@article{berntsen_fungal_2017,
	Abstract = {Penitrem A is a fungal neurotoxin that recurrently causes intoxication in animals, and occasionally also in humans. We have previously reported that penitrem A induced the production of reactive oxygen species (ROS) in rat cerebellar granule cells, opening for a new mechanism of action for the neurotoxin. The aim of this study was to examine the potential of penitrem A to induce ROS production in isolated human neutrophil granulocytes, and to study possible mechanisms involved. Penitrem A significantly increased the production of ROS in human neutrophils at concentrations as low as 0.25μM (40\% increase over basal levels), as measured with the DCF fluorescence assay. The EC50 determined for the production of ROS by penitrem A was 3.8μM. The maximal increase in ROS production was approximately 330\% over basal levels at a concentration of 12.5μM. ROS formation was significantly inhibited by the antioxidant vitamin E (50μM), the intracellular Ca+2 chelator BAPTA-AM (5μM), the mitogen activated protein kinase kinase (MEK) 1/2 and 5 inhibitor U0126 (1 and 10μM), the p38 mitogen activated protein kinase (MAPK) inhibitor SB203580 (1μM), the c-Jun amino-terminal kinase (JNK) inhibitor SP600125 (10μM), and the calcineurin inhibitors FK-506 and cyclosporine A (1.5 and 0.5μM, respectively). These finding suggest that penitrem A is able to induce an increase in ROS production in neutrophils via the activation of several MAPK-signalling pathways. We suggest that this increase may partly explain the pathophysiology generated by penitrem A neuromycotoxicosis in both humans and animals.},
	Author = {Berntsen, H. F. and Bogen, I. L. and Wigestrand, M. B. and Fonnum, F. and Walaas, S. I. and Moldes-Anaya, A.},
	Doi = {10.1016/j.tox.2017.10.008},
	Journal = {Toxicology},
	Keywords = {Neuromycotoxicosis, Neutrophil granulocytes, Penitrem A, Reactive oxygen species (ROS)},
	Pages = {64--70},
	Title = {The fungal neurotoxin penitrem {A} induces the production of reactive oxygen species in human neutrophils at submicromolar concentrations},
	Url = {http://www.sciencedirect.com/science/article/pii/S0300483X17303141},
	Volume = {392},
	Year = {2017},
	Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/pii/S0300483X17303141},
	Bdsk-Url-2 = {https://doi.org/10.1016/j.tox.2017.10.008}}

{"_id":"ypibCKjyT8HZYNEZv","bibbaseid":"berntsen-bogen-wigestrand-fonnum-walaas-moldesanaya-thefungalneurotoxinpenitremainducestheproductionofreactiveoxygenspeciesinhumanneutrophilsatsubmicromolarconcentrations-2017","authorIDs":[],"author_short":["Berntsen, H. F.","Bogen, I. L.","Wigestrand, M. B.","Fonnum, F.","Walaas, S. I.","Moldes-Anaya, A."],"bibdata":{"bibtype":"article","type":"article","abstract":"Penitrem A is a fungal neurotoxin that recurrently causes intoxication in animals, and occasionally also in humans. We have previously reported that penitrem A induced the production of reactive oxygen species (ROS) in rat cerebellar granule cells, opening for a new mechanism of action for the neurotoxin. The aim of this study was to examine the potential of penitrem A to induce ROS production in isolated human neutrophil granulocytes, and to study possible mechanisms involved. Penitrem A significantly increased the production of ROS in human neutrophils at concentrations as low as 0.25μM (40% increase over basal levels), as measured with the DCF fluorescence assay. The EC50 determined for the production of ROS by penitrem A was 3.8μM. The maximal increase in ROS production was approximately 330% over basal levels at a concentration of 12.5μM. ROS formation was significantly inhibited by the antioxidant vitamin E (50μM), the intracellular Ca+2 chelator BAPTA-AM (5μM), the mitogen activated protein kinase kinase (MEK) 1/2 and 5 inhibitor U0126 (1 and 10μM), the p38 mitogen activated protein kinase (MAPK) inhibitor SB203580 (1μM), the c-Jun amino-terminal kinase (JNK) inhibitor SP600125 (10μM), and the calcineurin inhibitors FK-506 and cyclosporine A (1.5 and 0.5μM, respectively). These finding suggest that penitrem A is able to induce an increase in ROS production in neutrophils via the activation of several MAPK-signalling pathways. We suggest that this increase may partly explain the pathophysiology generated by penitrem A neuromycotoxicosis in both humans and animals.","author":[{"propositions":[],"lastnames":["Berntsen"],"firstnames":["H.","F."],"suffixes":[]},{"propositions":[],"lastnames":["Bogen"],"firstnames":["I.","L."],"suffixes":[]},{"propositions":[],"lastnames":["Wigestrand"],"firstnames":["M.","B."],"suffixes":[]},{"propositions":[],"lastnames":["Fonnum"],"firstnames":["F."],"suffixes":[]},{"propositions":[],"lastnames":["Walaas"],"firstnames":["S.","I."],"suffixes":[]},{"propositions":[],"lastnames":["Moldes-Anaya"],"firstnames":["A."],"suffixes":[]}],"doi":"10.1016/j.tox.2017.10.008","journal":"Toxicology","keywords":"Neuromycotoxicosis, Neutrophil granulocytes, Penitrem A, Reactive oxygen species (ROS)","pages":"64–70","title":"The fungal neurotoxin penitrem A induces the production of reactive oxygen species in human neutrophils at submicromolar concentrations","url":"http://www.sciencedirect.com/science/article/pii/S0300483X17303141","volume":"392","year":"2017","bdsk-url-1":"http://www.sciencedirect.com/science/article/pii/S0300483X17303141","bdsk-url-2":"https://doi.org/10.1016/j.tox.2017.10.008","bibtex":"@article{berntsen_fungal_2017,\n\tAbstract = {Penitrem A is a fungal neurotoxin that recurrently causes intoxication in animals, and occasionally also in humans. We have previously reported that penitrem A induced the production of reactive oxygen species (ROS) in rat cerebellar granule cells, opening for a new mechanism of action for the neurotoxin. The aim of this study was to examine the potential of penitrem A to induce ROS production in isolated human neutrophil granulocytes, and to study possible mechanisms involved. Penitrem A significantly increased the production of ROS in human neutrophils at concentrations as low as 0.25μM (40\\% increase over basal levels), as measured with the DCF fluorescence assay. The EC50 determined for the production of ROS by penitrem A was 3.8μM. The maximal increase in ROS production was approximately 330\\% over basal levels at a concentration of 12.5μM. ROS formation was significantly inhibited by the antioxidant vitamin E (50μM), the intracellular Ca+2 chelator BAPTA-AM (5μM), the mitogen activated protein kinase kinase (MEK) 1/2 and 5 inhibitor U0126 (1 and 10μM), the p38 mitogen activated protein kinase (MAPK) inhibitor SB203580 (1μM), the c-Jun amino-terminal kinase (JNK) inhibitor SP600125 (10μM), and the calcineurin inhibitors FK-506 and cyclosporine A (1.5 and 0.5μM, respectively). These finding suggest that penitrem A is able to induce an increase in ROS production in neutrophils via the activation of several MAPK-signalling pathways. We suggest that this increase may partly explain the pathophysiology generated by penitrem A neuromycotoxicosis in both humans and animals.},\n\tAuthor = {Berntsen, H. F. and Bogen, I. L. and Wigestrand, M. B. and Fonnum, F. and Walaas, S. I. and Moldes-Anaya, A.},\n\tDoi = {10.1016/j.tox.2017.10.008},\n\tJournal = {Toxicology},\n\tKeywords = {Neuromycotoxicosis, Neutrophil granulocytes, Penitrem A, Reactive oxygen species (ROS)},\n\tPages = {64--70},\n\tTitle = {The fungal neurotoxin penitrem {A} induces the production of reactive oxygen species in human neutrophils at submicromolar concentrations},\n\tUrl = {http://www.sciencedirect.com/science/article/pii/S0300483X17303141},\n\tVolume = {392},\n\tYear = {2017},\n\tBdsk-Url-1 = {http://www.sciencedirect.com/science/article/pii/S0300483X17303141},\n\tBdsk-Url-2 = {https://doi.org/10.1016/j.tox.2017.10.008}}\n\n","author_short":["Berntsen, H. F.","Bogen, I. L.","Wigestrand, M. B.","Fonnum, F.","Walaas, S. 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