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The toxicity of Fusarium mycotoxins enniatin and moniliformin.
by Martina Jonsson
Institution: | University of Helsinki |
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Year: | 2017 |
Posted: | 02/01/2018 |
Record ID: | 2152050 |
Full text PDF: | http://hdl.handle.net/10138/227965 |
The red mold Fusarium, is a fungal pathogen, infecting mainly small-grain cereals in the temperate regions of the world. In Scandinavia, F. avenaceum, F. culmorum, F. poae, and F. sporotrichioides infections are most common, but in recent years F. graminearum and F. langsethiae infections have increased, as well. Most Fusarium species are capable of producing a variety of mycotoxins, possibly providing an edge over competing strains at the site of infection. Mycotoxins can evoke a broad range of toxic effects in humans and animals, including neurotoxicity, immunotoxicity, reproductive-, and developmental toxicity and carcinogenicity. The most toxic fusariatoxins include the tricothecenes, fumonisins and zearalenone. However, less studied mycotoxins, as enniatins (Enns) and moniliformin (MON) are frequently found in grain products, hence, causing a risk of a daily, low-level exposure of human and livestock, the significance of which is still unclear. The aim of this study was to provide further insights into the toxicity of Enns and MON, and into the mechanism of action of EnnB, monitored at gene expression level. Furthermore, the acute oral toxicity and repeated, low-dose, oral toxicity of MON in Sprague-Dawley rats was assessed, adapting OECD Guidelines 423 and 407.We report clear toxic outcomes of EnnB in vitro, as it affected cellular energy metabolism by reducing ATP levels in cell cultures and cell proliferation, already at low concentrations (below 10 M) in the cell lines Balb 3T3 and HepG2. EnnB exposure slightly increased the proportion of early apoptotic cells, as well. Gene expression studies revealed alteration of energy metabolism, due to effects on gene expression of genes associated with mitochondrial organization and function and assembly of complex I of the electron transport chain. Moniliformin (MON) did not induce significant toxicity in vitro. However, high doses of MON (50 mg/kg b.w.) caused acute toxicity in rats, seen as cardiovascular changes and respiratory distress, resulting in death. According to the OECD Globally Harmonized System, the toxicity of MON could be classified into category 2, and a LD50 cut of value of 25 mg/kg b.w. was determined. Long term, low dose exposure affected mainly the innate immunity, by reducing the phagocytic activity of rat neutrophils in all tested groups. Hence, a LOAEL of 3 mg/kg b.w. for MON was suggested. The rats of the lowest dose groups (3-6 mg/kg b.w.) remained clinically healthy. Two rats of five in the highest dose group (15 mg/kg b.w.) showed similar signs as in the acute oral toxicity test and died. Excretion kinetics revealed that MON is rapidly excreted in urine, in less than 6 h, but only 1-2% was found in feces. This indicates that the urinary excretion is the main route for elimination. Fusarium punahome on merkittv viljelyskasvien taudinaiheuttaja, joka aiheuttaa maailmanlaajuisesti suuria taloudellisia tappioita. Euroopassa erityisesti vilja-kasvit ovat alttiita Fusarium infektioille. Taudinaiheutuskyvyn lisksi Fusarium lajit
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