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- Gallo, Valentina, et al.
(författare)
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Proteomic Analysis Identifies Markers of Exposure to Cadmium Sulphide Quantum Dots (CdS QDs)
- 2020
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Ingår i: Nanomaterials. - : MDPI. - 2079-4991. ; 10:6
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Tidskriftsartikel (refereegranskat)abstract
- The use of cadmium sulphide quantum dot (CdS QD)-enabled products has become increasingly widespread. The prospect of their release in the environment is raising concerns. Here we have used the yeast modelSaccharomyces cerevisiaeto determine the potential impact of CdS QD nanoparticles on living organisms. Proteomic analyses and cell viability assays performed after 9 h exposure revealed expression of proteins involved in oxidative stress and reduced lethality, respectively, whereas oxidative stress declined, and lethality increased after 24 h incubation in the presence of CdS QDs. Quantitative proteomics using the iTRAQ approach (isobaric tags for relative and absolute quantitation) revealed that key proteins involved in essential biological pathways were differentially regulated over the time course of the experiment. At 9 h, most of the glycolytic functions increased, and the abundance of the number of heat shock proteins increased. This contrasts with the situation at 24 h where glycolytic functions, some heat shock proteins as well as oxidative phosphorylation and ATP synthesis were down-regulated. It can be concluded from our data that cell exposure to CdS QDs provokes a metabolic shift from respiration to fermentation, comparable to the situation reported in some cancer cell lines.
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| 2. |
- Peters, Susan, et al.
(författare)
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Alcohol Consumption and Risk of Parkinson's Disease : Data from a Large Prospective European Cohort
- 2020
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Ingår i: Movement Disorders. - : John Wiley & Sons. - 0885-3185 .- 1531-8257. ; 35:7, s. 1258-1263
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Tidskriftsartikel (refereegranskat)abstract
- Background: Parkinson's disease (PD) etiology is not well understood. Reported inverse associations with smoking and coffee consumption prompted the investigation of alcohol consumption as a risk factor, for which evidence is inconclusive.Objective: To assess the associations between alcohol consumption and PD risk.Methods: Within NeuroEPIC4PD, a prospective European population‐based cohort, 694 incident PD cases were ascertained from 209,998 PD‐free participants. Average alcohol consumption at different time points was self‐reported at recruitment. Cox regression hazard ratios were estimated for alcohol consumption and PD occurrence.Results: No associations between baseline or lifetime total alcohol consumption and PD risk were observed. Men with moderate lifetime consumption (5–29.9 g/day) were at ~50% higher risk compared with light consumption (0.1–4.9 g/day), but no linear exposure–response trend was observed. Analyses by beverage type also revealed no associations with PD.Conclusion: Our data reinforce previous findings from prospective studies showing no association between alcohol consumption and PD risk.
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