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Despite the abundance of promising studies, developments, and improvements about the elimination of microbial toxins from food matrices, they are still considered as one of the major food safety problems due to the lack of their complete avoidance even today. Every year, many crops and foodstuffs have to be discarded due to unconstrained contamination and/or production of microbial toxins. Furthermore, the difficulty for the detection of toxin presence and determination of its level in foods may lead to acute or chronic health problems in many individuals. On the other hand, phenolic compounds might be considered as microbial toxin detoxification agents because of their inhibition effect on the toxin synthesis of microorganisms or exhibiting protective effects against varying damaging mechanisms caused by toxins. In this study, the effect of phenolic compounds on the synthesis of bacterial toxins and mycotoxins is comprehensively reviewed. The potential curing effect of phenolic compounds against toxin-induced damages has also been discussed. Consequently, phenolic compounds are indicated as promising, and considerable natural preservatives against toxin damages and their detoxification potentials are pronounced. [Display omitted] • Microbial toxins cause serious safety problems in the food industry. • Phenolic compounds are natural preservatives used in the food industry. • Many toxin-producing microbes may be inhibited by phenolic compounds. • Phenolic compounds may protect or reduce the damage caused by microbial toxins. [ABSTRACT FROM AUTHOR]

Abstract: The aim of this study was to screen potential myelotoxicity of the emerging mycotoxins Beauvericin, Enniatin b and Moniliformin using human hematopoietic progenitor clonogenic assays. Depending on mycotoxins, inhibitory effects on proliferation of white blood cells progenitors (CFU-GM), platelet progenitors (CFU-MK) and red blood cells progenitors (BFU-E) have been detected at various concentrations. Beauvericin was cytotoxic at 32μM, 3.2μM and 6.4μM, had no effect on proliferation in the presence of 0.032μM, 0.16μM and 0.064μM, and the IC50 was equal to 3.4μM, 0.7μM and 3.7μM for CFU-GM, CFU-MK and BFU-E, respectively. Enniatin b was cytotoxic at 6μM, 1.8μM and 5μM, had no effect on proliferation in the presence of 1μM, 1.1μM and 1.2μM and the IC50 was equal to 4.4μM, 1.3μM and 3.3μM for CFU-GM, CFU-MK and BFU-E, respectively. Moniliformin was not cytotoxic at tested concentrations for CFU-GM and CFU-MK and cytotoxic at 10μM for BFU-E, had no effect on proliferation in the presence of 5μM, 0.1μM and 0.1μM and the IC50 was equal to 31μM, 39μM and 4.1μM for CFU-GM, CFU-MK and BFU-E, respectively. Inhibition of the BFU-E differentiation has been observed in the presence of Enniatin b or Moniliformin. For the three mycotoxins, variation of distribution of CFU-MK colonies according to their size has been observed. These in vitro effects may be responsible for in vivo hematological troubles in case of consumption of contaminated commodities. In vivo studies have to be performed to test this hypothesis. [Copyright &y& Elsevier]

Abstract: Although the theory of evolution was put forth about 150 years ago our understanding of how molecules drive evolution remains poor. It is well-established that proteins evolve at different rates, essentially based on their functional role and three-dimensional structure. However, the highly variable rates of evolution of different proteins – especially the rapidly evolving ones – within a single organism are poorly understood. Using examples of genes for fast-evolving toxins and human hereditary diseases, we show for the first time that specific nucleotide sequences appear to determine point mutation rates. Based on mutation rates, we have classified triplets (not just codons) into stable, unstable and intermediate groups. Toxin genes contain a relatively higher percentage of unstable triplets in their exons compared to introns, whereas non-toxin genes contain a higher percentage of unstable triplets in their introns. Thus the distribution of stable and unstable triplets is correlated with and may explain the accelerated evolution of point mutations in toxins. Similarly, at the genomic level, lower organisms with genes that evolve faster contain a higher percentage of unstable triplets compared to higher organisms. These findings show that mutation rates of proteins, and hence of the organisms, are DNA sequence-dependent and thus provide a proximate mechanism of evolution at the molecular level. [Copyright &y& Elsevier]

Abstract: Toxigenic isolate of Fusarium sporotrichioides was tested for the T-2 toxin production on PDA plates during 10 days under various glucose concentrations. T-2 toxin was determined by LC–MS and confirmed with LC–MS/MS. This analytical method has been applied, for the first time, to an extensive study of T-2 accumulation. Results showed that the production of this mycotoxin is directly correlated to the concentration of glucose present in the medium. Concentrations of T-2 toxin produced by the strain of F. sporotrichioides ranged from 0 to 1.45mg/kg. The better T-2 production was evidenced in the fermentation operated with 20% of glucose. [Copyright &y& Elsevier]

Abstract: There is growing evidence that adverse effects of microcystin-LR (MC-LR) are closely related to oxidative stress processes, free radicals and DNA damage, and involve major gene transcript changes. This study, utilizing gene expression analysis and plasma chemistries was the first to measure the effects of MC-LR in whitefish (Coregonus lavaretus L.), a feasible organism for pollution monitoring in aquatic systems. Fish were injected with different concentrations of MC-LR (0, 10 and 100μg/kg of body weight) and then sacrificed at either 0, 8, 24, 48 or 72h later, and their liver tissue were harvested for detailed investigation. Specifically, we were interested whether MC-LR is capable of: (i) modulating expression of two genes, tumor suppressor gene p53 and cdkn1a, p53 direct transcription target, and (ii) inducing apoptosis in whitefish liver. To study these effects, we developed a real-time qPCR assays useful for measuring both p53 and cdkn1a gene transcript levels in liver. To obtain necessary information for the study, either full-length p53 cDNA of whitefish (Wf-p53) was determined, using molecular cloning and rapid amplification of cDNA ends (RACE), or as for Wf-cdkn1a, specific primers were designed based on highly conserved regions of cdkn1a in fish. The Wf-p53 was found to share the same characteristics with a known p53 mRNA sequence of other vertebrates. Whitefish p53 amino acid sequence showed a high degree of homology with the sequences from fishes, amphibians, and mammals. The injection study showed that MC-LR at a higher dose, i.e. 100μg/kg body weight, up-regulated expression of p53 and cdkn1a genes in whitefish liver, as reflected by the continuous increase in their mRNA levels through the whole experiment. Furthermore, DNA fragmentation was observed in liver cells of whitefish after 24h of exposure to MC-LR (100μg/kg) that suggests the possibility of apoptosis. Finally, the study confirmed previous observations of severe injury of the liver and loss of normal organ functions as revealed by elevated levels of blood AspAT, AlaAT, and hepatosomatic index (HSI). [Copyright &y& Elsevier]

Abstract: The toxic activity of Aspergillus fumigatus is attributable to substances secreted by its cells. Specific toxic compounds synthesized by the fungi such as gliotoxin, can be detected by sensitive chemical procedures like TLC or HPLC. Measuring the total toxigenicity of a strain extract, however, requires a bioassay. In the present study, we evaluated the possibility of using the Microtox® bioassay to determine the toxigenicity of A. fumigatus, using 32 strains from different sources. The Microtox® method is based on the ability of Vibrio fischeri to produce luminescence, and their sensitivity to toxins. A. fumigatus strains, grouped according to their original sources, showed differences in toxigenicity. Strains isolated from invasive aspergillosis patients proved to be more toxigenic than environmental strains, or strains from colonized patients. Since the strains that were more toxigenic were isolated from sick patients, it is not surprising they showed more virulence than the other strains, and as expected, virulence could be correlated with high toxigenicity. The Microtox bioassay could be a useful tool in the study of toxigenicity of the mycelial fungi and their possible pathogenic roles, and for rapid assessment of secreted toxic compounds. [Copyright &y& Elsevier]

Abstract: The aim of the present study was to determine whether the intraperitoneal LD50 for yessotoxin (YTX) in mice varies with strain or gender. Thirty-six male and 36 female mice, of body weight 16–20g, from each of the strains ICR (CD-1), Swiss (CFW-1) and NMRI were employed. They were not fasted before YTX treatment. At each dose, nine mice were injected with YTX solutions at 1.0mL/20g body weight, and observed for 24h. Symptoms and time to death were recorded. Within each mouse strain and gender arm, the study was performed as a basic four level Response Surface Pathway designed trial with nine mice at each dose level. YTX was isolated from a culture of Protoceratium reticulatum. The LD50 values for female and male mice, respectively, were estimated as 380 and 462μg/kg for the ICR, 269 and 328μg/kg for the Swiss, and 314 and 412μg/kg for the NMRI strains. The increases in LD50 from female to male mice were found to be 22% for ICR, 22% for Swiss and 31% for NMRI. The largest difference in LD50 among mouse strains was detected between the ICR and Swiss strains, where the deviation was 41% in both females and males. The difference between mouse strains was found significant (p =0.03). For all three strains, females were more susceptible than males, with a difference in LD50 of 1.2–1.3-fold. The largest difference between the least- and most-susceptible strain was 1.4-fold for both females and males. The largest difference in LD50, 1.7-fold, was observed between female Swiss and male ICR mice. The difference between genders was not significant (p =0.12). These results indicate that other factors, like handling of the animals, and the source and handling of the toxin, may significantly influence the outcome of studies on acute toxicity since the reported differences in LD50 vary by a factor of about seven. [Copyright &y& Elsevier]

Abstract: Worldwide blooms of toxic cyanobacteria (blue-green algae) commonly occur in freshwater, often in drinking water sources, necessitating routine monitoring of water quality. Microcystin-LR and related cyanobacterial toxins strongly inhibit protein phosphatase 2A (PP2A) and are therefore assayable by measuring the extent of PP2A inhibition. In this study, we evaluated the suitability of the catalytic subunit of recombinant PP2A (rPP2Ac) expressed with a baculovirus system for use in a microplate microcystin assay. Five microcystin analogs, microcystin-LR, -RR, -YR, -LF, and -LW, and nodularin strongly inhibited rPP2Ac activity with IC50 values of 0.048, 0.072, 0.147, 0.096, 0.114, and 0.54nM, respectively. Microcystin-LR in a water sample could be assayed from 0.005 to 5ng/ml. The assay could detect the toxin at a far lower level than required by the World Health Organization for regulation of microcystin-LR or its equivalent (1μg/L). Pretreatment or concentration of water samples with low toxin concentrations was not necessary. The microplate assay using rPP2Ac was more sensitive than an enzyme-linked immunosorbent assay (ELISA) method and a cytotoxicity assay. The genetically engineered rPP2Ac was more stable than a commercially available dimeric enzyme, producing accurate and reproducible results. Our results confirm that the rPP2Ac we prepared is an excellent tool for detecting and quantifying microcystins in water. [Copyright &y& Elsevier]

Abstract: Receptor site-3 on voltage-gated sodium channels is targeted by a variety of structurally distinct toxins from scorpions, sea anemones, and spiders whose typical action is the inhibition of sodium current inactivation. This site interacts allosterically with other topologically distinct receptors that bind alkaloids, lypophilic polyether toxins, pyrethroids, and site-4 scorpion toxins. These features suggest that design of insecticides with specificity for site-3 might be rewarding due to the positive cooperativity with other toxins or insecticidal agents. Yet, despite the central role of scorpion α-toxins in envenomation and their vast use in the study of channel functions, molecular details on site-3 are scarce. Scorpion α-toxins vary greatly in preference for sodium channels of insects and mammals, and some of them are highly active on insects. This implies that despite its commonality, receptor site-3 varies on insect vs. mammalian channels, and that elucidation of these differences could potentially be exploited for manipulation of toxin preference. This review provides current perspectives on (i) the classification of scorpion α-toxins, (ii) their mode of interaction with sodium channels and pharmacological divergence, (iii) molecular details on their bioactive surfaces and differences associated with preference for channel subtypes, as well as (iv) a summary of the present knowledge about elements involved in constituting receptor site-3. These details, combined with the variations in allosteric interactions between site-3 and the other receptor sites on insect and mammalian sodium channels, may be useful in new strategies of insect control and future design of anti-insect selective ligands. [Copyright &y& Elsevier]

In order to investigate the transfer of nivalenol (NIV) and fusarenon-X (FX) from pregnant to fetal mice and from lactating to suckling mice, 3H-NIV or 3H-FX was given p.o. to pregnant or lactating mice. Radioactivity was detected in the whole fetal tissues as well as the fetal liver and kidney, the levels being comparable to those of the maternal tissues. Radioactivity was also detected in the milk, and liver and kidney tissues taken from suckling mice of both 3H-NIV or 3H-FX administered dams. HPLC analysis of fetal tissue homogenates from non-labeled FX- or NIV-administered pregnant mice revealed transmission of NIV to fetuses after administration of either toxin. In mice given the non-labeled FX, major and minor peaks of NIV and FX on HPLC were noted in suckling pup tissue homogenates. The results demonstrate that NIV transfers in unchanged form to fetal or suckling mice via placenta or milk, respectively, and that FX does so mainly after being metabolized to NIV in maternal body. [Copyright &y& Elsevier]