Biodegradation of atrazine, glyphosate and pendimetaline employing fungal consortia

The objective of the present study was to evaluate the bioremediation of soils artificially contaminated with atrazine, glyphosate and pendimethalin by fungal consortia in biodegradation processes in microcosms. Biodegradation was evaluated from microbial respiration over a period of 15 days and genotoxicity analysis in Allium cepa roots exposed to elutriate samples at zero and 50 μg mL-1 concentrations of the herbicides after the biodegradation process. The results were submitted to analysis of variance, the Tukey test and the Fischer test (p<0.05%) for comparison of means. The Aspergillus fumigatus - Penicillium citrinum consortium had a larger capacity to degrade atrazine but metabolism was inhibited in the presence of glyphosate and pendimethalin. There was a delay in the mitotic index in the meristematic cells of the Allium cepa roots exposed to the elutriates in the 50 μg mL-1 atrazine and pendimethalin concentration. There was a cellular alteration in the metaphase phase of the cells exposed to the elutriates at the 50 μg mL-1 concentration of the three herbicides. The changes occurred were low, indicating that there was degradation of part of the herbicides.

Ectonucleoside Triphosphate Diphosphohydrolase Type 5 (Entpd5)-Deficient Mice Develop Progressive Hepatopathy, Hepatocellular Tumors, and Spermatogenic Arrest

Ectonucleoside triphosphate diphosphohydrolase type 5 (ENTPD5, also CD39L4) is a soluble enzyme that hydrolyzes purine nucleoside diphosphates. Genetic inactivation of ENTPD5 in mice ( Entpd5-/-) resulted in 2 major histopathologic lesions: hepatopathy and aspermia. The hepatopathy was progressive and characterized by centrilobular hepatocyte hypertrophy, oval cell proliferation, bile staining of Kupffer cells, and hepatocyte degeneration with increasing incidence and severity of degenerative lesions, development of multiple foci of cellular alteration, and hepatocellular neoplasia with age. Greatly increased proliferation of hepatocytes in young adult as well as aged Entpd5-/- mice was demonstrated by Ki67 immunohistochemistry and 5î-bromo-3î-deoxyuridine incorporation. Of 15 Entpd5-/- mice between 44 and 69 weeks of age, all showed foci of cellular alteration in the liver, and at least 6 of 15 developed hepatocellular carcinoma (HCC), hepatocellular adenoma, or both. Significantly, none of these lesions were observed in 13 wild-type Entpd5++ littermates. These findings, combined with the historically low incidence (about 5%) of HCC in mice up to 2 years of age with the same genetic background, strongly suggest that loss of Entpd5 promotes hepatocellular neoplasia in mice. In humans, ENTPD5 has been found to be identical to the PCPH proto-oncogene, and dysregulation of this gene has been demonstrated in some human cancers. This mouse model could contribute to the understanding of the influence of ENTPD5/PCPH on cellular proliferation and neoplasia.