Foodborne Disease Outbreaks Caused by Biotoxins in Yantai City: A 10-Year Spatiotemporal Monitoring Study.

Unsafe food causes 600 million cases of foodborne diseases and 420,000 deaths every year. Meanwhile, biological toxins such as poisonous mushrooms, saponins, and aflatoxin can cause significant damage to humans. Therefore, it is particularly important to study foodborne disease outbreaks caused by biotoxins (FDOB). We collected FDOB in Yantai City from 2013 to 2022 and further established a corresponding database. Statistical analysis was carried out according to time, place, pathogen, and contamination of pathogenic factors. There were 128 FDOB, resulting in 417 patients and 6 deaths. The third quarter was a high season for foodborne disease outbreaks, the number of events, patients and deaths accounted for 65.63% (84/128), 55.88% (233/417), and 100% (6/6) of the total number, respectively. The highest number of outbreaks per 10,000 persons was Qixia (0.41), followed by Zhifu (0.36) and Laiyang (0.33). The top three causes of outbreaks were poisonous mushroom toxin, saponins and hemagglutinin, and Lagenaria siceraria (Molina) Standl. Sixty-five (50.78%) outbreaks were attributed to poisonous mushroom toxin, 18 (14.06%) outbreaks to saponin and hemagglutinin, and 12 (9.38%) outbreaks to L. siceraria (Molina) Standl. The largest number of outbreaks, patients and deaths all occurred in families, accounting for 82.81% (106/128) outbreaks, 66.19% (276/417) patients, and 100% (6/6) deaths, respectively. Followed by catering service establishments, accounting for 14.84% (19/128), 30.22% (126/417), and 0% (0/6), respectively. The main poisoning link of outbreaks was ingestion and misuse, accounting for 72.66% (93/128), followed by improper processing, accounting for 20.31% (26/128). It is necessary to carry out targeted family publicity and education, strengthen the integration of medical and prevention, explore innovative monitoring and early warning mechanisms for foodborne diseases, and reduce the occurrence of underreporting of foodborne disease outbreaks.

Maternal exposure to multiple mycotoxins and adverse pregnancy outcomes: a prospective cohort study in rural Bangladesh.

There is limited and inconsistent evidence, primarily from cross-sectional studies, linking mycotoxins to adverse birth outcomes. This study investigates the potential role of maternal dietary exposure to multiple mycotoxins in the development of several adverse pregnancy and birth outcomes. We analyzed data from 436 singleton pregnancies enrolled in a prospective cohort study in the rural Habiganj district, Bangladesh, between July 2018 and November 2019. Thirty-five urinary mycotoxin biomarkers were quantified using liquid chromatography coupled with tandem mass spectrometry and used to estimate dietary mycotoxin exposure. Multivariable regression models, adjusted for potential confounding and clustering, were fitted to assess the associations between maternal exposure to frequently occurring mycotoxins (ochratoxin A-OTA, citrinin- CIT, and Deoxynivalenol- DON) and pregnancy loss, preterm birth (PTB), low birth weight (LBW), born small-for-gestational-age (SGA) and small-vulnerable newborn. The results indicate that only in 16 of 436 pregnancies (4%) were urine samples free from all investigated mycotoxins. Biomarkers for six major mycotoxins were detected in the urine samples. OTA (95%), CIT (61%), and DON (6%) were most frequently detected, with at least two mycotoxins co-occurring in the majority of women (63%). There was evidence that maternal dietary intake of OTA was associated with higher odds of having an LBW baby, with the odds increasing in a dose-dependent manner. We found no evidence of associations between pregnancy loss, PTB, SGA, small-vulnerable newborns, and maternal dietary exposure to OTA, CIT, and DON, albeit with large confidence intervals, so findings are consistent with protective as well as large harmful effects. Exposure to multiple mycotoxins during pregnancy is widespread in this rural community and represents a health risk for mothers and babies. Tailored public health policies and interventions must be implemented to reduce mycotoxin exposure to the lowest possible level.

Zearalenone damages the male reproductive system of rats by destroying testicular focal adhesion.

Zearalenone (ZEA), a common mycotoxin in animal feed, is harmful to public health and causes huge economic losses. The potential target proteins of ZEA and its derivatives were screened using the PharmMapper database and the related genes (proteins) of the testis were obtained from Genecards. We obtained 144 potential targets of ZEA and its derivatives related to the testis using Venn diagrams. The PPI analysis showed that ZEA had the most targets in testis, followed by ZAN, α-ZAL, ß-ZEL, α-ZEL, and ß-ZAL. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses evaluated the metabolic and cancer pathways. We further screened four hub genes: RAC3, CCND1, EP300, and CTNNB1. Eight key biological processes were obtained by GO analysis, and four important pathways were identified by KEGG analysis. Animal and cell experimental results confirmed that ZEA could inhibit the expression of four key KEGG pathway protein components and four hub proteins that interfere with cell adhesion by inhibiting the focal adhesion structure of the testis, Leydig cells, and Sertoli cells. Collectively, our findings reveal that the destruction of the focal adhesion structure in the testis is the mechanism through which ZEA damages the male reproductive system.

Nivalenol affects spindle formation and organelle functions during mouse oocyte maturation.

Oocyte maturation is essential for fertilization and early embryo development, and proper organelle functions guarantee this process to maintain high-quality oocytes. The type B trichothecene nivalenol (NIV) is a mycotoxin produced by Fusarium oxysporum and is commonly found in contaminated food. NIV intake affect growth, the immune system, and the female reproductive system. Here, we investigated NIV toxicity on mouse oocyte quality. Transcriptome analysis results showed that NIV exposure altered the expression of multiple genes involved in spindle formation and organelle function in mouse oocytes, indicating its toxicity on mouse oocyte maturation. Further analysis indicated that NIV exposure disrupted spindle structure and chromosome alignment, possibly through tubulin acetylation. NIV exposure induced aberrant mitochondria distribution and reduced mitochondria number, mitochondria membrane potential (MMP), and ATP levels. In addition, NIV caused the abnormal distribution of the Golgi apparatus and altered the expression of the vesicle trafficking protein Rab11. ER distribution was also disturbed under NIV exposure, indicating the effects of NIV on protein modification and transport in oocytes. Thus, our results demonstrated that NIV exposure affected spindle structure and organelles function in mouse oocytes.

Deoxynivalenol damages the intestinal barrier and biota of the broiler chickens.

BACKGROUND: In the livestock feed industry, feed and feed raw materials are extremely susceptible to mycotoxin contamination. Deoxynivalenol (DON) is one of the main risk factors for mycotoxin contamination in broiler feed and feedstuff, however, there is still little knowledge about this. Hence, the purpose of this study was to explore the toxicity effect of DON on the intestinal barrier and the microecological balance of the biota in broiler chickens. RESULTS: In our present study, we compared the pathological scores of the small intestines of broilers on the 5th, 7th, and 10th day, and chose the 7th day to analyze the small intestine histomorphology, tight junctions, and cecal biota of the broilers. The results showed the damage to the small intestine worsened over time, the small intestinal villi of broilers were breakage, the tight junctions of the small intestine were destroyed, the cecal biota was unbalanced, and the growth performance of broilers was reduced on the 7th day. CONCLUSIONS: DON could damage the functional and structural completeness of the intestinal tract, disorder the Intestinal biota, and finally lead to declined broiler performance. Our study provided a basis for the prevention and treatment of DON in broiler production.

Obesity alters the ovarian proteomic response to zearalenone exposure†.

Zearalenone (ZEN), a nonsteroidal estrogenic mycotoxin, is detrimental to female reproduction. Altered chemical biotransformation, depleted primordial follicles and a blunted genotoxicant response have been discovered in obese female ovaries, thus, this study investigated the hypothesis that obesity would enhance ovarian sensitivity to ZEN exposure. Seven-week-old female wild-type nonagouti KK.Cg-a/a mice (lean) and agouti lethal yellow KK.Cg-Ay/J mice (obese) received food and water ad libitum, and either saline or ZEN (40 µg/kg) per os for 15 days. Body and organ weights, and estrous cyclicity were recorded, and ovaries collected posteuthanasia for protein analysis. Body and liver weights were increased (P < 0.05) in the obese mice, but obesity did not affect (P > 0.05) heart, kidney, spleen, uterus, or ovary weight and there was no impact (P > 0.05) of ZEN exposure on body or organ weight in lean or obese mice. Obese mice had shorter proestrus (P < 0.05) and a tendency (P = 0.055) for longer metestrus/diestrus. ZEN exposure in obese mice increased estrus but shortened metestrus/diestrus length. Neither obesity nor ZEN exposure impacted (P > 0.05) circulating progesterone, or ovarian abundance of EPHX1, GSTP1, CYP2E1, ATM, BRCA1, DNMT1, HDAC1, H4K16ac, or H3K9me3. Lean mice exposed to ZEN had a minor increase in γH2AX abundance (P < 0.05). In lean and obese mice, LC-MS/MS identified alterations to proteins involved in chemical metabolism, DNA repair and reproduction. These data identify ZEN-induced adverse ovarian modes of action and suggest that obesity is additive to ZEN-induced ovotoxicity.

Melatonin alleviates deoxynivalenol-induced apoptosis of human granulosa cells by reducing mutually accentuated FOXO1 and ER stress‡.

Deoxynivalenol (DON) is one of the most prevalent Fusarium mycotoxins, which cause detrimental effects on human and animal reproductive systems by inducing oxidative stress. Increasing evidence has suggested the potential roles of melatonin in protecting granulosa cells from oxidative injury, but the underlying mechanisms remain largely elusive. Here, we demonstrated that suppression of FOXO1 and endoplasmic reticulum (ER) stress was engaged in melatonin-mediated protection against oxidative damage in human granulosa cells upon DON exposure in vitro. DON induced excess reactive oxygen species accumulation, cells viability loss, reduced estradiol-17ß, and progesterone production in human granulosa cells, whereas melatonin ameliorated these phenotypes. Next, we found that the protective effect of melatonin against apoptosis was via reducing ER stress because the inhibition of ER stress displayed similar protective effects during DON treatment. Moreover, melatonin provided no additional protection when ER stress was inhibited. We further found that FOXO1 is a pivotal downstream effector of melatonin and ER stress in regulating DON-induced apoptosis in human granulosa cells. Blocking of FOXO1 reduced DON-induced cells death and FOXO1 activation could be suppressed by melatonin or ER stress inhibitor. However, melatonin failed to further restore cells viability in the presence of FOXO1 inhibitor. Collectively, our results reveal a new mechanism of melatonin in protecting against DON-induced apoptosis and dysfunction by suppressing ER stress and FOXO1 in human granulosa cells.

Ginsenoside Rb1 prevents deoxynivalenol-induced immune injury via alleviating oxidative stress and apoptosis in mice.

Deoxynivalenol (DON) is considered to be a grave threat to humans and animals. Ginsenoside Rb1 (Rb1) has been reported for its antioxidant potential and medicinal properties. However, the shielding effects of Rb1 and the precise molecular mechanisms against DON-induced immunotoxicity in mice have not been reported yet. In the present research, 4-weeks old healthy C57BL/6 mice were randomly assigned into four experimental groups (n = 12), viz., CON, DON 3 mg/kg BW, Rb1 50 mg/kg BW and DON 3 mg/kg + Rb1 50 mg/kg BW (DON + Rb1). Feed intake and body weight gain were monitored during the entire experiment (15 d). Our results demonstrated that Rb1 markedly increased the ADG (30%) and ADFI (25.10%) of mice compared with DON group. Furthermore, Rb1 alleviated the DON-induced immune injury by relieving the splenic histopathological alteration, enhancing the T-lymphocytes subsets (CD4+, CD8+), the levels of cytokines (IL-2, IL-6, IFN-γ, and TNF-α), as well as production of immunoglobulins (IgA, IgM, and IgG). Moreover, Rb1 ameliorated DON-inflicted oxidative stress by reducing the ROS, MDA and H2O2 contents and boosting the antioxidant defense system (T-AOC, T-SOD, CAT, and GSH-Px). Additionally, Rb1 significantly reversed the DON-induced excessive splenic apoptosis via modulating the mitochondria-mediated apoptosis pathway in mice, depicting the decreased percentage of splenocyte apoptotic cells by 26.65%, down-regulated the mRNA abundance of Bax, caspase-3, caspase-9, and protein expression of Bax, cleaved caspase-3, and Cyt-c. Simultaneously, Rb1 markedly rescued both Bcl-2 mRNA and protein expression levels. Taken together, Rb1 mitigates DON-induced immune injury by suppressing the oxidative damage and regulating the mitochondria-mediated apoptosis pathway in mice. Conclusively, our current research provides an insight into the preventive mechanism of Rb1 against DON-induced immune injury in mice and thus, presents a scientific baseline for the therapeutic application of Rb1.

Mycotoxin management in a developing country context: A critical review of strategies aimed at decreasing dietary exposure to mycotoxins in Zimbabwe.

Mycotoxins are unavoidable environmental contaminants, which are found throughout the food chain, particularly in cereals. Mycotoxin management is not effective in developing countries, such as Zimbabwe, due to resource constraints, yet human health risk is evident. Various practical mitigation strategies that can be employed to decrease human dietary exposure to mycotoxins as a means of preliminary steps towards risk management are discussed. These strategies were stratified into two categories. First, crop/commodity-centred strategies, mainly the pre-harvest actions of cultivar selection, bio-control, as well as good agricultural practices (GAP), and the post-harvest actions including timeous harvesting, appropriate drying and storage technologies, are elaborated making use of hazard analysis critical control points (HACCP) principles. The role of legislation is also explored as a crop/commodity centred mitigation strategy. Second, human-centred strategies anchored on dietary diversity and the use of socio-cultural approaches as a direct means of reducing mycotoxin exposure are discussed. Finally, an integrated science-based mycotoxin management strategy, encompassing targeted legislation on mycotoxins, consumer education and information sharing, human and institutional capacity building, training and financing, is suggested in addition to GAP, as a means of reducing human health risk associated with mycotoxin exposure in Zimbabwe.HighlightsFarm-to-fork HACCP-based mycotoxin managementHuman-centred mycotoxin management approaches are keyAgronomy, technology and legislation critical in reducing mycotoxin exposure.

Mycotoxin exposure and human cancer risk: A systematic review of epidemiological studies.

In recent years, there has been an increasing interest in investigating the carcinogenicity of mycotoxins in humans. This systematic review aims to provide an overview of data linking exposure to different mycotoxins with human cancer risk. Publications (2019 and earlier) of case-control or longitudinal cohort studies were identified in PubMed and EMBASE. These articles were then screened by independent reviewers and their quality was assessed according to the Newcastle-Ottawa scale. Animal, cross-sectional, and molecular studies satisfied criteria for exclusion. In total, 14 articles were included: 13 case-control studies and 1 longitudinal cohort study. Included articles focused on associations of mycotoxin exposure with primary liver, breast, and cervical cancer. Overall, a positive association between the consumption of aflatoxin-contaminated foods and primary liver cancer risk was verified. Two case-control studies in Africa investigated the relationship between zearalenone and its metabolites and breast cancer risk, though conflicting results were reported. Two case-control studies investigated the association between hepatocellular carcinoma and fumonisin B1 exposure, but no significant associations were observed. This systematic review incorporates several clear observations of dose-dependent associations between aflatoxins and liver cancer risk, in keeping with IARC Monograph conclusions. Only few human epidemiological studies investigated the associations between mycotoxin exposures and cancer risk. To close this gap, more in-depth research is needed to unravel evidence for other common mycotoxins, such as deoxynivalenol and ochratoxin A. The link between mycotoxin exposures and cancer risk has mainly been established in experimental studies, and needs to be confirmed in human epidemiological studies to support the evidence-based public health strategies.

The effects of feed naturally contaminated with Fusarium mycotoxins on the thymus in suckling piglets.

In this study, feed naturally containing Fusarium mycotoxins was fed to gilts during the perinatal period, and the effects on the thymus were investigated in one-week-old piglets. Twenty gilts were divided into equal control (0.26 mg deoxynivalenol, DON) and experimental (5.08 mg DON, 0.09 mg zearalenone and 21.61 mg fusaric acid per kg of feed) groups. One suckling piglet from each litter (n = 20) was sacrificed at one week of age to obtain thymus samples for further analysis. The cortex to medulla ratio of the thymus was morphometrically analysed using NIS Elements BR (Nikon) software. Paraffin-embedded thymus sections were stained to quantify apoptosis (with terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling - TUNEL method), cellular proliferation (Ki-67) and macrophages (MAC 387). The results showed that the thymus cortex (P = 0.023) to medulla (P = 0.023) ratio was significantly lower in the experimental group. The number of apoptotic cells (cortex, P = 0.010, medulla, P = 0.001) and the number of proliferating cells in the thymus cortex (P = 0.001) and medulla (P < 0.001) were significantly higher in the experimental group. Our results indicate that feeding Fusarium mycotoxins to a parent animal during the perinatal period induces significant alterations in the thymus of one-week-old piglets, which indicates an immunosuppressive effect in piglets.

Factors adversely influencing neurodevelopment.

Neurodevelopment has been studied extensively, especially in respect to abuse, anoxia, nutritional status and prematurity/low birth weight. However, less attention has been paid to innate and environmental factors, as well as to inflammatory conditions that may adversely affect neurodevelopment and learning in children. These include heavy metals, herbicides and polyvinyl chlorides (PVCs), mycotoxins, viral infections and Lyme disease-associated pathogens, as well as number of conditions such as chronic inflammatory response syndrome (CIRS) and Mast cell activation syndrome (MCAS). Early recognition of factors/conditions that could interfere with neurodevelopment is critical. Corrective actions, including the use of some unique natural flavonoids, could have lasting beneficial results.

Fusarium graminearum Chemotype-Spring Wheat Genotype Interaction Effects in Type I and II Resistance Response Assays.

Fusarium head blight (FHB), caused by several Fusarium spp., is a worldwide problem that severely impacts cereal grain yield and poses major risks to human and animal health due to production of the mycotoxin deoxynivalenol (DON) and its acetylated forms, 3-acetyl-DON (3-ADON) and 15-acetyl-DON (15-ADON). Recent studies suggest an inconsistent effect of F. graminearum chemotypes and resistance of wheat (Triticum aestivum) genotypes. To gain insight into the interaction effects of F. graminearum chemotypes and spring wheat genotypes on FHB resistance response, 10 spring wheat genotypes with varying levels of FHB resistance were inoculated with 10 F. graminearum isolates, consisting of 5 3-ADON- and 5 15-ADON-producing isolates and evaluated in type I (spray inoculation) and type II (point inoculation) resistance assays. Wheat genotypes carrying the resistance allele of the Fhb1 quantitative trait locus on chromosome 3BS had lower disease in type II evaluations, regardless of F. graminearum isolate or chemotype. Isolates of F. graminearum were also significantly different for disease aggressiveness. In addition, the 3-ADON-producing isolates were 18% more aggressive than the 15-ADON isolates in type I resistance assays. No difference in aggressiveness of the two chemotypes was observed, when tested in type II resistance assays. There was no interaction effect between F. graminearum chemotypes and spring wheat genotypes, suggesting that screening of germplasm for resistance can be performed with limited number of aggressive isolates.

Systematic review of clinician awareness of mycotoxin impact in neural tube defects and best practices for pediatric neurosurgeons: implications for public health and policy.

PURPOSE: In lower-income populations, high rates of neural tube defects (NTDs) are a concern. Nutritional folate deficiencies and mycotoxins in contaminated food supplies increase risk of NTDs. As physicians in public health and involved in the care of children with NTDs, pediatric neurosurgeons have an interest in the treatment and prevention of NTDs. We aimed to evaluate the literature to assess the awareness and the existence of best practices/educational materials on this issue to better guide management. METHODS: A systematic review using the National Library of Medicine PubMed database was conducted to find articles related to mycotoxins in foods causing neural tube defects. Additional citation searches of key publications and personal collections were used. Two reviewers evaluated the resulting studies for subject area analysis. Best practice recommendations were drawn from articles selected for full-text review. RESULTS: Seventy-three articles were identified. Most articles were found in "nutritional sciences" (18), "teratology" (14), and "toxicology" (13). No articles were found in neurosurgery. Thirty-two additional articles were identified through other sources to screen best practice recommendations. Of the 105 articles, 34 journal articles were included in best practice recommendation guidelines. Key recommendations included education of proper food storage, hygienic agricultural practices, decontamination techniques, diet diversification, folate supplementation, risk assessment, and food safety policy and public health initiatives. CONCLUSION: There is an absence of neurosurgical literature-related mycotoxins and NTDs. We suggest a set of best practices/educational materials on this topic and advocate pediatric neurosurgery engagement in public health initiatives targeted towards populations most affected by mycotoxins.

Effects of fed mycotoxin contaminated diets supplemented with spray-dried porcine plasma on cholinergic response and behavior in piglets.

The aim of this study was to evaluate the effect of spray-dried porcine plasma (SDPP) supplementation on cholinesterase enzymes and its relationship with animal behavior of weaning piglets exposed to mycotoxin contaminated diets. To achieve these objectives, two experimental design approaches were used. Male piglets (7.15±0.61kg) were allocated in four groups: CTL group received a regular diet; SDPP group received a regular diet and 6% SDPP; MYC group received a diet containing desired contamination of 210 µg/kg aflatoxins and 6.690 µg/kg fumonisins; group MYC+SDPP received 253 µg/kg aflatoxins, 6930 µg/kg fumonisins and 6% SDPP. The animals treated with mycotoxin co-contaminated diets showed an increase in AChE and BChE activities in peripheral system (MYC) when compared to control (CTL). Furthermore, supplementation with SDPP (MYC+SDPP group) prevented the mycotoxin-related reduction of AChE in blood and brain. Behavioral tests showed that sleeping and resting behaviors were more often observed in the MYC group; this group also fed fewer times when compared to the other groups, characterizing the deleterious effect of mycotoxins. Taken together, the data suggest changes in AChE and BChE activities may indicate alterations in cholinergic neurotransmission and consequently in the behavior of piglets.

Treatment with potassium bromide mitigates ataxia and reduces tremor in lambs with perennial ryegrass toxicosis.

Aims: To assess the use of potassium bromide (KBr) as a therapeutic intervention for perennial ryegrass toxicosis (PRGT) in lambs fed ryegrass seed containing lolitrem B. Methods: Male lambs aged 10-12 months (n = 43) were assigned to receive ryegrass seed containing lolitrem B, at a dose of 0.16 mg/kg/day (Groups 2, 3 and 4), or lucerne chaff and molasses (Groups 1 and 5). Lambs in Groups 2 and 3 were observed for clinical signs and gait changes until defined signs of PGRT were observed, when they were transferred, with lambs in Group 1, to the Testing phase of the trial. Lambs in Group 3 were then treated with a single oral dose of 300 mg/kg bromide. Lambs in Groups 4 and 5 received KBr daily from the start of the trial (540 mg/kg bromide over 3 days then 20 mg/kg daily) and were transferred to the Testing phase after 18 days. Clinical examination and gait assessment, and surface electromyography of the triceps muscle, measuring root-mean-square (RMS) voltages, were carried out on Days 0, 1 and 2 of the Testing phase followed by necropsy, histopathology, measurement of concentrations of bromide in serum and CSF and faecal cortisol metabolites (FCM). Results: In Group 3 lambs, mean composite gait scores decreased between Testing phase Day 0 and Days 1 and 2 (p < 0.001), but increased in lambs in Group 2 between Day 0 and Day 2 (p = 0.015). Scores for lambs in Group 3 on Day 2 were lower than for lambs in Group 2 (p < 0.001). Mean RMS voltages on Day 2 were higher in lambs in Group 2 than Group 3 (p = 0.045). Mean concentrations of bromide in serum were >800 µg/mL in lambs in Groups 3 and 4 on Day 2. Concentrations of FCM were higher in lambs from Group 2 than in Groups 1 or 5, but were similar in Groups 2, 3 and 4. Histopathological findings in the cerebellum of lambs from Groups 2, 3 and 4 were similar, showing pyknosis of neurons within the granular layer of the cerebellum and Purkinje neuron proximal axonal spheroid formation. Conclusions and clinical relevance: A single oral dose of 300 mg/kg bromide in lambs with neurological signs of PRGT resulted in reduced composite gait scores and reduced RMS voltages, indicating a significant improvement in clinical signs of ataxia, movement disorder and muscle tremor associated with the neurotoxic effects of lolitrem B.

Effect of deoxynivalenol on growth performance, histological morphology, anti-oxidative ability and immune response of juvenile Pacific white shrimp, Litopenaeus vannamei.

A 5-weeks experiment was conducted to evaluate the effect of deoxynivalenol on growth performance, histological morphology, anti-oxidative ability and immune capacity of Litopenaeus vannamei. White shrimp (mean initial weight 1.02 g) were fed seven isonitrogenous diets, Diet 1 as the control, Diet 2-4 was supplemented with grade levels (250, 500 and 1000 µg kg-1) of deoxynivalenol (DON), Diet 5-7 were formulated to contain graded levels of contaminated wheat flour. Each diet was assigned to four tanks (30 shrimp). The weight gain was decreased with the increasing dietary DON levels, survival was lower in shrimp fed high levels of DON-contaminated wheat flour (P < 0.05). Feed intake and feed conversion ratio did not show any difference among all the groups. After 4 h hypoxia stress, survival of shrimp was decreased in shrimp fed high levels of DON-contaminated wheat flour (P < 0.05). Total antioxidant capacity in hepatopancreas was higher in shrimp fed the control diet, glutathione S-transferase (GST) activity were higher in shrimp fed the Diet 3 and Diet 6, superoxide dismutase (SOD) activity was higher in shrimp fed the highest dietary DON (Diet 4), while the gene expression of SOD and GPx were lower in shrimp fed the Diet 3-7. The expression of HSP70, Toll 1 and Dorsal were higher in shrimp fed the Diet 2, the expression of AKT were higher in shrimp fed the Diet 1 and Diet 2. The expression of proPO, LGBP and PPAF were higher in shrimp fed the Diet 4 and Diet 7. The H&E stain indicated intestinal mucosal folds were impaired in shrimp fed the Diet 3-7, and B cells number and diameters of the hepatopancreas tubules were affected by DON levels, and transmission electron microscope (TEM) analysis indicated the apopotosis occurs in intestinal epithelial cell of shrimp fed the Diet 2-7. Based on the present results, the safety level of DON for white shrimp should below 0.5 ppm, which was much less than the European Communities recommendation values for aquatic animals (5 ppm). High level of DON would damage the cell structural and affect the NF-κB pathway and proPO system of shrimp.

Development of a model for investigation of perennial ryegrass toxicosis in sheep.

AIMS To develop a clinical model of perennial ryegrass toxicosis (PRGT) based on feeding a known dose of lolitrem B and ergotamine, and to produce a consistent clinical presentation for assessment of disease pathophysiology, neurological changes and neurohistopathology. METHODS Male lambs, aged between 10-12 months, were randomly assigned to either Treatment (n=9) or Control (n=9) groups. Lambs in the Treatment group received feed containing a novel endophyte-infested perennial ryegrass seed, commencing on Day 0 of the Feeding phase with a low induction dose, then increasing after 3 days to provide 0.16 mg/kg live bodywight (LBW)/day of lolitrem B and 0.054 mg/kg LBW/day ergotamine. Lambs were examined daily and when defined signs of PRGT were observed they were transferred to the Testing phase. Neurological examinations, assessment of gait, surface electromyography (EMG) and mechanosensory nociceptive threshold testing were carried out and blood samples collected during both phases of the trial, with a full necropsy, histopathological examination and measurement of faecal cortisol metabolites (FCM) performed on Day 2 of the Testing phase. RESULTS Typical clinical signs of PRGT, including ataxia of vestibulocerebellar origin leading to stumbling, were observed in all Treatment lambs. The median interval from the start of the Feeding phase to entry into the Testing phase was 21 (min 18, max 34) days. Histopathological characterisation of neurological lesions included the presence of Purkinje cell vacuolation, pyknotic granular layer neurons and proximal axonal Purkinje cell spheroids. Lesions were most apparent within the vestibulocerebellum. Mean root-mean-square voltages from triceps EMG increased in Treatment lambs between Feeding phase Day 0 and Testing phase Day 2 (p<0.001). Daily water intake during the Testing phase for the Treatment group was less than in Control group lambs (p=0.002), and concentrations of FCM at necropsy were higher in Treatment compared to Control lambs (p=0.02). CONCLUSIONS AND CLINICAL RELEVANCE Lolitrem B and ergotamine dosing in feed on a live weight basis combined with neurological/gait assessment provides an effective model for investigation of PRGT and potential therapeutics. Assessment of gait changes using defined criteria and RMS voltages from EMG appear to be useful tools for the assessment of the severity of neurological changes.

Impact of mycotoxins on the intestine: are mucus and microbiota new targets?

There is an increasing awareness of the deleterious effects attributed to mycotoxins during their fate within the gut, particularly for deoxynivalenol (DON), zearalenone (ZEN), ochratoxin A (OTA), fumonisin B1 (FB1), aflatoxin B1 (AFB1), and patulin (PAT). Evidence indicates that disruption of the epithelial barrier is well established. However, intestinal barrier function on its luminal side involves two other partners, mucus and microbiota, which have rarely been considered in the context of mycotoxin exposure. The current review aimed at providing a summary of DON, ZEN, OTA, FB1, AFB1, and PAT effects on intestinal barrier function, with special focus on mucus and microbiota. DON, ZEN, OTA, FB1, AFB1, and PAT are known to markedly affect epithelial cell integrity and functions. Regarding mucus, DON is the most documentated mycotoxin. In vivo, toxicological impact of DON generally has only been assessed through goblet cell number. Evaluation of the mycotoxins/mucus interplay considering other indicators such as composition, thickness, and penetrability of mucus, mucin O-glycosylation thus warrants further attention. With respect to microbiota, few short-term studies to date have been reported indicating deleterious effects. However, long-term exposure to mycotoxins may also produce significant changes in microbiota composition and metabolic activity, which requires further experimentation. In conclusion, mucus and microbiota are key targets for dietary mycotoxins although assessment of induced effects is preliminary. A significant research effort is now underway to determine the adverse consequences of mycotoxins on mucus and microbiota considered as individual but also as tightly connected gut players.

Positive and negative aspects of green coffee consumption - antioxidant activity versus mycotoxins.

BACKGROUND: The quality of coffee depends not only on the contents of healthy compounds but also on its contamination with microorganisms that can produce mycotoxins during development, harvesting, preparation, transport and storage. RESULTS: The antioxidant activity of green coffee brews measured in this study by ABTS, DPPH and Folin-Ciocalteu assays showed that coffee extracts from Robusta beans possessed higher activity in all assays than extracts from Arabica beans. The occurrence of ochratoxin A and aflatoxins (B1, B2, G1 and G2) in green coffee beans was studied using liquid chromatography/mass spectrometry. Apart from mycotoxins, the content of ergosterol as a marker indicating fungal occurrence was also determined. Among aflatoxins, aflatoxin B1 was the dominant mycotoxin in coffee bean samples, with the highest level at 17.45 ng g-1 . Ochratoxin A was detected in four samples at levels ranging from 1.27 to 4.34 ng g-1 , and fungi potentially producing this toxin, namely Aspergillus oryzae, Alternaria sp., Aspergillus foetidus, Aspergillus tamarii and Penicillium citrinum, were isolated. CONCLUSION: Steaming and decaffeination of coffee beans increased antioxidant activities of brews in comparison with those prepared from unprocessed beans. Although toxins can be quantified in green coffee beans and novel fungi were isolated, their concentrations are acceptable according to legal limits. © 2017 Society of Chemical Industry.