Chlorpyrifos [HRP]

In 2015, after the Fundao dam failure, in Minas Gerais State, Brazil, around 50 million cubic meters of sludge from iron mining tailings were discharged into the Doce River. After the dam collapse, surpassing concentrations of metals were observed in the river sediment, which could be harmful to aquatic organisms, including the fishes. The present study aimed to evaluate the toxic effects of both elutriate and water, collected from the Doce River, on Astyanax lacustris three years after the dam failure. A bioassay was carried out through subchronic exposure to Doce River water (E0) and three elutriate concentrations (10, 50 and 100%). Biochemical analyses (CAT, GST, AChE), metal bioaccumulation assays and calculation of the integrated biomarker response index, version 2 (IBRv2) were performed. The outcomes uncovered deleterious consequences on organisms exposed to E0, with AChE inhibition and bioaccumulation of Fe and Mn in both liver and gills. IBRv2 values were more elevated in fishes exposed to E0 for all tissues. Thus, the elutriate was not harmful for the assessed fishes, since complexing agents presented in the sediment, such as goethite and hematite, may have triggered metals' chelation. In this scenario, the elutriate may have acted as a protective agent for the subjected organisms, unlike the Doce River waters, in which contaminants were proven to be hazardous for the aquatic biota. (c) 2020 Elsevier B.V. All rights reserved.

The fungal metabolism of diazinon was investigated and the microbial model (Cunninghamella elegans ATCC36112) could effectively degrade the organophosphorus pesticide (diazinon) mediated by cytochrome P450, which was mainly involved in oxidation and hydrolysis of phase I metabolism. Approximately 89% of diazinon was removed within 7 days and was not observed after 13 days with concomitant accumulation of eight metabolites. Structures of the metabolites were fully or tentatively identified with GC-MS and H-1, C-13 NMR. The major metabolites of diazinon were diethyl (2-isopropyl-6-methylpyrimidin-4-yl) phosphate (diazoxon) and 2-isopropyl-6-methyl-4-pyrimidinol (pyrimidinol), and formation of minor metabolites was primarily the result of hydroxylation. To determine the responsible enzymes in diazinon metabolism, piperonyl butoxide and methimazole were treated, and the kinetic responses of diazinon and its metabolites by Cunninghamella elegans were measured. Results indirectly demonstrated that cytochrome P450 and flavin monooxygenase were involved in the metabolism of diazinon, but methimazole inhibited the metabolism less effectively. Based on the metabolic profiling, a possible metabolic pathway involved in phase I metabolism of diazinon was proposed, which would contribute to providing insight into understanding the toxicological effects of diazinon and the potential application of fungi on organophosphorus pesticides.