The mycotoxins beauvericin and T-2 induce cell death and alteration to the ascorbate metabolism in tomato protoplasts

Paciolla, Costantino; Dipierro, Nunzio; Mulé, Giuseppina; Logrieco, A.; Dipierro, Silvio

doi:10.1016/j.pmpp.2004.07.006

Cited by 68 publications

(52 citation statements)

References 37 publications

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“…Lucia indicates its direct involvement in the detoxification processes, which is probably one of the key factors in the tolerance mechanisms of this cultivar to FUS. No significant differences in reduced glutathione (GSH) or oxidized glutathione (GSSG) were found either with beauvericin or T-2 toxin treated tomato cells but these two toxins, both produced by Fussarium spp., significantly affected ascorbate system (Paciolla et al 2004).…”

Section: Discussionmentioning

confidence: 96%

Impact of fusaproliferin on primary roots of maize cultivars differing in their susceptibility to Fusarium

et al. 2011

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Effects of fusaproliferin (FUS) on membrane potential (EM), electrolyte leakage, enzymes activity and respiration of roots, were studied in two maize cultivars (Zea mays L.), differing in their susceptibility to this toxin. In short-term experiments (≤ 6 h), EM has been rapidly and significantly depolarized by FUS. The rapidity of EM depolarization in tolerant cv. Lucia was more expressive in comparison with susceptible cv. Pavla, but the extent of EM depolarization was higher in cv. Pavla. In both maize cultivars, higher depolarization of EM was registered in cells of root zone I. In long-term experiments after the first EM depolarization, which occurred during the first 6 h of FUS treatment, gradual depolarization continued up to 24 h and was represented not only by the active component (EP) but also by the passive component (ED) of EM. The decrease in EM and ED was followed by a loss of K + ions from FUS treated roots of both cultivars. The leak of K + ions from the root cells of both root zones as well as both maize cultivars increased with the time of FUS treatment and was significantly higher in susceptible cv. Pavla than in tolerant cv. Lucia. FUS treatment of maize roots resulted in a significant decrease of root respiration which was higher in susceptible cv. Pavla than in tolerant cv. Lucia. The analysis of enzyme activities revealed that FUS significantly stimulated POD activity in both maize cultivars. SOD activity was significantly increased only in susceptible cv. Pavla, while APX activity was not affected by the presence of FUS. GST activity was specifically induced by FUS only in tolerant cv. Lucia. Due to the observed correlation between the extent of depolarization and the sensitivity of the studied maize cultivars to fusaproliferin, the EM parameters should be used for rapid screening of FUS-resistant cultivars for agricultural practice.

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Section: Discussionmentioning

confidence: 96%

Impact of fusaproliferin on primary roots of maize cultivars differing in their susceptibility to Fusarium

et al. 2011

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“…BEA is a cyclic hexadepsipeptide produced by various phytopathogenic Fusarium species (Moretti et al 1995) with apoptotic properties (Ojcius et al 1991, Paciolla et al 2004) influencing membrane properties of root cells (Lemmens et al 1997, Pavlovkin et al 2006, Santini et al 2008, Šrobárová et al 2009). …”

Section: Discussionmentioning

confidence: 99%

“…BEA is a specific cholesterol acyltransferase inhibitor (Tomoda et al 1992), induces apoptosis in mammalian cells , human leukemia cells (Chen et al 2006) and shows cytotoxicity of the invertebrate cell line SF-9 (Ojcius et al 1991. However, until now, phytotoxic activity of BEA has only been sporadically investigated (Paciolla et al 2004, Pavlovkin et al 2006. Paciolla et al (2004) reported that BEA-induced tomato protoplast death is caused by imbalance of the ascorbate system and subsequent oxidative stress.…”

mentioning

confidence: 99%

“…However, until now, phytotoxic activity of BEA has only been sporadically investigated (Paciolla et al 2004, Pavlovkin et al 2006. Paciolla et al (2004) reported that BEA-induced tomato protoplast death is caused by imbalance of the ascorbate system and subsequent oxidative stress. Šrobárová et al (2009) suggested that the nuclear fragmentation in BEA-treated cells is an important feature of apoptosis and implies that the intracellular phytotoxin BEA plays an important role, possibly as a mediator in cell-death signalling.…”

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confidence: 99%

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Impact of beauvericin on membrane properties of young initial leaves of maize with different susceptibility to Fusarium

Pavlovkin¹,

Mistríková²,

Jašková³

et al. 2012

PLANT SOIL ENVIRON

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In the present study the impact of beauvericin (BEA) on the cell membrane properties and respiration of young initial leaves of maize were studied using two maize cultivars differing in their susceptibility to Fusarium sp. BEA significantly depolarized E M of leaf parenchymal cells and this depolarization showed time and dose dependency regardless on the sensitivity of maize cultivars to Fusarium. However, the extent of BEA-induced depolarization was 2-5 times higher in sensitive cv. Pavla than in tolerant cv. Lucia. Membrane permeability and K + leakage from leaves cells treated with BEA was higher in sensitive cv. Pavla but the differences were not so considerable than the depolarization of E M . Treatment of maize young initial leaves with 40 μmol BEA significantly inhibited respiration. In accord with electrophysiological measurements inhibition of respiration was higher in sensitive cv. Pavla showing 70% inhibition already after 90 min of BEA treatment while in tolerant cv. Lucia inhibition represented only 27%. The biological activity of BEA seems to be mediated by the ability of BEA to affect membrane permeability and ion transport. This is probably the initial effect of BEA on plant cell leading to subsequent effect on other cell organelles (mitochondria) and cell metabolism.

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“…Toxic level of ROS usually reacts with numerous cell components causing a cascade of oxidative reactions and the consequent inactivation of enzymes, protein degradation, and nucleic acid damage. In addition, excessive ROS can react with membrane lipids, generating lipid peroxides that can in turn lead to further damaging intermediates such as malondialdehyde (MDA), to the point of inducing cellular dysfunction and/or cell death [14], [15]. The present investigation portrays the elicitation of defence responses in tomato after the treatment of FA (Fusarium toxin).…”

Section: Induction Of Defence Responses By Fusaricmentioning

confidence: 95%

Induction of Defence Responses by Fusaric Acid (Fusarium Toxin) in Tomato Plant

2016

6th International Conference on Advances in Engineering Sciences and Applied Mathematics (ICAESAM-2016) Dec. 21-22, 2016 Kuala

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Abstract-Fusaric acid (FA) is a host non-specific toxin produced by a number of Fusarium species. The most expansive producer of this toxin is Fusarium oxysporum and its special forms (f. sp.) lycopersici (causal agent of Fusarium wilt of tomato). FA is suspected to be a potent pathogenicity factor in tomato wilt disease development. With this rationale the present study was carried out with biochemical and molecular perspectives. In the present study, the treatment of FA was given to the leaves of tomato directly through infiltration to assess the induction of defence responses. The phytotoxic effect of FA was assessed in the form of cell death in tomato leaves which was observed by increased uptake of Evans blue stain. This cell death inducer (FA) produced an enormous oxidative burst during which large quantities of reactive oxygen species (ROS) like H 2 O 2 was generated in the treated leaf tissues of tomato plants which was evident from enhancement in lipid peroxidation. However, to cope with the toxicity of FA, tomato plants develop a cellular strategy involving activation of antioxidative defence system. This modulation of antioxidative system could reflect a defence response to the cellular damage provoked by treatment of FA. Results demonstrate that production of phytohormone (SA) potentiates the oxidative burst, while ROS increases its production. In this way these signaling molecules stimulate each other's production, thus amplifying the initial signal, ultimately leading to plant cell death. A significant increase of PAL activity in tomato plants confirmed the responsiveness of PAL-mediated primary defence system against the FA exposure. In the present study, the level of total phenols (important component of plant defence machinery) increased significantly in consonance with increase in the ROS level.Furthermore, proteomic study was used as a powerful tool to understand the alterations in cellular protein expression in response to FA exposure. Differential expression in several proteins was observed in the present study. The present study provides clues to understand the biochemical and molecular changes that occurred in the host plant, Solanum lycopersicum L., during the FA treatment. The study provides valuable outputs regarding vulnerability of such vegetable crop plant under FA exposure, which can be used in future breeding to design effective ameliorative strategy for the generation of resistant plants.

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The mycotoxins beauvericin and T-2 induce cell death and alteration to the ascorbate metabolism in tomato protoplasts

Cited by 68 publications

References 37 publications

Impact of fusaproliferin on primary roots of maize cultivars differing in their susceptibility to Fusarium

Impact of fusaproliferin on primary roots of maize cultivars differing in their susceptibility to Fusarium

Impact of beauvericin on membrane properties of young initial leaves of maize with different susceptibility to Fusarium

Induction of Defence Responses by Fusaric Acid (Fusarium Toxin) in Tomato Plant

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