H. Yazdanpanah, F. Roshanzamir, B. Shafaghi, M. Faizi, M. Elhami, H. Rasekh
The efficacy of two free radical scavengers, selenium and zinc, and a microsomal epoxide hydrolase-inducing agent, cis-stilbene oxide on the acute toxicity of T-2 toxin, a potent cytotoxic trichothecene, was investigated. Mice were pretreated daily for 3 consecutive days with either zinc sulfate (4.4 mg/kg, intraperitoneally [i.p.]), sodium selenite (1, 2, and 3 mg/kg i.p.) or cis-stilbene oxide (50 mg/kg i.p.). A full 24-hr after the final dosing with these agents, mice were given T-2 toxin (2, 2.5, or 3 mg/kg i.p.). The acute lethal toxicity of T-2 toxin (2.5 mg/kg) was reduced by administration of only sodium selenite (3 mg/kg) and cis-stilbene oxide (50 mg/kg). No significant effect on weight gain was observed.
{"title":"Assessment of possible protective roles of selenium, zinc, and cis-stilbene oxide against acute T-2 toxin poisoning: a preliminary report.","authors":"H. Yazdanpanah, F. Roshanzamir, B. Shafaghi, M. Faizi, M. Elhami, H. Rasekh","doi":"10.1002/19970504NT1","DOIUrl":"https://doi.org/10.1002/19970504NT1","url":null,"abstract":"The efficacy of two free radical scavengers, selenium and zinc, and a microsomal epoxide hydrolase-inducing agent, cis-stilbene oxide on the acute toxicity of T-2 toxin, a potent cytotoxic trichothecene, was investigated. Mice were pretreated daily for 3 consecutive days with either zinc sulfate (4.4 mg/kg, intraperitoneally [i.p.]), sodium selenite (1, 2, and 3 mg/kg i.p.) or cis-stilbene oxide (50 mg/kg i.p.). A full 24-hr after the final dosing with these agents, mice were given T-2 toxin (2, 2.5, or 3 mg/kg i.p.). The acute lethal toxicity of T-2 toxin (2.5 mg/kg) was reduced by administration of only sodium selenite (3 mg/kg) and cis-stilbene oxide (50 mg/kg). No significant effect on weight gain was observed.","PeriodicalId":18777,"journal":{"name":"Natural toxins","volume":"5 1","pages":"133-5"},"PeriodicalIF":0.0,"publicationDate":"1998-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90818268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Total nucleated cellularity and total erythroid cell populations were measured in spleen and bone marrow of mice at different times after treatment with 3 daily doses of T-2 toxin (2.0 mg/kg). It was found that the initial depletion of hematopoietic cells produced by the toxin was rapidly reverted in spleen, giving way after 48 hr to a significant hypercellularity which after 10 days was 2.5 times the normal levels, but this effect was not observed in bone marrow, which slowly recovered normal cellularity after 5 days. The cytological analysis revealed that there was a highly significant shift in the ratio of erythroid to non-erythroid cells, since erythroid cell populations increased by about 8-fold in spleen and nearly 2-fold in bone marrow between 10 and 35 days after intoxication. In order to test the integrity of the hematopoietic reserve capacity, a hemorrhagic stress was produced in intoxicated animals at 10-50 days after toxin exposure. It was found that the erythroid response capacity was significantly higher in the intoxicated animals compared to anemic controls. The results suggest that the initial cytotoxic damage produced by T-2 toxin in the hematopoietic system is followed by a significant erythroid hypercellularity, which can confer an increased capacity for response to a hemorrhagic emergency.
{"title":"Effects of multiple doses of T-2 toxin on the erythroid response capacity of mice following an extensive experimental bleeding.","authors":"H. Godoy, G. C. Faifer, V. Velazco","doi":"10.1002/19970504NT5","DOIUrl":"https://doi.org/10.1002/19970504NT5","url":null,"abstract":"Total nucleated cellularity and total erythroid cell populations were measured in spleen and bone marrow of mice at different times after treatment with 3 daily doses of T-2 toxin (2.0 mg/kg). It was found that the initial depletion of hematopoietic cells produced by the toxin was rapidly reverted in spleen, giving way after 48 hr to a significant hypercellularity which after 10 days was 2.5 times the normal levels, but this effect was not observed in bone marrow, which slowly recovered normal cellularity after 5 days. The cytological analysis revealed that there was a highly significant shift in the ratio of erythroid to non-erythroid cells, since erythroid cell populations increased by about 8-fold in spleen and nearly 2-fold in bone marrow between 10 and 35 days after intoxication. In order to test the integrity of the hematopoietic reserve capacity, a hemorrhagic stress was produced in intoxicated animals at 10-50 days after toxin exposure. It was found that the erythroid response capacity was significantly higher in the intoxicated animals compared to anemic controls. The results suggest that the initial cytotoxic damage produced by T-2 toxin in the hematopoietic system is followed by a significant erythroid hypercellularity, which can confer an increased capacity for response to a hemorrhagic emergency.","PeriodicalId":18777,"journal":{"name":"Natural toxins","volume":"23 1","pages":"152-6"},"PeriodicalIF":0.0,"publicationDate":"1998-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87614651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
We report a retrospective study of the clinical signs and symptoms associated with a point-source outbreak of fish poisoning that occurred with a fish captured from the Arafura Sea, northern Australia. Twenty cases (16 Aboriginal and 4 non-Aboriginal) characteristic of ciguatera, including 4 inpatients and 16 outpatients from the Gove Hospital, were identified based on the pattern of clinical symptoms and signs after ingestion of a large coral cod from a known ciguatera-prone coral reef. In the absence of a serologic test for the victim, laboratory analysis of a 230-g sample of the coral cod (Cephalopolis miniatus), using both mouse bioassay and HPLC/mass spectometry, showed that Pacific ciguatoxin-1 was the principal toxin involved. Intravenous mannitol was administered to one patient without clear benefit. Risk factors for ciguatera poisoning are ingestion of larger portions of reef fish from ciguatera-prone areas. Despite apparent local awareness of the distribution and etiology of the disease, large common-source outbreaks of ciguatera still occur.
{"title":"Pacific ciguatoxin-1 associated with a large common-source outbreak of ciguatera in east Arnhem Land, Australia.","authors":"R. E. Lucas, R. Lewis, J. M. Taylor","doi":"10.1002/19970504NT2","DOIUrl":"https://doi.org/10.1002/19970504NT2","url":null,"abstract":"We report a retrospective study of the clinical signs and symptoms associated with a point-source outbreak of fish poisoning that occurred with a fish captured from the Arafura Sea, northern Australia. Twenty cases (16 Aboriginal and 4 non-Aboriginal) characteristic of ciguatera, including 4 inpatients and 16 outpatients from the Gove Hospital, were identified based on the pattern of clinical symptoms and signs after ingestion of a large coral cod from a known ciguatera-prone coral reef. In the absence of a serologic test for the victim, laboratory analysis of a 230-g sample of the coral cod (Cephalopolis miniatus), using both mouse bioassay and HPLC/mass spectometry, showed that Pacific ciguatoxin-1 was the principal toxin involved. Intravenous mannitol was administered to one patient without clear benefit. Risk factors for ciguatera poisoning are ingestion of larger portions of reef fish from ciguatera-prone areas. Despite apparent local awareness of the distribution and etiology of the disease, large common-source outbreaks of ciguatera still occur.","PeriodicalId":18777,"journal":{"name":"Natural toxins","volume":"86 1","pages":"136-40"},"PeriodicalIF":0.0,"publicationDate":"1998-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85623140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Brevetoxins are produced by the marine dinoflagellate Ptychodiscus brevis, an organism linked to red tide outbreaks, and the accompanying toxicity to marine animals and to neurotoxic shellfish poisoning in humans. Brevetoxins bind with high affinity to voltage-sensitive sodium channels and cause increased sodium ion conductance and nerve cell depolarization. The brevetoxin competitive binding assay with tritium-labeled brevetoxin 3 (3H-PbTx-3) and rat brain synaptosomes is a sensitive and specific assay for pure brevetoxins. Here we report that extracts of manatee, turtle, fish, and clam tissues contain components that interfere with the assay by cooperative, noncompetitive inhibition of 3H-PbTx-3 specific binding and increased nonspecific binding to synaptosomes. By determining the "apparent" toxin concentration ("[Toxin]") in the extract at several assay concentrations, a reasonable correction for the complex inhibition could be made using a semilog plot to extrapolate [Toxin] to zero extract concentration to obtain [Toxin]0. Spiking 4 extracts with 60 nM PbTx-3 caused [Toxin]0 to increase by 41 +/- 8 nM, indicating that the noncompetitive components did not prevent the assay of toxin but did reduce the accuracy of the result. Fourfold repetition of the assay of 4 samples gave standard deviations of 25 to 60% of the value of [Toxin]0, so the error can be fairly large, especially for samples with little toxin. Purification of an extract with a 1 g sample prep column of C-18 decreased the complex inhibition by about 3-fold but did not eliminate interference in the assay.
短鞭藻毒素是由海洋甲藻短鞭藻(Ptychodiscus brevis)产生的，这种生物与赤潮爆发有关，并对海洋动物和人类造成神经毒性贝类中毒。短链毒素与电压敏感的钠离子通道高亲和力结合，引起钠离子电导增加和神经细胞去极化。短叶草毒素与氚标记短叶草毒素3 (3H-PbTx-3)和大鼠脑突触体的竞争结合试验是一种对纯短叶草毒素敏感和特异的试验。在这里，我们报道了海牛、海龟、鱼类和蛤蜊组织的提取物含有通过合作、非竞争性抑制3H-PbTx-3特异性结合和增加对突触体的非特异性结合来干扰测定的成分。通过确定几种测定浓度下提取物中的“表观”毒素浓度(“[毒素]”)，可以使用半对数图将[毒素]外推到零提取物浓度，从而得到[毒素]0，从而对复杂抑制进行合理的修正。用60 nM PbTx-3加药可使[毒素]0增加41 +/- 8 nM，表明非竞争性成分不妨碍毒素测定，但降低了结果的准确性。对4个样品进行四次重复分析，得出[Toxin]0值的标准偏差为25%至60%，因此误差可能相当大，特别是对于毒素含量很少的样品。用1 g C-18样品制备柱纯化提取物后，复合物抑制作用降低了约3倍，但不能消除实验中的干扰。
{"title":"Complex behavior of marine animal tissue extracts in the competitive binding assay of brevetoxins with rat brain synaptosomes.","authors":"P. Whitney, J. Delgado, D. Baden","doi":"10.1002/19970505NT4","DOIUrl":"https://doi.org/10.1002/19970505NT4","url":null,"abstract":"Brevetoxins are produced by the marine dinoflagellate Ptychodiscus brevis, an organism linked to red tide outbreaks, and the accompanying toxicity to marine animals and to neurotoxic shellfish poisoning in humans. Brevetoxins bind with high affinity to voltage-sensitive sodium channels and cause increased sodium ion conductance and nerve cell depolarization. The brevetoxin competitive binding assay with tritium-labeled brevetoxin 3 (3H-PbTx-3) and rat brain synaptosomes is a sensitive and specific assay for pure brevetoxins. Here we report that extracts of manatee, turtle, fish, and clam tissues contain components that interfere with the assay by cooperative, noncompetitive inhibition of 3H-PbTx-3 specific binding and increased nonspecific binding to synaptosomes. By determining the \"apparent\" toxin concentration (\"[Toxin]\") in the extract at several assay concentrations, a reasonable correction for the complex inhibition could be made using a semilog plot to extrapolate [Toxin] to zero extract concentration to obtain [Toxin]0. Spiking 4 extracts with 60 nM PbTx-3 caused [Toxin]0 to increase by 41 +/- 8 nM, indicating that the noncompetitive components did not prevent the assay of toxin but did reduce the accuracy of the result. Fourfold repetition of the assay of 4 samples gave standard deviations of 25 to 60% of the value of [Toxin]0, so the error can be fairly large, especially for samples with little toxin. Purification of an extract with a 1 g sample prep column of C-18 decreased the complex inhibition by about 3-fold but did not eliminate interference in the assay.","PeriodicalId":18777,"journal":{"name":"Natural toxins","volume":"61 1","pages":"193-200"},"PeriodicalIF":0.0,"publicationDate":"1998-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87539067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ultrastructural changes in the alveolar tissue of rats intraperitoneally injected with the Cerastes cerastes cerastes venom were studied in 2 different experimental groups. In the first group, each rat was given 0.73 mg/Kg as a single dose and sacrificed after 24 hours. In the second group, each rat was given a daily dose of 0.42 mg/Kg for 7 days and sacrificed 24 hours after the last injection. Proliferative changes were seen in type II alveolar cells, fibroblasts, lymphocytes, and macrophages. Type II alveolar cells of the lungs developed a large number of surfactant granules. In the 24-hour-envenomated rats, type I alveolar cells displayed swollen nuclei and masses of dilated endoplasmic reticulum. In the 7-day-treated rats, several plasma cells, adjacent interstitial cells as well as alveolar brush cells, with their characteristic short microvilli, were detected. Large masses of collagen and elastic fibers were also located in the vicinity of the alveolar brush cells and type II alveolar cells. These histopathological changes may be attributed to the body-immune response and possibly to the development of hyperplasia due to venom-induced trauma.
{"title":"Ultrastructural changes in the alveolar cells of rats injected with Cerastes cerastes cerastes venom.","authors":"N. Fares, A. Abd el-Aal","doi":"10.1002/19970505NT6","DOIUrl":"https://doi.org/10.1002/19970505NT6","url":null,"abstract":"Ultrastructural changes in the alveolar tissue of rats intraperitoneally injected with the Cerastes cerastes cerastes venom were studied in 2 different experimental groups. In the first group, each rat was given 0.73 mg/Kg as a single dose and sacrificed after 24 hours. In the second group, each rat was given a daily dose of 0.42 mg/Kg for 7 days and sacrificed 24 hours after the last injection. Proliferative changes were seen in type II alveolar cells, fibroblasts, lymphocytes, and macrophages. Type II alveolar cells of the lungs developed a large number of surfactant granules. In the 24-hour-envenomated rats, type I alveolar cells displayed swollen nuclei and masses of dilated endoplasmic reticulum. In the 7-day-treated rats, several plasma cells, adjacent interstitial cells as well as alveolar brush cells, with their characteristic short microvilli, were detected. Large masses of collagen and elastic fibers were also located in the vicinity of the alveolar brush cells and type II alveolar cells. These histopathological changes may be attributed to the body-immune response and possibly to the development of hyperplasia due to venom-induced trauma.","PeriodicalId":18777,"journal":{"name":"Natural toxins","volume":"27 1","pages":"208-21"},"PeriodicalIF":0.0,"publicationDate":"1998-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78996873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
U. Vinitketkumnuen, T. Chewonarin, P. Kongtawelert, A. Lertjanyarak, S. Peerakhom, C. Wild
Aflatoxin-albumin (AFB-albumin) adducts and hepatitis B markers (anti-HBs, and anti-HBc) were measured in vegetarians and nonvegetarians from Chiang Mai, Thailand. The AFB-albumin adduct levels were detected in 62% (37 of 60) of the vegetarian samples and 22% (22 of 100) of nonvegetarians. Somewhat higher levels were detected in vegetarians sera collected in the summer than in the winter, although this difference was not statistically significant. Subjects who were hepatitis B surface antigen (HBsAg)-positive had slightly higher AFB-albumin adduct levels than subjects who had evidence of past exposure (anti-HBc-positive) or no HB virus infection. This study indicated that vegetarians may have a higher frequency of aflatoxin exposure than nonvegetarians. Thai vegetarians consume various vegetables, grains, peanut, soybean, and fermented products, which have been reported to be sources of aflatoxin.
{"title":"Aflatoxin exposure is higher in vegetarians than nonvegetarians in Thailand.","authors":"U. Vinitketkumnuen, T. Chewonarin, P. Kongtawelert, A. Lertjanyarak, S. Peerakhom, C. Wild","doi":"10.1002/19970504NT8","DOIUrl":"https://doi.org/10.1002/19970504NT8","url":null,"abstract":"Aflatoxin-albumin (AFB-albumin) adducts and hepatitis B markers (anti-HBs, and anti-HBc) were measured in vegetarians and nonvegetarians from Chiang Mai, Thailand. The AFB-albumin adduct levels were detected in 62% (37 of 60) of the vegetarian samples and 22% (22 of 100) of nonvegetarians. Somewhat higher levels were detected in vegetarians sera collected in the summer than in the winter, although this difference was not statistically significant. Subjects who were hepatitis B surface antigen (HBsAg)-positive had slightly higher AFB-albumin adduct levels than subjects who had evidence of past exposure (anti-HBc-positive) or no HB virus infection. This study indicated that vegetarians may have a higher frequency of aflatoxin exposure than nonvegetarians. Thai vegetarians consume various vegetables, grains, peanut, soybean, and fermented products, which have been reported to be sources of aflatoxin.","PeriodicalId":18777,"journal":{"name":"Natural toxins","volume":"88 1","pages":"168-71"},"PeriodicalIF":0.0,"publicationDate":"1998-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85541618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The amyloid precursor protein (APP) is abnormally cleaved during the progression of Alzheimer's disease, resulting in production of the toxic beta-amyloid peptide, which forms neuritic plaques in the brain. To develop a pharmacological approach for treatment of Alzheimer's disease, natural compounds which may inhibit APP synthesis and/or beta-amyloid production are required. Staurosporine, a toxin isolated from Streptomyces staurospores bacteria, is widely used as a protein kinase C inhibitor in signal transduction research. Using rat pheochromocytoma PC12 sympathetic neurons, which express APP, we characterised staurosporine effect on APP level by western blotting, using an anti-APP monoclonal antibody. PC12 APP levels were increased or decreased upon exposure to either 50-200 nM or 10-20 nM phorbol 12-myristate 13-acetate (PMA, a protein kinase C activator), respectively. An apparent relationship was found between the change in APP level and a differential down regulation process of different PKC isoforms. The PMA-induced increase in intracellular APP level was dose-dependently inhibited by staurosporine (natural alkaloid) or GF 109203X (synthetic analogue), protein kinase C (PKC) inhibitors. This inhibition was mainly observed upon treatment of the cells before the exposure to PMA. These results suggest PKC regulation of APP levels in PC12 cells, and provide staurosporine as a leader compound for the development of drugs to control the expression of APP in Alzheimer's research.
{"title":"The microbial alkaloid toxin staurosporine blocks the phorbol ester-induced increase in beta-amyloid precursor protein in PC12 cells.","authors":"L. Friedman, Y. Matsuda, P. Lazarovici","doi":"10.1002/19970505NT1","DOIUrl":"https://doi.org/10.1002/19970505NT1","url":null,"abstract":"The amyloid precursor protein (APP) is abnormally cleaved during the progression of Alzheimer's disease, resulting in production of the toxic beta-amyloid peptide, which forms neuritic plaques in the brain. To develop a pharmacological approach for treatment of Alzheimer's disease, natural compounds which may inhibit APP synthesis and/or beta-amyloid production are required. Staurosporine, a toxin isolated from Streptomyces staurospores bacteria, is widely used as a protein kinase C inhibitor in signal transduction research. Using rat pheochromocytoma PC12 sympathetic neurons, which express APP, we characterised staurosporine effect on APP level by western blotting, using an anti-APP monoclonal antibody. PC12 APP levels were increased or decreased upon exposure to either 50-200 nM or 10-20 nM phorbol 12-myristate 13-acetate (PMA, a protein kinase C activator), respectively. An apparent relationship was found between the change in APP level and a differential down regulation process of different PKC isoforms. The PMA-induced increase in intracellular APP level was dose-dependently inhibited by staurosporine (natural alkaloid) or GF 109203X (synthetic analogue), protein kinase C (PKC) inhibitors. This inhibition was mainly observed upon treatment of the cells before the exposure to PMA. These results suggest PKC regulation of APP levels in PC12 cells, and provide staurosporine as a leader compound for the development of drugs to control the expression of APP in Alzheimer's research.","PeriodicalId":18777,"journal":{"name":"Natural toxins","volume":"2 1","pages":"173-9"},"PeriodicalIF":0.0,"publicationDate":"1998-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88632118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yessotoxin (YTX), a disulfated polyether toxin, was isolated from cultured cells of the marine dinoflagellate Protoceratium reticulatum and unambiguously identified by high-performance liquid chromatography, 1H NMR, and MS data. The result is the first to confirm toxigenicity of this species and demonstrate it as one of the biogenetic origins of YTX found in shellfish.
{"title":"Identification of Protoceratium reticulatum as the biogenetic origin of yessotoxin.","authors":"M. Satake, L. Mackenzie, T. Yasumoto","doi":"10.1002/19970504NT7","DOIUrl":"https://doi.org/10.1002/19970504NT7","url":null,"abstract":"Yessotoxin (YTX), a disulfated polyether toxin, was isolated from cultured cells of the marine dinoflagellate Protoceratium reticulatum and unambiguously identified by high-performance liquid chromatography, 1H NMR, and MS data. The result is the first to confirm toxigenicity of this species and demonstrate it as one of the biogenetic origins of YTX found in shellfish.","PeriodicalId":18777,"journal":{"name":"Natural toxins","volume":"52 1","pages":"164-7"},"PeriodicalIF":0.0,"publicationDate":"1998-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81123433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A series of stable quinones and their precursors, and enzymatic oxidation products of plant allelochemicals were tested for their effect on maize fungal pathogens, primarily Fusarium graminearum. Benzoquinone was typically significantly more toxic than hydroquinone, while 1,2-naphthoquinone was typically significantly more toxic than 1,2-dihydroxynaphthalene. Aspergillus flavus was the most resistant fungus to these compounds, while Phoma medicaginis was the most susceptible. Applying tyrosinase in conjunction with several phenolic compounds only increased the toxicity of gallic acid to Fusarium graminearum. Applying peroxidase generally increased toxicity of all compounds tested to this fungus in a dose-dependent fashion. Ferulic acid was generally the most toxic compound, both alone and when combined with peroxidase and H2O2, followed by coumaric acid. These results suggest that enzymatic oxidation of plant allelochemicals may result in the generation of products that either are directly toxic to maize pathogens, or indirectly inhibitory due to their ability to tie up nutrients.
{"title":"Comparative toxicity of allelochemicals and their enzymatic oxidation products to maize fungal pathogens, emphasizing Fusarium graminearum.","authors":"P. Dowd, J. Duvick, T. Rood","doi":"10.1002/19970505NT2","DOIUrl":"https://doi.org/10.1002/19970505NT2","url":null,"abstract":"A series of stable quinones and their precursors, and enzymatic oxidation products of plant allelochemicals were tested for their effect on maize fungal pathogens, primarily Fusarium graminearum. Benzoquinone was typically significantly more toxic than hydroquinone, while 1,2-naphthoquinone was typically significantly more toxic than 1,2-dihydroxynaphthalene. Aspergillus flavus was the most resistant fungus to these compounds, while Phoma medicaginis was the most susceptible. Applying tyrosinase in conjunction with several phenolic compounds only increased the toxicity of gallic acid to Fusarium graminearum. Applying peroxidase generally increased toxicity of all compounds tested to this fungus in a dose-dependent fashion. Ferulic acid was generally the most toxic compound, both alone and when combined with peroxidase and H2O2, followed by coumaric acid. These results suggest that enzymatic oxidation of plant allelochemicals may result in the generation of products that either are directly toxic to maize pathogens, or indirectly inhibitory due to their ability to tie up nutrients.","PeriodicalId":18777,"journal":{"name":"Natural toxins","volume":"18 1","pages":"180-5"},"PeriodicalIF":0.0,"publicationDate":"1998-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81966159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
K. Harada, M. Oshikata, T. Shimada, Akiko Nagata, Nami Ishikawa, Makoto Suzuki, F. Kondo, M. Shimizu, Sachiko Yamada
Microcystins are potent hepatotoxins produced by cyanobacteria, and are also tumor promoters as well as potent inhibitors of the catalytic subunits of protein phosphatases 1 and 2A. In order to establish a physicochemical method for individual detection and determination of trace amounts of microcystins, we developed a derivatization method for fluorescence (FL) and chemiluminescence (CL) detection, in which a highly fluorescent dienophile, DMEQ-TAD (4-[2-(6,7-dimethoxy-4-methyl-3-oxo-3,4-dihydroquinoxalinyl) ethyl]-1,2,4-triazoline-3,5-dione), was used as the labeling reagent. DMEQ-TAD reacted smoothly with the conjugated diene of the Adda moiety to give 2 stereoisomers of the adducts. As a result of the extensive experiments, the following reaction conditions were optimized for the labeling: sample amount, 10 micrograms; reaction solvent, DMF:acetonitrile (1:1); reaction time, 15 minutes; reaction temperature, 70 degrees C; amount of DMEQ-TAD used relative to that of microcystin, 80 equivalent. The resulting 6 adducts from microcystins-LR, -YR, and -RR can be separated from one another using the following reversed phase HPLC conditions in combination with a clean-up using ODS silica gel: column, Cosmosil 5C18-AR (150 x 4.6 I.D. mm); mobile phase, methanol:0.05M phosphate buffer (pH 3) (1:1); flow rate, 1.0 ml/min; detection, FL lambda ex 370 nm, lambda em 440 nm. The detection limits of the DMEQ-TAD derivatives were estimated to be 100 and 500 pg for LR, and 65 and 2,500 pg for RR using FL and CL detections, respectively; and the detection behavior was different from that of the Dns-Cys derivatives, which were more sensitive to CL than FL.
微囊藻毒素是由蓝藻产生的强效肝毒素，也是肿瘤促进剂以及蛋白磷酸酶1和2A催化亚基的强效抑制剂。为建立微量微囊藻毒素个体检测和测定的理化方法，以高荧光亲和试剂DMEQ-TAD(4-[2-(6,7-二甲氧基-4-甲基-3-氧-3,4-二氢喹啉基)乙基]-1,2,4-三唑啉-3,5-二酮)为标记试剂，建立了一种衍生化荧光和化学发光检测方法。DMEQ-TAD与Adda部分的共轭二烯反应顺利，得到2个加合物的立体异构体。经过大量的实验，优化了标记的反应条件:进样量为10微克;反应溶剂DMF:乙腈(1:1);反应时间:15分钟;反应温度70℃;与微囊藻毒素相比，DMEQ-TAD用量为80当量。从微囊藻藻中得到的6个加合物- lr， -YR和-RR可以通过以下反相高效液相色谱条件相互分离，并使用ODS硅胶进行清理:色谱柱，Cosmosil 5C18-AR (150 x 4.6 I.D. mm);流动相:甲醇:0.05M磷酸盐缓冲液(pH 3) (1:1);流速:1.0 ml/min;检测，FL λ ex 370 nm， λ em 440 nm。使用FL和CL检测，DMEQ-TAD衍生物对LR的检出限分别为100和500 pg，对RR的检出限分别为65和2500 pg;与Dns-Cys衍生物的检测行为不同，对CL比FL更敏感。
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