplc
Journal of Agricultural and Food Chemistry, 2009Co-Authors: Stephen T. Lee, Dale R. Gardner, Bryan L. Stegelmeier, Zane T Davis, Tim J. EvansAbstract:White snakeroot ( Ageratina Altissima ) and rayless goldenrod ( Isocoma pluriflora ) can cause "trembles" and "milk sickness" in livestock and humans, respectively. Tremetol, a complex mixture of sterols and derivatives of methyl ketone benzofuran has been extracted from white snakeroot and rayless goldenrod and is reported to be the toxic substance in plant material. In this study, the three major benzofuran ketones, tremetone, dehydrotremetone, and 3-oxyangeloyl-tremetone, were isolated from rayless goldenrod. Using these compounds as standards, a quantitative high-performance liquid chromatography (HPLC) method was developed to measure these compounds in white snakeroot and rayless goldenrod. Concentrations of tremetone, dehydrotremetone, and 3-oxyangeloyl-tremetone were found to vary considerably among the different white snakeroot and rayless goldenrod plant collections. Differences in concentrations of tremetone, dehydrotremetone, and 3-oxyangeloyl-tremetone in white snakeroot and rayless goldenrod plants may explain the historical sporadic and unpredictable toxicity of these plants to livestock and humans.
