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Diazinon is an organophosphorus pesticide, which may have potential toxic effects on the liver and immune system; however, the underlying mechanisms remain mostly unidentified. This work is aimed at evaluating the oxidative stress and cell cycle alterations elicited by low-dose diazinon in a rat liver cell line (BRL-3A) and spleen mononuclear cells (SMC) from Wistar rats. Diazinon (10–50 μM) caused early reactive oxygen species (ROS) generation (from 4 h) as well as increased O2•- level (from 0.5 h), which led to subsequent lipid peroxidation at 24 h, in BRL-3A cells. In SMC, diazinon (20 μM) produced similar increases in ROS levels, at 4 and 24 h, with the highest O2•- level being found at 4 h. Low-dose diazinon induced G1-phase arrest and cell death in hepatic cells and SMC. Therefore, diazinon could affect the liver and the immunological system through the premature oxidative stress induction. Abbreviations: O2•-: superoxide anion radical; ROS: reactive oxygen species; SMC: spleen mononuclear cells; TBARS: thiobarbituric acid reactive substances [ABSTRACT FROM AUTHOR]

Fungal and plant secondary metabolites modulate host-pathogen interactions. However, the participation of fumonisin B1 (FB1) in the Fusarium verticillioides-maize pathosystem is unclear. In this work, cell death and the reactive oxygen species-phytohormone imbalance interplay as well as their correlation with the FB1 phytotoxicity in two maize genotypes with contrasting resistance to Fusarium ear rot were studied. Resistant (RH) and susceptible hybrid (SH) maize seedlings, grown from uninoculated seeds irrigated with FB1 (1 and 20 μg/mL), were harvested at 7, 14 and 21 days after planting, and were examined for electrolyte leakage (aerial parts) and for oxidative stress biomarkers (aerial parts and roots). The salicylic/jasmonic acid levels associated with cytotoxicity were further explored in seedlings exposed 24 h to FB1 (1 μg/mL) in hydroponics, with and without pre-treatment with the antioxidant ascorbic acid (AA). Cell death increased in RH and SH watered with 1 and 20 μg/mL of mycotoxin, respectively. Both toxin concentrations were pro-oxidant, and the major perturbations were found in roots. The overall plant stress, estimated by an Integrated Biomarker Response index, was higher in plants treated with 20 μg/mL of FB1, while treatment with 1 μg/mL caused more stress in RH at 21 days. Different phytohormone changes were found in both hybrids: salicylic acid increases (prevented by AA) in RH, and jasmonic acid decreases in both germplasms (although prevented by AA pre-treatment only in SH). Cell death induced by FB1 was associated with different phytohormonal regulatory mechanisms in both maize genotypes, some of which were mediated by the redox status. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Considering the impact of Aspergillus species on crops, it appears to be highly desirable to apply strategies to prevent their growth, as well as to eliminate or reduce their presence in food products. For this reason, the aims of this investigation were to evaluate the effects of ten natural phenolic compounds on the Aspergillus parasiticus growth and to determine which physicochemical properties are involved in the antifungal activity. According to the results of minimum inhibitory concentration (MIC) values of the individual compounds, isoeugenol, carvacrol, and thymol were the most active phenolic components (1.26 mM, 1.47 mM, and 1.50 mM, resp.), followed by eugenol (2.23 mM). On the other hand, creosol, p-cresol, o-cresol, m-cresol, vanillin, and phenol had no effects on fungal development. Logarithm of the octanol/water partition coefficient (log P), refractivity index (RI), and molar volume (MV) were demonstrated to be the descriptors that best explained the antifungal activity correlated to lipophilicity, reactivity of the components, and steric aspect. These findings make an important contribution to the search for new compounds with antifungal activity. [ABSTRACT FROM AUTHOR]