Karwinskia humboldtiana

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Jaime Garciajuarez - One of the best experts on this subject based on the ideXlab platform.

  • damage to pancreatic acinar cells and preservation of islets of langerhans in a rat model of acute pancreatitis induced by Karwinskia humboldtiana buckthorn
    Histology and Histopathology, 2016
    Co-Authors: Katya Carcanodiaz, Aracely Garciagarcia, Juan Carlos Segovianoramirez, Humberto Rodriguezrocha, Maria De Jesus Loeraarias, Jaime Garciajuarez
    Abstract:

    Karwinskia humboldtiana (Kh) is a poisonous plant that grows in some regions of the American continent. Consuming large amounts of Kh fruit results in acute intoxication leading to respiratory failure, culminating in death within days. There is evidence of histological damage to the lungs, liver, and kidneys following accidental and experimental Kh intoxication. To date, the microscopic effect of Kh consumption on the pancreas has not been described. We examined the early effects of Kh fruit on pancreatic tissue at different stages of acute intoxication in the Wistar rat. We found progressive damage confined to the exocrine pancreas, starting with a reduction in the number of zymogen granules, loss of acinar architecture, the presence of autophagy-like vesicles, apoptosis and inflammatory infiltrate. The pancreatic pathology culminated in damaged acini characterized by necrosis and edema, with a complete loss of lobular architecture. Interestingly, the morphology of the islets of Langerhans was conserved throughout our evaluations. Taken together, our results indicate the damage induced by a high dose of Kh fruit in the Wistar rat is consistent with an early acute necrotizing pancreatitis that exclusively affects the exocrine pancreas. Therefore, this system might be useful as an animal model to study the treatment of pancreatic diseases. More importantly, as the islets of Langerhans were preserved, the active compounds of Kh fruit could be utilized for the treatment of acinar pancreatic cancer. Further studies might provide insight into the severity of acute Kh intoxication in humans and influence the design of treatments for pancreatic diseases and acinar pancreatic cancer.

  • histopathological alterations in the striatum caused by Karwinskia humboldtiana buckthorn fruit in an experimental model of peripheral neuropathy
    Histology and Histopathology, 2016
    Co-Authors: R N Diazperez, Jaime Garciajuarez, Martha E Salazarleal, Odila Saucedocardenas, J A Castillogonzalez, K Carcanodiaz, Gerardo Enrique Munozmaldonado, Roberto Montesdeocaluna, Adolfo Sotodominguez
    Abstract:

    The accidental ingestion of Karwinskia humboldtiana (Kh) fruit in humans and animals causes chronic or acute intoxication. Acute poisoning induces respiratory failure that progresses rapidly to death. Studies in animals intoxicated with Kh describe lesions in cerebral cortex, cerebellum, spinal cord, hippocampus and caudate nucleus. Kh intoxication in Wistar rats models the sub-lethal clinical phase observed in humans. Considering these reports, the present study analyzed the histopathological alterations within the striatum following experimental Kh intoxication. Twenty Wistar rats were divided into three groups (n=5) and were intoxicated with Kh fruit. A control group (n=5) was included. Animals were euthanized at several time points (48, 58 and 170 days post-intoxication). The brain was collected, divided and processed for conventional histology or electron microscopy. Sections were stained with hematoxylin and eosin, cresyl violet, Kluver-Barrera, and toluidine blue. Immunolabeling was performed for glial cells in the striatum, and the samples were analyzed with light microscopy. Morphometric and statistical analyses were performed. In control group, neurons, axon bundles and neuropil had a normal appearance. At 48 days, hyperchromic neurons with apparent decreased size were observed interspersed among the normal neurons. At 58 days, we observed an increased number of hyperchromic neurons and disorganization of the myelin sheath and neuropil. At 170 days, these alterations persisted in the paralysis group. In treated groups, we observed signs of gliosis and increased axonal diameters. This study is the first report that describes the histopathological alterations within the striatum caused by chronic intoxication with Kh fruit in the Wistar rat

  • evaluacion del efecto del tratamiento con acido lipoico administrado a la rata wistar intoxicada con el fruto de Karwinskia humboldtiana
    International Journal of Morphology, 2012
    Co-Authors: Jaime Garciajuarez, Martha E Salazarleal, Santos Guzmanlopez, Viktor J Romerodiaz, Rosalba Ramirezduron, Julio Sepulvedasaavedra
    Abstract:

    La ingesta accidental de fruto de Karwinskia humboldtiana ocasiona una paralisis flacida, simetrica, progresiva y ascendente, similar al sindrome de Guillain-Barre. Evoluciona en el transcurso de 3 a 12 meses hasta su recuperacion total, pero los casos graves terminan en la muerte por insuficiencia respiratoria. No existe un tratamiento especifico. La lesion histopatologica descrita en nervio periferico de pacientes, y animales de experimentacion corresponde a una desmielinizacion segmentaria acompanada de degeneracion Walleriana. Una de las toxinas extraidas a partir de la semilla, la T-514, ocasiona un incremento de radicales libres in vitro. Los radicales libres se han relacionado con la desmielinizacion que se presenta en otros tipos de neuropatias como en la diabetica. Ya que la lesion ultraestructural que se presenta en los modelos animales de diabetes es similar a la que se observa en la intoxicacion experimental con fruto de K. humboldtiana, se decidio administrar un potente agente antioxidante, el acido a-lipoico en un modelo de intoxicacion cronica por fruto de K. humboldtiana. Sin embargo, no se observo mejoria sobre las manifestaciones clinicas evaluadas en los animales o sobre las lesiones histopatologicas presentes en el nervio periferico. Estos resultados sugieren que los radicales libres no son el mecanismo principal de lesion sobre el nervio periferico en la polineuropatia causada por K. humboldtiana.

  • evaluacion del efecto del tratamiento con acido lipoico administrado a la rata wistar intoxicada con el fruto de Karwinskia humboldtiana evaluation of the effect of treatment with lipoic acid administered to the wistar rat intoxicated with the fruit
    2012
    Co-Authors: Jaime Garciajuarez, Martha E Salazarleal, Santos Guzmanlopez, Viktor J Romerodiaz, Rosalba Ramirezduron
    Abstract:

    Julio Sepulveda-SaavedraGARCIA-JUAREZ, J.; SALAZAR-LEAL, M. E.; GUZMAN-LOPEZ, S.; ROMERO-DIAZ, V. J.; RAMIREZ-DURON, R. S Acido lipoico; Polineuropatia; Desmielinizacion; Paralisis.

Martha E Salazarleal - One of the best experts on this subject based on the ideXlab platform.

  • histopathological alterations in the striatum caused by Karwinskia humboldtiana buckthorn fruit in an experimental model of peripheral neuropathy
    Histology and Histopathology, 2016
    Co-Authors: R N Diazperez, Jaime Garciajuarez, Martha E Salazarleal, Odila Saucedocardenas, J A Castillogonzalez, K Carcanodiaz, Gerardo Enrique Munozmaldonado, Roberto Montesdeocaluna, Adolfo Sotodominguez
    Abstract:

    The accidental ingestion of Karwinskia humboldtiana (Kh) fruit in humans and animals causes chronic or acute intoxication. Acute poisoning induces respiratory failure that progresses rapidly to death. Studies in animals intoxicated with Kh describe lesions in cerebral cortex, cerebellum, spinal cord, hippocampus and caudate nucleus. Kh intoxication in Wistar rats models the sub-lethal clinical phase observed in humans. Considering these reports, the present study analyzed the histopathological alterations within the striatum following experimental Kh intoxication. Twenty Wistar rats were divided into three groups (n=5) and were intoxicated with Kh fruit. A control group (n=5) was included. Animals were euthanized at several time points (48, 58 and 170 days post-intoxication). The brain was collected, divided and processed for conventional histology or electron microscopy. Sections were stained with hematoxylin and eosin, cresyl violet, Kluver-Barrera, and toluidine blue. Immunolabeling was performed for glial cells in the striatum, and the samples were analyzed with light microscopy. Morphometric and statistical analyses were performed. In control group, neurons, axon bundles and neuropil had a normal appearance. At 48 days, hyperchromic neurons with apparent decreased size were observed interspersed among the normal neurons. At 58 days, we observed an increased number of hyperchromic neurons and disorganization of the myelin sheath and neuropil. At 170 days, these alterations persisted in the paralysis group. In treated groups, we observed signs of gliosis and increased axonal diameters. This study is the first report that describes the histopathological alterations within the striatum caused by chronic intoxication with Kh fruit in the Wistar rat

  • evaluacion del efecto del tratamiento con acido lipoico administrado a la rata wistar intoxicada con el fruto de Karwinskia humboldtiana
    International Journal of Morphology, 2012
    Co-Authors: Jaime Garciajuarez, Martha E Salazarleal, Santos Guzmanlopez, Viktor J Romerodiaz, Rosalba Ramirezduron, Julio Sepulvedasaavedra
    Abstract:

    La ingesta accidental de fruto de Karwinskia humboldtiana ocasiona una paralisis flacida, simetrica, progresiva y ascendente, similar al sindrome de Guillain-Barre. Evoluciona en el transcurso de 3 a 12 meses hasta su recuperacion total, pero los casos graves terminan en la muerte por insuficiencia respiratoria. No existe un tratamiento especifico. La lesion histopatologica descrita en nervio periferico de pacientes, y animales de experimentacion corresponde a una desmielinizacion segmentaria acompanada de degeneracion Walleriana. Una de las toxinas extraidas a partir de la semilla, la T-514, ocasiona un incremento de radicales libres in vitro. Los radicales libres se han relacionado con la desmielinizacion que se presenta en otros tipos de neuropatias como en la diabetica. Ya que la lesion ultraestructural que se presenta en los modelos animales de diabetes es similar a la que se observa en la intoxicacion experimental con fruto de K. humboldtiana, se decidio administrar un potente agente antioxidante, el acido a-lipoico en un modelo de intoxicacion cronica por fruto de K. humboldtiana. Sin embargo, no se observo mejoria sobre las manifestaciones clinicas evaluadas en los animales o sobre las lesiones histopatologicas presentes en el nervio periferico. Estos resultados sugieren que los radicales libres no son el mecanismo principal de lesion sobre el nervio periferico en la polineuropatia causada por K. humboldtiana.

  • evaluacion del efecto del tratamiento con acido lipoico administrado a la rata wistar intoxicada con el fruto de Karwinskia humboldtiana evaluation of the effect of treatment with lipoic acid administered to the wistar rat intoxicated with the fruit
    2012
    Co-Authors: Jaime Garciajuarez, Martha E Salazarleal, Santos Guzmanlopez, Viktor J Romerodiaz, Rosalba Ramirezduron
    Abstract:

    Julio Sepulveda-SaavedraGARCIA-JUAREZ, J.; SALAZAR-LEAL, M. E.; GUZMAN-LOPEZ, S.; ROMERO-DIAZ, V. J.; RAMIREZ-DURON, R. S Acido lipoico; Polineuropatia; Desmielinizacion; Paralisis.

  • Karwinskia humboldtiana buckthorn fruit causes central nervous system damage during chronic intoxication in the rat
    Toxicon, 2009
    Co-Authors: Eduardo M Becerraverdin, Martha E Salazarleal, Viktor J Romerodiaz, M V Bermudezbarba, Ancer J Rodriguez, Adolfo Sotodominguez, Raquel G Ballesteroseliozondo, Odila Saucedocardenas, Alfredo Pineyro Lopez
    Abstract:

    Abstract Karwinskia humboldtiana fruit (Kh) causes a neurological disorder 3–4 weeks after ingestion, characterized by flaccid, symmetrical, ascending paralysis, similar to the Guillain–Barre syndrome. In this polyneuropathy the lesion (demyelization) in peripheral nerves has been described in several animal species, both in acute and in chronic intoxication. However, no reports exist about the presence of lesions in the Central Nervous System (CNS), in chronic intoxication. We considered it important to evaluate, with histological techniques, the possible presence of lesions in the brain, by using a model of chronic intoxication that reproduces the same stages present in the human intoxication, to better understanding of this pathological process. In our present work we fed the ground Kh fruit to Wistar rats and samples of brain, cerebellum, and pons were embedded in paraffin. Sections were stained with Hematoxylin & Eosin (HE) and special stains for nerve tissue. Histopathological changes were evaluated in the CNS through the different stages of the polyneuropathy and comparison to a control group. With this methodology, we found lesions in the motor pathway. This is the first report about the presence of neuronal damage caused by Kh in the Central Nervous System in chronic intoxication.

  • an experimental model of peripheral neuropathy induced in rats by Karwinskia humboldtiana buckthorn fruit
    Journal of The Peripheral Nervous System, 2006
    Co-Authors: Martha E Salazarleal, Viktor J Romerodiaz, Julio Sepulvedasaavedra, Hector R Martinez, Alfredo Pineyrolopez, Victor Armando Tamezrodriguez, M S Flores, Eduardo M Becerraverdin, Maria Victoria Bermudez
    Abstract:

    Abstract  Intoxication by Karwinskia humboldtiana (buckthorn) fruit presents a neurological picture similar to that of Guillain-Barre syndrome. In this report, we describe an experimental animal model of peripheral neuropathy induced by buckthorn fruit. Four groups of Wistar rats received one oral dose of 1.5 g/kg followed by oral doses of 0.5 g/kg at days 3, 7, 10, and 14 of dried and ground buckthorn fruit in aqueous suspension. Rats were sacrificed at 24, 48, 58, and 112 days after initial dose. Treated animals developed progressive paralysis through 58 days, then completely recovered by 112 days. Sciatic nerves showed segmental demyelination and cellular infiltrates until 58 days after exposure and then remyelinating changes at 112 days. This experimental model for peripheral neuropathy is reproducible and easy to handle. Its manipulation is relatively innocuous and allows us to study reversible peripheral nerve damage. This model can be developed in other animal species and may be useful to test new therapies for peripheral neuropathy.

Viktor J Romerodiaz - One of the best experts on this subject based on the ideXlab platform.

  • evaluacion del efecto del tratamiento con acido lipoico administrado a la rata wistar intoxicada con el fruto de Karwinskia humboldtiana
    International Journal of Morphology, 2012
    Co-Authors: Jaime Garciajuarez, Martha E Salazarleal, Santos Guzmanlopez, Viktor J Romerodiaz, Rosalba Ramirezduron, Julio Sepulvedasaavedra
    Abstract:

    La ingesta accidental de fruto de Karwinskia humboldtiana ocasiona una paralisis flacida, simetrica, progresiva y ascendente, similar al sindrome de Guillain-Barre. Evoluciona en el transcurso de 3 a 12 meses hasta su recuperacion total, pero los casos graves terminan en la muerte por insuficiencia respiratoria. No existe un tratamiento especifico. La lesion histopatologica descrita en nervio periferico de pacientes, y animales de experimentacion corresponde a una desmielinizacion segmentaria acompanada de degeneracion Walleriana. Una de las toxinas extraidas a partir de la semilla, la T-514, ocasiona un incremento de radicales libres in vitro. Los radicales libres se han relacionado con la desmielinizacion que se presenta en otros tipos de neuropatias como en la diabetica. Ya que la lesion ultraestructural que se presenta en los modelos animales de diabetes es similar a la que se observa en la intoxicacion experimental con fruto de K. humboldtiana, se decidio administrar un potente agente antioxidante, el acido a-lipoico en un modelo de intoxicacion cronica por fruto de K. humboldtiana. Sin embargo, no se observo mejoria sobre las manifestaciones clinicas evaluadas en los animales o sobre las lesiones histopatologicas presentes en el nervio periferico. Estos resultados sugieren que los radicales libres no son el mecanismo principal de lesion sobre el nervio periferico en la polineuropatia causada por K. humboldtiana.

  • evaluacion del efecto del tratamiento con acido lipoico administrado a la rata wistar intoxicada con el fruto de Karwinskia humboldtiana evaluation of the effect of treatment with lipoic acid administered to the wistar rat intoxicated with the fruit
    2012
    Co-Authors: Jaime Garciajuarez, Martha E Salazarleal, Santos Guzmanlopez, Viktor J Romerodiaz, Rosalba Ramirezduron
    Abstract:

    Julio Sepulveda-SaavedraGARCIA-JUAREZ, J.; SALAZAR-LEAL, M. E.; GUZMAN-LOPEZ, S.; ROMERO-DIAZ, V. J.; RAMIREZ-DURON, R. S Acido lipoico; Polineuropatia; Desmielinizacion; Paralisis.

  • Karwinskia humboldtiana buckthorn fruit causes central nervous system damage during chronic intoxication in the rat
    Toxicon, 2009
    Co-Authors: Eduardo M Becerraverdin, Martha E Salazarleal, Viktor J Romerodiaz, M V Bermudezbarba, Ancer J Rodriguez, Adolfo Sotodominguez, Raquel G Ballesteroseliozondo, Odila Saucedocardenas, Alfredo Pineyro Lopez
    Abstract:

    Abstract Karwinskia humboldtiana fruit (Kh) causes a neurological disorder 3–4 weeks after ingestion, characterized by flaccid, symmetrical, ascending paralysis, similar to the Guillain–Barre syndrome. In this polyneuropathy the lesion (demyelization) in peripheral nerves has been described in several animal species, both in acute and in chronic intoxication. However, no reports exist about the presence of lesions in the Central Nervous System (CNS), in chronic intoxication. We considered it important to evaluate, with histological techniques, the possible presence of lesions in the brain, by using a model of chronic intoxication that reproduces the same stages present in the human intoxication, to better understanding of this pathological process. In our present work we fed the ground Kh fruit to Wistar rats and samples of brain, cerebellum, and pons were embedded in paraffin. Sections were stained with Hematoxylin & Eosin (HE) and special stains for nerve tissue. Histopathological changes were evaluated in the CNS through the different stages of the polyneuropathy and comparison to a control group. With this methodology, we found lesions in the motor pathway. This is the first report about the presence of neuronal damage caused by Kh in the Central Nervous System in chronic intoxication.

  • an experimental model of peripheral neuropathy induced in rats by Karwinskia humboldtiana buckthorn fruit
    Journal of The Peripheral Nervous System, 2006
    Co-Authors: Martha E Salazarleal, Viktor J Romerodiaz, Julio Sepulvedasaavedra, Hector R Martinez, Alfredo Pineyrolopez, Victor Armando Tamezrodriguez, M S Flores, Eduardo M Becerraverdin, Maria Victoria Bermudez
    Abstract:

    Abstract  Intoxication by Karwinskia humboldtiana (buckthorn) fruit presents a neurological picture similar to that of Guillain-Barre syndrome. In this report, we describe an experimental animal model of peripheral neuropathy induced by buckthorn fruit. Four groups of Wistar rats received one oral dose of 1.5 g/kg followed by oral doses of 0.5 g/kg at days 3, 7, 10, and 14 of dried and ground buckthorn fruit in aqueous suspension. Rats were sacrificed at 24, 48, 58, and 112 days after initial dose. Treated animals developed progressive paralysis through 58 days, then completely recovered by 112 days. Sciatic nerves showed segmental demyelination and cellular infiltrates until 58 days after exposure and then remyelinating changes at 112 days. This experimental model for peripheral neuropathy is reproducible and easy to handle. Its manipulation is relatively innocuous and allows us to study reversible peripheral nerve damage. This model can be developed in other animal species and may be useful to test new therapies for peripheral neuropathy.

Maria Victoria Bermudez - One of the best experts on this subject based on the ideXlab platform.

  • an experimental model of peripheral neuropathy induced in rats by Karwinskia humboldtiana buckthorn fruit
    Journal of The Peripheral Nervous System, 2006
    Co-Authors: Martha E Salazarleal, Viktor J Romerodiaz, Julio Sepulvedasaavedra, Hector R Martinez, Alfredo Pineyrolopez, Victor Armando Tamezrodriguez, M S Flores, Eduardo M Becerraverdin, Maria Victoria Bermudez
    Abstract:

    Abstract  Intoxication by Karwinskia humboldtiana (buckthorn) fruit presents a neurological picture similar to that of Guillain-Barre syndrome. In this report, we describe an experimental animal model of peripheral neuropathy induced by buckthorn fruit. Four groups of Wistar rats received one oral dose of 1.5 g/kg followed by oral doses of 0.5 g/kg at days 3, 7, 10, and 14 of dried and ground buckthorn fruit in aqueous suspension. Rats were sacrificed at 24, 48, 58, and 112 days after initial dose. Treated animals developed progressive paralysis through 58 days, then completely recovered by 112 days. Sciatic nerves showed segmental demyelination and cellular infiltrates until 58 days after exposure and then remyelinating changes at 112 days. This experimental model for peripheral neuropathy is reproducible and easy to handle. Its manipulation is relatively innocuous and allows us to study reversible peripheral nerve damage. This model can be developed in other animal species and may be useful to test new therapies for peripheral neuropathy.

  • clinical diagnosis in Karwinskia humboldtiana polyneuropathy
    Journal of the Neurological Sciences, 1998
    Co-Authors: Hector R Martinez, Ricardo A Rangelguerra, Maria Victoria Bermudez, Laura De Leon Flores
    Abstract:

    Intoxication by Karwinskia humboldtiana presents a neurological picture similar to that for Guillain-Barre syndrome or other polyradiculoneuropathies. Clinical diagnosis in poisoned humans may be difficult if no evidence of previous fruit ingestion is available. We present our experience in the clinical diagnosis of Karwinskia humboldtiana polyneuropathy, as confirmed by toxin detection in blood. We designed an open trial at the Pediatric Neurology service and included all cases with acute ascending paralysis that were admitted to our hospital in the last two years. In all cases, we performed hematological, immunological and biochemical profiles, CSF analysis including immunological studies, oligoclonal bands and myelin basic protein determinations. Electrodiagnostic studies were performed, including motor conduction velocities, distal latencies, F-wave latency and compound muscle action potential (CAMP) amplitude. The presence of Karwinskia humboldtiana toxins in blood were determined by thin layer chromatography. In six cases, T-514 Karwinskia humboldtiana toxin was detected. These cases had a symmetric motor polyneuropathy with the absence of tendon reflexes and no sensory signs or cranial nerve involvement. Only one patient required assisted ventilation due to bulbar paralysis. In two of these cases, a sural nerve biopsy revealed a segmental demyelination with swelling and phagocytic chambers in Schwann cells and without lymphocytic infiltration. All six cases survived, with complete recovery in five. We conclude that this intoxication is common in Mexico. The availability of toxin detection in blood samples allows the clinician to establish an accurate diagnosis and should be included in the study of children with polyradiculoneuropathy, especially in countries where this poisonous plant grows.

  • frecuencia de intoxicacion con Karwinskia humboldtiana en mexico
    Salud Publica De Mexico, 1995
    Co-Authors: Maria Victoria Bermudez, Fabiola Eugenia Lozano, Victor Armando Tamez, Genaro Diaz, Alfredo Pineyro
    Abstract:

    Ii~toxication produced by Karwinskia humboldtiana preseirts a neurological pichm similar to that of poliomielitis, Guillain-Basre qndrome or otherpolyr.adi...

  • experimental acute intoxication with ripe fruit of Karwinskia humboldtiana tullidora in rat guinea pig hamster and dog
    Toxicon, 1992
    Co-Authors: Maria Victoria Bermudez, M E Salazar, Noemí Waksman, F. J. Martínez, Alfredo Pineyro
    Abstract:

    Previous acute toxicity studies with ‘Tullidora’ in mice showed mainly hepatic and pulmonary complications. We tested samples in rat, guinea-pig, hamster and dog, searching for the mechanism of death. A single oral preparation of ripe fruit of Karwinskia humboldtiana was given to all animals. Clinical signs and histopathology were reproduced in all species except dogs. We propose a selective toxicity of the toxins of this fruit to the lungs and liver.

Alfredo Pineyrolopez - One of the best experts on this subject based on the ideXlab platform.

  • an experimental model of peripheral neuropathy induced in rats by Karwinskia humboldtiana buckthorn fruit
    Journal of The Peripheral Nervous System, 2006
    Co-Authors: Martha E Salazarleal, Viktor J Romerodiaz, Julio Sepulvedasaavedra, Hector R Martinez, Alfredo Pineyrolopez, Victor Armando Tamezrodriguez, M S Flores, Eduardo M Becerraverdin, Maria Victoria Bermudez
    Abstract:

    Abstract  Intoxication by Karwinskia humboldtiana (buckthorn) fruit presents a neurological picture similar to that of Guillain-Barre syndrome. In this report, we describe an experimental animal model of peripheral neuropathy induced by buckthorn fruit. Four groups of Wistar rats received one oral dose of 1.5 g/kg followed by oral doses of 0.5 g/kg at days 3, 7, 10, and 14 of dried and ground buckthorn fruit in aqueous suspension. Rats were sacrificed at 24, 48, 58, and 112 days after initial dose. Treated animals developed progressive paralysis through 58 days, then completely recovered by 112 days. Sciatic nerves showed segmental demyelination and cellular infiltrates until 58 days after exposure and then remyelinating changes at 112 days. This experimental model for peripheral neuropathy is reproducible and easy to handle. Its manipulation is relatively innocuous and allows us to study reversible peripheral nerve damage. This model can be developed in other animal species and may be useful to test new therapies for peripheral neuropathy.

  • in vitro metabolism and toxicity assessment of toxin t 514 peroxisomicine a1 of Karwinskia humboldtiana in microsomes and primary cultured hepatocytes
    Toxicology in Vitro, 2005
    Co-Authors: Magdalena Gomezsilva, Noemí Waksman, Lourdes Garzaocanas, V Rivas, Alfredo Pineyrolopez
    Abstract:

    Abstract T-514 (Peroxisomicine A1) from Karwinskia humboldtiana is a dimeric hydroxyanthracenone with a highly selective cytotoxic effect on tumor cells. We evaluated the metabolism of this compound in two in vitro systems (liver microsomes and hepatocytes) and assessed the cytotoxicity of its metabolites on normal and tumor cells. Microsomes (12.5, 125 and 250 μg of protein/ml) and hepatocytes (1 × 106 cells/ml) were incubated with the toxin (25 μM) for 0.5, 1, 3, 6, 9, 12 and 24 h and the samples were examined using chromatographic analysis and UV spectra. Two metabolites (M1 and M2) were detected in the rat microsomes and one (M1) in the monkey microsomes. The retention times and UV spectra of the peaks were very similar to those of the toxin T-514. M1 was isolated and identified as a mixture of two isomers. The cytotoxicity of the metabolites was evaluated in Chang liver and Hep G2 cells but they did not show the selective cytotoxic effect on tumor cells seen in the original compound.

  • comparison of the hepatotoxicity of toxin t 514 of Karwinskia humboldtiana and its diastereoisomer in primary liver cell cultures
    Toxicon, 1994
    Co-Authors: Lourdes Garzaocanas, O Torresalanis, Waksman N De Torres, T Jiang, Daniel Acosta, Alfredo Pineyrolopez
    Abstract:

    Toxin T-514 of Karwinskia humboldtiana has been demonstrated to be hepatotoxic in vivo and in vitro. Recently a diastereoisomer of T-514 has been isolated. In the present study we have evaluated and compared the in vitro hepatoxicity of the diastereoisomer of T-514 using primary cultures of rat hepatocytes. Cytotoxicity was evaluated by release of cytoplasmic enzyme lactate dehydrogenase (LDH), and mitochondrial metabolic function (MTT reduction). The diastereoisomer was shown to be almost as hepatoxic in vitro as toxin T-514.

  • in vitro selective toxicity of toxin t 514 from Karwinskia humboldtiana buckthorn plant on various human tumor cell lines
    Toxicology, 1994
    Co-Authors: Alfredo Pineyrolopez, Laura Martinez E De Villarreal, Rogerio Gonzalezalanis
    Abstract:

    Abstract Toxin T-514 is a dimeric anthracenone isolated from the Karwinskia humboldtiana (buckthorn) plant. Its potential anti-neoplastic effect was evaluated in vitro and the results obtained were compared with the effect of other known anti-cancer agents. Normal and malignant continuous cell lines were tested. After a 72-h exposure, neoplastic cells derived from hepatic, pulmonary and colonic tissues were more sensitive to toxin T-514 than normal cells from the corresponding organ. Hepatoma cells and colon adenocarcinoma CT 50 values were μ g/ml. Lung adenocarcinoma, undifferentiated bronchogenic cancer cells and small cell carcinoma CT 50 values were μ g/ml. All benign cell CT 50 levels tested were > 113 μ g/ml. Thin in vitro selective toxicity found with toxin T-514 was also seen with 5-fluorouracil and mitomycin for colon adenocarcinoma and with epidoxorubicin for undifferentiated bronchogenic cancer cells.

  • effect of toxins 544 and 514 from Karwinskia humboldtiana buckthorn plant upon fetal development of the mouse
    Toxicon, 1993
    Co-Authors: R Valadezalvizo, A Rodriguezalvarado, María Luisa Villarreal, Rogerio Gonzalezalanis, Alfredo Pineyrolopez
    Abstract:

    R. Valadez-Alvizo, A. Rodriguez-Alvarado, L. Martinez de Villarreal, R. Gonzalez-Alanis and A. Pineyro-Lopez. Effect of toxins 544 and 514 from Karwinskia humboldtiana (buckthorn) plant upon fetal development of the mouse. Toxicon31, 1329–1332, 1993.—The teratogenic effect of toxins 544 and 514 from K. humboldtiana upon the mouse embryo was evaluated. One half of the ld50 dose for the mouse was administered at day 8 of gestation. At the end of pregnancy, reproduction and fetal data were recorded. Dams treated with toxin 544, but not with toxin 514, showed a higher incidence of reabsorptions, malformations, as well as lower fetal length compared to the control group.