Role of proliferation in the toxicity of fumonisin B1: enhanced hepatotoxic response in the partially hepatectomized rat

Fumonisin mycotoxins are common contaminants of maize and cause several fatal animal diseases. Liver is a target organ of fumonisins in intact animals, but liver slices and primary hepatocytes, which do not proliferate in culture, are resistant to fumonisin exposure. Hepatoma cell lines, on the other hand, undergo cell division in culture and are sensitive to the toxic effects of fumonisins. It was therefore hypothesized that fumonisin cytotoxicity is dependent on cell proliferation. To test this hypothesis, the partially hepatectomized rat was used as a model to determine whether fumonisin produced greater toxicity in rapidly proliferating liver in vivo. Rats were dosed intraperitoneally with fumonisin B1 (FB1) 24 h after sham operation or partial hepatectomy (PH) and were killed 24 h later. The dose-related increase in free sphingoid bases (a biomarker of fumonisin exposure) was enhanced in the PH-treated rats. Serum cholesterol and enzymes were higher in PH-treated rats dosed with FB1 than in those given PH without FB1 or in sham-operated, FB1-dosed rats. Multiple daily doses of FB1 after surgery elevated the number of apoptotic hepatocytes in both sham-operated and PH-treated rats to about the same degree, suggesting that apoptosis is not associated with the enhanced cytotoxicity of FB1 in regenerating liver. Proliferating cells appear to be more sensitive to the toxic effects of fumonisins. This enhanced cytotoxicity may be related to the increased ability of fumonisins to disrupt sphingolipid metabolism in hepatectomized rats, but this is yet to be determined.     

Cytotoxicity of Fumonisin B1 in Spheroid and Monolayer Cultures of Rat Hepatocytes

Fumonisin B₁ (FB₁), the most prevalent member of toxins produced by several species of Fusarium molds, which occur mainly in maize, causes several fatal hepatopathies and nephropathies of animals. The current study was scrutinized to ascertain different cytotoxic and morphological transformations in rat hepatocytes induced by the treatments of diverse concentrations (300, 500, or 1000 μM) of fumonisin B₁ in vitro, using both monolayer and spheroid cultures. In each hepatocyte culture, the cytotoxicity of FB₁ was augmented in dose- and time-response manners. Morphological transformations among FB₁-treated groups integrated accumulation of lipid droplets, cytoplasmic vacuolation in hepatocyte monolayers, and bleb formation in the hepatocyte spheroids. Additionally, electron microscopy revealed the loss of microvilli, mitochondrial swelling, and formation of lamellar membranous whorl in the vacuoles and bile canaliculi-like structures. Appearance of electron dense bodies in the monolayers, and loss of cell-to-cell contact in spheroids were depicted in 1000 μM FB₁-treated hepatocytes. These outcomes insinuate different vital events in explaining morphological transformations in the cell membrane and organelles, induced by fumonisins in rat hepatocytes.     

Paradoxical role of tumor necrosis factor α in fumonisin-induced hepatotoxicity in mice

Tumor necrosis factor α (TNFα) is involved in fumonisin-induced hepatotoxic effects in mice. The hepatic response to fumonisin B₁ (FB₁) was reduced in transgenic animals lacking either of the two TNFα receptors. In the present study, we hypothesized that the effect of a similar fumonisin treatment in animals lacking either TNFα or both TNFα receptors would be considerably less than their wild type (WT) counterparts. The FB₁-induced increase in circulating liver enzymes was enhanced by deletion of TNFα or unchanged in mice lacking both TNFα receptors. These findings corresponded with the degree of toxicity as established by microscopic examination of liver. FB₁ induced the expression of TNFα in the liver of all strains, except the animals with a deleted TNFα gene. The FB₁-mediated increases in liver sphingosine or sphinganine paralleled the hepatotoxic responses. It is apparent that the presence of TNFα is not necessary for FB₁-induced hepatotoxicity in mice and a lack of the function of this cytokine may aggravate the hepatotoxic responses to fumonisins, perhaps by preventing repair mechanisms or by expression of other signaling molecules. These observations were in accordance with our previous finding where over-expression of TNFα also protected against FB₁-mediated hepatotoxicity, and with the reported beneficial functions of low-level TNFα in tissue regeneration.     

Toxicity assessment of fumonisins using the brine shrimp (Artemia salina) bioassay

The Fusarium mycotoxins fumonisin B₁ (FB₁) (1) and B₂ (FB₂) (2), their hydrolysed analogues HFB₁ (3) and HFB₂ (4) and the recently discovered fumonisin derivatives N-palmitoyl-HFB₁ (5) and N-carboxymethyl-FB₁ (6) were compared for their toxicity in a short term bioassay using brine shrimp (Artemia salina). The brine shrimp were hatched in artificial sea water and exposed to the fumonisins in microwell plates with a mortality endpoint after 48 hours. LC₅₀ values were calculated after Probit transformation of the resulting data. Of the substances tested, fumonisin B₁ emerged to be the most toxic whereas its N-carboxymethyl analogue was 100-fold less effective. The hydrolysed fumonisins showed a four- to sixfold reduced toxicity compared to FB₁. N-Palmitoyl-HFB₁ had a higher LC₅₀ value than its precursor HFB₁. The brine shrimp assay proved to be a convenient and rapid system for toxicity assessment of this group of mycotoxins.     

Effects of orally administered fumonisin B1 (FB1), partially hydrolysed FB1, hydrolysed FB1 and N-(1-deoxy-D-fructos-1-yl) FB1 on the sphingolipid metabolism in rats

Fumonisin B₁ (FB₁) is a Fusarium mycotoxin frequently occurring in maize-based food and feed. Alkaline processing like nixtamalisation of maize generates partially and fully hydrolysed FB₁ (pHFB₁ and HFB₁) and thermal treatment in the presence of reducing sugars leads to formation of N-(1-deoxy-D-fructos-1-yl) fumonisin B₁ (NDF). The toxicity of these metabolites, in particular their effect on the sphingolipid metabolism, is either unknown or discussed controversially. We produced high purity FB₁, pHFB₁a+b, HFB₁ and NDF and fed them to male Sprague Dawley rats for three weeks. Once a week, urine and faeces samples were collected over 24 h and analysed for fumonisin metabolites as well as for the sphinganine (Sa) to sphingosine (So) ratio by validated LC–MS/MS based methods. While the latter was significantly increased in the FB₁ positive control group, the Sa/So ratios of the partially and fully hydrolysed fumonisins were indifferent from the negative control group. Although NDF was partly cleaved during digestion, the liberated amounts of FB₁ did not raise the Sa/So ratio. These results show that the investigated alkaline and thermal processing products of FB₁ were, at the tested concentrations, non-toxic for rats, and suggest that according food processing can reduce fumonisin toxicity for humans.     

Fumonisin B1-induced mitochondrial toxicity and hepatoprotective potential of rooibos: An update

Fumonisins are a family of potentially carcinogenic mycotoxins produced by Fusarium verticillioides. Several fumonisins have been identified with fumonisin B₁ (FB₁) being the most toxic. The canonical mechanism of FB₁ toxicity is centered on its structural resemblance with sphinganine and consequent competitive inhibition of ceramide synthase and disruption of lipidomic profiles. Recent and emerging evidence at the molecular level has identified the disruption of mitochondria and excessive generation of toxic reactive oxygen species (ROS) as alternative/additional mechanisms of toxicity. The understanding of how these pathways contribute to FB₁ toxicity can lead to the identification of novel, effective approaches to protecting vulnerable populations. Natural compounds with antioxidant properties seem to protect against the induced toxic effects of FB₁. Rooibos (Aspalathus linearis), endemic to South Africa, has traditionally been used as a medicinal herbal tea with strong scientific evidence supporting its anecdotal claims. The unique composition of phytochemicals and combination of metabolic activators, adaptogens and antioxidants make rooibos an attractive yet underappreciated intervention for FB₁ toxicoses. In the search for a means to address FB₁ toxicoses as a food safety problem in developing countries, phytomedicine and traditional knowledge systems must play an integral part. This review aims to summarize the growing body of evidence succinctly, which highlights mitochondrial dysfunction as a secondary toxic effect responsible for the FB₁-induced generation of ROS. We further propose the potential of rooibos to combat this induced toxicity based on its integrated bioactive properties, as a socio-economically viable strategy to prevent and/or repair cellular damage caused by FB₁.     

Chronic Effects of Dietary Fumonisin on the Heart and Pulmonary Vasculature of Swine

Fumonisins, mycotoxins produced in Fusarium moniliforme infectedcorn, are hepatotoxic in several species and induce hepatocarcinomasin laboratory rats, leukoencephalomalacia in equine species,and fulminant pulmonary edema in swine. To date, the effectsof fumonisin on pigs has dealt solely with the high levels requiredto induce the dramatic development of acute fulminant, and usuallylethal, pulmonary edema. Less sensational, but equally important,are the chronic effects of fumonisin on swine health. In thefirst trial, six gilts were fed, ad libitum, a formulated completeration containing 100 mg fumonisin B₁ (FB₁ )/kg for 10 daysfollowed by a ration containing 190 mg FB₁/kg for up to 83 days.In the second trial, five gilts were fed, ad libitum, rationscontaining 150–170 mg FB₁/kg for up to 210 days. The concentrationof fumonisin B₂ (FB₂) was 31 ± 2% that of the FB₁ Weight-matchedcontrols were selected for cardiac parameter comparison. Pigsfed fumonisin for at least 93 days developed nodular hyperplasiaof the liver. Evidence from the microscopic examination of heartand lungs and gravimetric measurements of cardiac tissues fromfour pigs exposed to dietary fumonisins for 6 months suggeststhat the pulmonary vasculature is a target of chronic exposure.This study provides additional evidence linking the pathogenesisof fumonisin-induced lesions in a variety of organ systems ofvarious animal species to a vascular mechanism.     

Fumonisins: Abiogenic Conversions of an Environmental Tumor Promoter and Common Food Contaminant

Fumonisins are a series of sphingosine‐analog mycotoxins produced by Fusarium verticillioides, a ubiquitous contaminant of stored corn (maize) world‐wide. Extensive alterations in the structures of fumonisins are possible without complete loss of in vitro toxicity. Numerous laboratories have reported that fumonisin B₁ (FB₁) levels in corn‐derived foods are reduced during roasting and frying. We have conducted radiotracer studies to determine the fate of tritium‐labeled FB₁ added in laboratory models of corn flake manufacture (roasting), and tortilla chip manufacture (frying). These studies have confirmed that most, but not all, FB₁ is converted to other substances during cooking. Under roasting conditions the major conversion pathway resulted in radiolabeled FB₁ becoming covalently bound to proteins. Several lines of evidence supported a proposed role for FB₁‐anhydride, an intermediate formed by loss of water from a FB₁ side chain, which enabled the toxin to bind covalently to proteins by reacting with amino groups. Under nixtamalization/frying conditions in preheated cooking oil, both FB₁ and hydrolyzed FB₁ were efficiently N‐fatty acylated to the corresponding ceramide derivatives, presumably by fatty acid anhydrides or other degradation products formed from the fat by non‐oxidative thermal degradation. The N‐fatty acylated fumonisin derivatives were efficiently extracted from the chips into the hot oil. We will not understand the full threat to food safety posed by the fumonisins until we know what they are converted to during cooking, and what is the toxicity of those conversion products.     

Phytotoxicity of Fumonisins and Rfzated Compounds

Abstract

The fumonisins and AAL-toxin are related long-chain alkylamines with propane carboxylic acid moieties. The fumonisins, especially fumonisin B₁ (FB₁), were initially described as mammalian toxins; however, they are also potent phytotoxins. The fumonisins have a spectrum of susceptible plant species similar to that of AAL-toxin. The aminopentol derivatives of the B fumonisins are generally less toxic than the parent compounds, while the A series of fumonisins (acetylated forms) are essentially inactive. AAL-toxin was first thought to be host-specific for certain tomato cultivars, but now is known to affect many weed and crops species. Monocotyledonous species are less affected than dicotyledonous species. Tomatoes with the asc/asc genotype, jimsonweed, black nightshade, and duckweeds are the most susceptible species tested thus far. FB, causes toxicity on contact with plant tissue and at sites distal from wounds, demonstrating xylem mobility. AAL-toxin is an important virulence factor for infection of certain susceptible tomato cultivars by Alternaria altemata f. sp. lycopersici. Ultrastructural studies show that FB₁ and AAL-toxin both cause rapid plasma membrane disruption. Both FBI and AAL-toxin are thought to interfere with plasma membrane function through disruption of sphingolipid metabolism by inhibition of sphinganine (sphingosine) N-acyltransferase (ceramide synthase), the same mechanism of toxicity as in animals. As in animals, high levels of ceramide synthase precursors accumulate in fumonisin-and AAL-toxin-treated plants. In addition, high concentrations of long chain sphingoid bases applied to plants cause phytotoxicity symptoms similar to those of fumonisins and AAL-toxin. Thus, the phytotoxicity of fumonisins and AAL-toxin are likely to be due to the accumulation of phytotoxic sphingolipid intermediates.     

Current Issues in Research on Fumonisins,Mycotoxins Which May Cause Nephropathy

The fumonsins are a series of mycotoxins produced by the ubiquitous corn (maize) contaminant, Fusarium moniliforme, and several other Fusarium species. Fumonisin B₁ (FB₁), the major component of the fumonisins, causes leukoencephalomalacia in horses, pulmonary edema in swine and hepatocellular carcinoma, cirrhosis and chronic interstitial nephritis in rats. Also, consumption of corn-derived food products contaminated with F. moniliforme has been correlated with increased risk of human esophageal cancer in epidemiological stumes in South Africa and China. In the kidneys of rodents, dietary exposure to FB₁ produces a dose-related non-inflammatory nephrosis with regeneration at low doses. Individual cells die by induction of apoptosis. The fumonisins have chemcal structures analogous to sphingosine, a putative intracellular regulatory molecule, and a component of sphingolipids. The alkylamine structure of FB₁ makes possible sensitive high performance liquid chromatography (HPLC) assays based on pre-column derivatization of the amino group with fluorogenic reagents. These assays have been used to demonstrate that FB₁ contaminates most corn and corn-derived processed food products intended for human consumption. Conventional thermal food processing techniques reduce FB₁ levels, but do not completely eliminate it. Structure-activity relationship studies carried out in our laboratories on natural and synthetic fumonisins indicate that extensive alterations in structure are possible without loss of biological activity. This observation raises the concern that the FB₁ eliminated during food processing may actually be converted to other biologically active forms. The full extent of the threat to food safety posed by fumonisins will not be known until it is determjned what substances the toxin is converted to during food processing, the bioavailability of those substances, the extent they retain biological activity and the additivity of their toxic effects with other nephrotoxic mycotoxins such as ochratoxins A and B.     

Gastrointestinal Degradation of Fumonisin B1 by Carboxylesterase FumD Prevents Fumonisin Induced Alteration of Sphingolipid Metabolism in Turkey and Swine

The mycotoxin fumonisin B₁ (FB₁) is a frequent contaminant of feed and causes various adverse health effects in domestic animals. Hence, effective strategies are needed to prevent the impact of fumonisins on livestock productivity. Here we evaluated the capability of the fumonisin carboxylesterase FumD to degrade FB₁ to its less toxic metabolite hydrolyzed FB₁ (HFB₁) in the gastrointestinal tract of turkeys and pigs. First, an ex vivo pig model was used to examine the activity of FumD under digestive conditions. Within 2 h of incubation with FumD, FB₁ was completely degraded to HFB₁ in the duodenum and jejunum, respectively. To test the efficacy of the commercial application of FumD (FUMzyme) in vivo, female turkeys (n = 5) received either basal feed (CON), fumonisin-contaminated feed (15 mg/kg FB₁+FB₂; FB) or fumonisin-contaminated feed supplemented with FUMzyme (15 U/kg; FB+FUMzyme) for 14 days ad libitum. Addition of FUMzyme resulted in significantly decreased levels of FB₁ in excreta, whereas HFB₁ concentrations were significantly increased. Compared to the FB group (0.24 ± 0.02), the mean serum sphinganine-to-sphingosine (Sa/So) ratio was significantly reduced in the FB+FUMzyme group (0.19 ± 0.02), thus resembling values of the CON group (0.16 ± 0.02). Similarly, exposure of piglets (n = 10) to 2 mg/kg FB₁+FB₂ for 42 days caused significantly elevated serum Sa/So ratios (0.39 ± 0.15) compared to the CON group (0.14 ± 0.01). Supplementation with FUMzyme (60 U/kg) resulted in gastrointestinal degradation of FB₁ and unaffected Sa/So ratios (0.16 ± 0.02). Thus, the carboxylesterase FumD represents an effective strategy to detoxify FB₁ in the digestive tract of turkeys and pigs.     

Fumonisin B1 Inhibits Cell Proliferation and Decreases Barrier Function of Swine Umbilical Vein Endothelial Cells

The fumonisins are a group of common mycotoxins found around the world that mainly contaminate maize. As environmental toxins, they pose a threat to human and animal health. Fumonisin B₁ (FB₁) is the most widely distributed and the most toxic. FB₁ can cause pulmonary edema in pigs. However, the current toxicity mechanism of fumonisins is still in the exploratory stage, which may be related to sphingolipid metabolism. Our study is designed to investigate the effect of FB₁ on the cell proliferation and barrier function of swine umbilical vein endothelial cells (SUVECs). We show that FB₁ can inhibit the cell viability of SUVECs. FB₁ prevents cells from entering the S phase from the G1 phase by regulating the expression of the cell cycle-related genes cyclin B1, cyclin D1, cyclin E1, Cdc25c, and the cyclin-dependent kinase-4 (CDK-4). This results in an inhibition of cell proliferation. In addition, FB₁ can also change the cell morphology, increase paracellular permeability, destroy tight junctions and the cytoskeleton, and reduce the expression of tight junction-related genes claudin 1, occludin, and ZO-1. This indicates that FB₁ can cause cell barrier dysfunction of SUVECs and promote the weakening or even destruction of the connections between endothelial cells. In turn, this leads to increased blood vessel permeability and promotes exudation. Our findings suggest that FB₁ induces toxicity in SUVECs by affecting cell proliferation and disrupting the barrier function.     

The aflatoxin B1‐fumonisin B1 toxicity in BRL‐3A hepatocytes is associated to induction of cytochrome P450 activity and arachidonic acid metabolism

Human oral exposure to aflatoxin B₁ (AFB₁) and fumonisin B₁ (FB₁) is associated with increased hepatocellular carcinoma. Although evidence suggested interactive AFB₁–FB₁ hepatotoxicity, the underlying mechanisms remain mostly unidentified. This work was aimed at evaluating the possible AFB₁–FB₁ interplay to induce genetic and cell cycle toxicities in BRL‐3A rat hepatocytes, reactive oxygen species (ROS) involvement, and the AFB₁ metabolizing pathways cytochrome P450 (CYP) and arachidonic acid (ArAc) metabolism as ROS contributors. Flow cytometry of stained BRL‐3A hepatocytes was used to study the cell cycle (propidium iodide), ROS intracellular production (DCFH‐DA, HE, DAF‐2 DA), and phospholipase A activity (staining with bis‐BODIPY FL C11‐PC). The CYP1A activity was assessed by the 7‐ethoxyresorufin‐O‐deethylase (EROD) assay. Despite a 48‐h exposure to FB₁ (30 μM) not being genotoxic, the AFB₁ (20 μM)‐induced micronucleus frequency was overcome by the AFB₁–FB₁ mixture (MIX), presumably showing toxin interaction. The mycotoxins blocked G1/S‐phase, but only MIX caused cell death. Overall, the oxidative stress led these alterations as the pretreatment with N‐acetyl‐l‐cysteine reduced such toxic effects. While AFB₁ had a major input to the MIX pro‐oxidant activity, with CYP and ArAc metabolism being ROS contributors, these pathways were not involved in the FB₁‐elicited weak oxidative stress. The MIX‐induced micronucleus frequency in N‐acetyl‐l ‐cysteine pretreated cells was greater than that caused by AFB₁ without antioxidants, suggesting enhanced AFB₁ direct genotoxicity probably owing to the higher CYP activity and ArAc metabolism found in MIX. The metabolic pathways modulation by AFB₁–FB₁ mixtures could raise its hepatocarcinogenic properties.     

Isolation,purification, LC–MS/MS characterization and reactive oxygen species induced by fumonisin B1 in VERO cells

Fumonisins are mycotoxins produced by Fusarium verticillioides that commonly contaminate maize and maize products. The present work shows the results of a comparative study of three different fermentation’s techniques (solid and liquid medium of corn and a solid agarized medium) for the production of fumonisins B₁, B₂ and B₃ with strains of F. verticillioides. The solid medium of corn was the most effective in the production of fumonisins, being Fumonisin B₁ the one produced with higher concentration, so the extract obtained by solid fermentation process was used for FB₁ purification. Fumonisins characterization and quantification were performed with reversed-phase high-performance liquid chromatography with electrospray ionization triple quadrupole tandem mass spectrometry. The role of production of reactive oxygen species (ROS) in Fumonisin B₁ mediated toxicology has not been fully addresses in studies exploring FB₁ toxicity. It is evaluated the level of ROS production in kidney cell line (VERO) exposed to 1, 5 and 10 μM of FB₁ for 0.5–100 min. The ROS level was detected using a fluorescence probe, 2′,7′-dichlorofluorescein diacetate (DCFH-DA), which could be converted to highly fluorescent dichlorofluorescein (DCF) with the presence of intracellular ROS. Significant increase of ROS products was observed in VERO cells at 10 μM dose. These results indicate that ROS production by FB₁ on renal cells is a mechanism of fumonisin mediated toxicity.     

Detection of N-(1-deoxy-d-fructos-1-yl) Fumonisins B2 and B3 in Corn by High-Resolution LC-Orbitrap MS

The existence of glucose conjugates of fumonisin B₂ (FB₂) and fumonisin B₃ (FB₃) in corn powder was confirmed for the first time. These “bound-fumonisins” (FB₂ and FB₃ bound to glucose) were identified as N-(1-deoxy-d-fructos-1-yl) fumonisin B₂ (NDfrc-FB₂) and N-(1-deoxy-d-fructos-1-yl) fumonisin B₃ (NDfrc-FB₃) respectively, based on the accurate mass measurements of characteristic ions and fragmentation patterns using high-resolution liquid chromatography-Orbitrap mass spectrometry (LC-Orbitrap MS) analysis. Treatment on NDfrc-FB₂ and NDfrc-FB₃ with the o-phthalaldehyde (OPA) reagent also supported that d-glucose binding to FB₂ and FB₃ molecules occurred to their primary amine residues.     

Fumonisin B1 and the kidney: Modes of action for renal tumor formation by fumonisin B1 in rodents

The mycotoxin fumonisin B₁ (FB₁) is an important contaminant of maize and maize-based products. In rodent toxicity studies, FB₁ was shown to be hepato- and nephrotoxic, and to induce renal tumors in rats when administered via the diet. Of particular note are the aggressive growth characteristics of FB₁-induced tumors with a high potential to metastasize. While genotoxicity does not appear to contribute to FB₁ carcinogenicity, it is well established that FB₁-mediated disruption of sphingolipid metabolism plays a key role in FB₁ toxicity. This review provides an overview on human dietary exposure to FB₁, FB₁ toxicity and carcinogenicity, and potential mechanisms involved in FB₁-mediated tumor formation, with a particular focus on cellular functions of sphingolipids and biological consequences of FB₁-mediated perturbation of sphingolipid metabolism.     

Grape Seed Proanthocyanidin Ameliorates FB1-Induced Meiotic Defects in Porcine Oocytes

Fumonisin B₁ (FB₁), as the most prevalent and toxic fumonisin, poses a health threat to humans and animals. The cytotoxicity of FB₁ is closely related to oxidative stress and apoptosis. The purpose of this study is to explore whether Grape seed proanthocyanidin (GSP), a natural antioxidant, could alleviate the meiotic maturation defects of oocytes caused by FB₁ exposure. Porcine cumulus oocyte complexes (COCs) were treated with 30 μM FB₁ alone or cotreated with 100, 200 and 300 μM GSP during in vitro maturation for 44 h. The results show that 200 μM GSP cotreatment observably ameliorated the toxic effects of FB₁ exposure, showing to be promoting first polar body extrusion and improving the subsequent cleavage rate and blastocyst development rate. Moreover, 200 μM GSP cotreatment restored cell cycle progression, reduced the proportion of aberrant spindles, improved actin distribution and protected mitochondrial function in FB₁-exposed oocytes. Furthermore, reactive oxygen species (ROS) generation was significantly decreased and the mRNA levels of CAT, SOD2 and GSH-PX were obviously increased in the 200 μM GSP cotreatment group. Notably, the incidence of early apoptosis and autophagy level were also significantly decreased after GSP cotreatment and the mRNA expression levels of BAX, CASPASE3, LC3 and ATG5 were markedly decreased, whereas BCL2 and mTOR were observably increased in the oocytes after GSP cotreatment. Together, these results indicate that GSP could exert significant preventive effects on FB₁-induced oocyte defects by ameliorating oxidative stress through repairing mitochondrial dysfunction.     

Diversity of Pea-Associated F. proliferatum and F. verticillioides Populations Revealed by FUM1 Sequence Analysis and Fumonisin Biosynthesis

Fusarium proliferatum and F. verticillioides are considered as minor pathogens of pea (Pisum sativum L.). Both species can survive in seed material without visible disease symptoms, but still contaminating it with fumonisins. Two populations of pea-derived F. proliferatum and F. verticillioides strains were subjected to FUM1 sequence divergence analysis, forming a distinct group when compared to the collection strains originating from different host species. Furthermore, the mycotoxigenic abilities of those strains were evaluated on the basis of in planta and in vitro fumonisin biosynthesis. No differences were observed in fumonisin B (FB) levels measured in pea seeds (maximum level reached 1.5 μg g⁻¹); however, in rice cultures, the majority of F. proliferatum genotypes produced higher amounts of FB₁–FB₃ than F. verticillioides strains.     

Chemoprotective properties of rooibos (Aspalathus linearis), honeybush (Cyclopia intermedia) herbal and green and black (Camellia sinensis) teas against cancer promotion induced by fumonisin B1 in rat liver

The chemoprotective properties of unfermented and fermented rooibos (Aspalathus linearis) and honeybush (Cyclopia intermedia) herbal teas, and green and black teas (Camellia sinensis) were investigated against fumonisin B₁ (FB₁) promotion in rat liver utilizing diethylnitrosamine (DEN) as cancer initiator. The various teas differently affected the clinical chemical parameters associated with liver and kidney damage associated with FB₁ suggesting specific FB₁/iron/polyphenolic interactions. Green tea enhanced (P < 0.05) the FB₁-induced reduction of the oxygen radical absorbance capacity, while fermented herbal teas and unfermented honeybush significantly (P < 0.05) decreased FB₁-induced lipid peroxidation in the liver. The teas exhibited varying effects on FB₁-induced changes in the activities of catalase, glutathione peroxidase (GPx) glutathione reductase (GR) as well as the glutathione (GSH) status. Unfermented rooibos and honeybush significantly (P < 0.05) to marginally (P < 0.1) reduced the total number of foci (>10 μm), respectively, while all the teas reduced the relative amount of the larger foci. Fermentation seems to reduce the protective effect of the herbal teas. Differences in the major polyphenolic components and certain FB₁/polyphenolic/tissue interactions may explain the varying effects of the different teas on the oxidative parameters, hepatotoxic effects and cancer promotion in rat liver.