The extracts obtained have promising antibacterial capacities which need further investigation for them to be incorporated in medical or nutritional applications.

Microplastic (MP) pollution is everywhere. In terrestrial environments, microfibres (MFs) generated from textile laundering are believed to form a significant component of MPs entering soils, mainly through sewage sludge and compost applications. The aim of this study was to assess the effect of MFs on a keystone soil organism. We exposed the earthworm Lumbricus terrestris to soil with polyester MFs incorporated at rates of 0, 0.1 and 2 1.0 %w/w MF for a period of 35 days (in the dark at 15 o C; n = 4 for each treatment). Dried plant litter was applied at the soil surface as a food source for the earthworms. We assessed earthworm vitality through mortality, weight change, depurate production and MF avoidance testing. In addition, we measured stress biomarker responses via the expression of metallothionein-2 (mt-2), heat shock protein (hsp70) and superoxide dismutase (sod-1). Our results showed that exposure and ingestion of MFs (as evidenced by subsequent retrieval of MFs within earthworm depurates) were not lethal to earthworms, nor did earthworms actively avoid MFs. However, earthworms in the MF1.0% treatment showed a 1.5-fold lower cast production, a 24.3-fold increase in expression of mt-2 (p < 0.001) and a 9.9-fold decline in hsp70 expression (p < 0.001). Further analysis of soil and MF samples indicated that metal content was not a contributor to the biomarker results. Given that burrowing and feeding behaviour, as well as molecular genetic biomarkers, were modulated in earthworms exposed to MFs, our study highlights potential implications for soil ecosystem processes due to MF contamination.

Prurigo pigmentosa (PP) is a rare idiopathic inflammatory dermatosis that typically presents as pruritic erythematous papulovesicles in a reticular pattern predominantly on the trunk of young women. [1][2][3] The lesions then resolve with residual hyperpigmentation. The pathogenesis of PP is not completely clear. However, it has mainly been associated with ketotic states such as those seen in dieting, fasting, diabetes mellitus, and softdrink ketosis. [1][2][3] Herein we report the first case to our knowledge of PP occurring after bariatric surgery, which provides further evidence of a possible role of ketosis in PP pathogenesis.

Benzo[a]pyrene (BaP) is bioactivated in most organisms by the cytochrome P450 (CYP) enzymes, mainly CYP1A1, ultimately resulting in the reactive metabolite BaP-7,8-dihydrodiol-9,10-epoxide (BPDE) capable of covalently binding to DNA and forming adducts. This step has been defined as the key process in cancer initiation in humans. However, limited knowledge is available about the consequences of BaP exposure in organisms lacking this classical CYP1A1 pathway, one example is the model nematode Caenorhabditis elegans. The aim of this study was to define the genotoxic potential of BaP in C. elegans and to advance our understanding of xenobiotic processing in the absence of the CYP1A1 pathway. Exposure to high concentrations of BaP (0–40 µM) significantly affected life cycle endpoints of C. elegans, which were manifested by a reduced reproductive output and shortened life span. An optimised comet assay revealed that DNA damage increased in a dose-dependent manner; however, no bulky DNA adducts (dG-N2-BPDE) were observed by 32P-postlabelling. Global transcriptomic analysis by RNA-Seq identified responsive transcript families, most prominently members of the cyp-35 and UDP-glucuronosyltransferases (UGTs) enzyme families, both of which are linked to xenobiotic metabolism. Strains harbouring mutations in the cyp-35A2 and cyp-35A3 genes were notably less prone to BaP-mediated toxicity, and BaP led to longevity in cyp-35A5 mutants. In summary, BaP induces transcriptional, genotoxic and phenotypic responses in C. elegans, despite the absence of the classical CYP1A1 bioactivation pathway. This provides first evidence that parallel pathways are implicated in BaP metabolism in C. elegans and this seems to be mediated via the cyp-35 pathway.

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