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Toxins, Volume 2, Issue 3 (March 2010), Pages 310-366

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Research

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Open AccessArticle A Pilot Study of Nuclear Instability in Archived Renal and Upper Urinary Tract Tumours with Putative Ochratoxin Aetiology
Toxins 2010, 2(3), 326-340; doi:10.3390/toxins2030326
Received: 21 January 2010 / Revised: 22 February 2010 / Accepted: 24 February 2010 / Published: 9 March 2010
Cited by 3 | PDF Full-text (2219 KB) | HTML Full-text | XML Full-text
Abstract
DNA ploidy measurement has been applied uniquely to wax-embedded tissue of primary renal cell and metastatic tumours of a key experimental researcher on porcine ochratoxicosis, a control, and four transitional cell carcinomas from cases of Balkan endemic nephropathy. Primary renal tumour was [...] Read more.
DNA ploidy measurement has been applied uniquely to wax-embedded tissue of primary renal cell and metastatic tumours of a key experimental researcher on porcine ochratoxicosis, a control, and four transitional cell carcinomas from cases of Balkan endemic nephropathy. Primary renal tumour was diploid, and hyperdiploid metastasis was within the lower ploidy range for typical renal cell carcinoma. Three Balkan primary tumours showed extensive aneuploidy indicating marked nuclear instability, similar to model rat renal carcinoma caused by ochratoxin A. In contrast, much less nuclear instability in the putative occupational ochratoxicosis case fitted poorly with the ochratoxin A model. Full article
(This article belongs to the Special Issue Ochratoxins)
Open AccessArticle Porphyromonas gingivalis Gingipains Trigger a Proinflammatory Response in Human Monocyte-derived Macrophages Through the p38α Mitogen-activated Protein Kinase Signal Transduction Pathway
Toxins 2010, 2(3), 341-352; doi:10.3390/toxins2030341
Received: 8 February 2010 / Revised: 4 March 2010 / Accepted: 8 March 2010 / Published: 10 March 2010
Cited by 11 | PDF Full-text (109 KB) | HTML Full-text | XML Full-text
Abstract
Porphyromonas gingivalis, the major etiologic agent of chronic periodontitis, produces a broad spectrum of virulence factors, including Arg- and Lys-gingipain cysteine proteinases. In this study, we investigated the capacity of P. gingivalis gingipains to trigger a proinflammatory response in human monocyte-derived macrophages. [...] Read more.
Porphyromonas gingivalis, the major etiologic agent of chronic periodontitis, produces a broad spectrum of virulence factors, including Arg- and Lys-gingipain cysteine proteinases. In this study, we investigated the capacity of P. gingivalis gingipains to trigger a proinflammatory response in human monocyte-derived macrophages. Both Arg- and Lys-gingipain preparations induced the secretion of TNF-α and IL-8 by macrophages. Stimulation of macrophages with Arg-gingipain A/B preparation at the highest concentration was associated with lower amounts of cytokines detected, a phenomenon likely related to proteolytic degradation. The inflammatory response induced by gingipains was not dependent of their catalytic activity since heat-inactivated preparations were still effective. Stimulating macrophages with gingipain preparations was associated with increased levels of phosphorylated p38α MAPK suggesting its involvement in cell activation. In conclusion, our study brought clear evidence that P. gingivalis Arg- and Lys-gingipains may contribute to the host inflammatory response, a critical factor in periodontitis-associated tissue destruction. Full article
(This article belongs to the Special Issue Protein Toxins as Proteases)
Figures

Open AccessArticle Environmental Factors and Interactions with Mycobiota of Grain and Grapes: Effects on Growth, Deoxynivalenol and Ochratoxin Production by Fusarium culmorum and Aspergillus carbonarius
Toxins 2010, 2(3), 353-366; doi:10.3390/toxins2030353
Received: 28 January 2010 / Revised: 12 March 2010 / Accepted: 15 March 2010 / Published: 18 March 2010
Cited by 18 | PDF Full-text (283 KB) | HTML Full-text | XML Full-text
Abstract
Mycotoxigenic fungi colonizing food matrices are inevitably competing with a wide range of other resident fungi. The outcomes of these interactions are influenced by the prevailing environmental conditions and the competing species. We have evaluated the competitiveness of F. culmorum and A. [...] Read more.
Mycotoxigenic fungi colonizing food matrices are inevitably competing with a wide range of other resident fungi. The outcomes of these interactions are influenced by the prevailing environmental conditions and the competing species. We have evaluated the competitiveness of F. culmorum and A. carbonarius in the grain and grape food chain for their in vitro and in situ dominance in the presence of other fungi, and the effect that such interactions have on colony interactions, growth and deoxynivalenol (DON) and ochratoxin A (OTA) production. The Index of Dominance shows that changes in water activity (aw) and temperature affect the competitiveness of F. culmorum and A. carbonarius against up to nine different fungi. Growth of both mycotoxigenic species was sometimes inhibited by the presence of other competing fungi. For example, A. niger uniseriate and biseriate species decreased growth of A. carbonarius, while Aureobasidium pullulans and Cladosporium species stimulated growth. Similar changes were observed when F. graminearum was interacting with other grain fungi such as Alternaria alternata, Cladopsorium herbarum and Epicoccum nigrum. The impact on DON and OTA production was very different. For F. culmorum, the presence of other species often inhibited DON production over a range of environmental conditions. For A.carbonarius, on a grape–based medium, the presence of certain species resulted in a significant stimulation of OTA production. However, this was influenced by both temperature and aw level. This suggests that the final mycotoxin concentrations observed in food matrices may be due to complex interactions between species and the environmental history of the samples analyzed. Full article
(This article belongs to the Special Issue Advances in Mycotoxin Research)

Review

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Open AccessReview Cholera Toxin: An Intracellular Journey into the Cytosol by Way of the Endoplasmic Reticulum
Toxins 2010, 2(3), 310-325; doi:10.3390/toxins2030310
Received: 27 January 2010 / Revised: 27 February 2010 / Accepted: 2 March 2010 / Published: 5 March 2010
Cited by 54 | PDF Full-text (333 KB) | HTML Full-text | XML Full-text
Abstract
Cholera toxin (CT), an AB5-subunit toxin, enters host cells by binding the ganglioside GM1 at the plasma membrane (PM) and travels retrograde through the trans-Golgi Network into the endoplasmic reticulum (ER). In the ER, a portion of CT, the [...] Read more.
Cholera toxin (CT), an AB5-subunit toxin, enters host cells by binding the ganglioside GM1 at the plasma membrane (PM) and travels retrograde through the trans-Golgi Network into the endoplasmic reticulum (ER). In the ER, a portion of CT, the enzymatic A1-chain, is unfolded by protein disulfide isomerase and retro-translocated to the cytosol by hijacking components of the ER associated degradation pathway for misfolded proteins. After crossing the ER membrane, the A1-chain refolds in the cytosol and escapes rapid degradation by the proteasome to induce disease by ADP-ribosylating the large G-protein Gs and activating adenylyl cyclase. Here, we review the mechanisms of toxin trafficking by GM1 and retro-translocation of the A1-chain to the cytosol. Full article
(This article belongs to the Special Issue Enterotoxins)

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