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The Science of the Total Environment Sep 2020Microplastic ingestion in invertebrates reduces somatic and reproductive growth. This could be caused by energy reserves being detracted from growth processes and...
Microplastic ingestion in invertebrates reduces somatic and reproductive growth. This could be caused by energy reserves being detracted from growth processes and redistributed to maintenance processes that preserve life. A potential sink for this diverted energy is the antioxidant system, which minimises oxidative damage and reinstates redox homeostasis following disturbances caused by exposure to pollution. Several microplastic studies have used genetic and molecular redox biomarkers to assess how microplastic ingestion affects the functioning of the antioxidant system. This systematic review synthesises the current understanding of redox biomarker responses in invertebrates that have ingested microplastics. We found that biomarker response information exists for only seven invertebrate taxa, and early life stages have received little scientific attention. The microplastics used by most studies were polystyrene (45% of studies), spherical (51% of studies), and were < 10 μm in diameter (31% of studies). We found multiple examples of microplastic ingestion posing an oxidative challenge to invertebrates, which required upregulation of antioxidant system components. However, the lack of systematic experiments prevented us from clearly identifying which characteristic of microplastics caused these responses. We identify several areas for consideration when investigating biomarker responses to microplastic ingestion and offer research priorities for future studies.
Topics: Animals; Antioxidants; Environmental Monitoring; Invertebrates; Microplastics; Water Pollutants, Chemical
PubMed: 32470656
DOI: 10.1016/j.scitotenv.2020.138559 -
Frontiers in Medicine 2021This manuscript presents findings from the first dichotomous data pooling analysis on clinical trials (CT) regarding the effectiveness of binding potassium. The results...
Binding Potassium to Improve Treatment With Renin-Angiotensin-Aldosterone System Inhibitors: Results From Multiple One-Stage Pairwise and Network Meta-Analyses of Clinical Trials.
This manuscript presents findings from the first dichotomous data pooling analysis on clinical trials (CT) regarding the effectiveness of binding potassium. The results emanated from pairwise and network meta-analyses aiming evaluation of response to commercial potassium-binding polymers, that is, to achieve and maintain normal serum potassium ( = 1,722), and the association between this response and an optimal dosing of renin-angiotensin-aldosterone system inhibitors (RAASi) needing individuals affected by heart failure (HF) or resistant hypertension, who may be consuming other hyperkalemia-inducing drugs (HKID) (e.g., β-blockers, heparin, etc.), and frequently are affected by chronic kidney disease (CKD) ( = 1,044): According to the surface under the cumulative ranking area (SUCRA), sodium zirconium cyclosilicate (SZC) (SUCRA >0.78), patiromer (SUCRA >0.58) and sodium polystyrene sulfonate (SPS) (SUCRA <0.39) were different concerning their capacity to achieve normokalemia (serum potassium level (sK+) 3.5-5.0 mEq/L) or acceptable kalemia (sK+ ≤ 5.1 mEq/L) in individuals with hyperkalemia (sK+ >5.1 mEq/L), and, when normokalemia is achieved, patiromer 16.8-25.2 g/day (SUCRA = 0.94) and patiromer 8.4-16.8 g/day (SUCRA = 0.41) can allow to increase the dose of spironolactone up to 50 mg/day in subjects affected by heart failure (HF) or with resistant hypertension needing treatment with other RAASi. The potential of zirconium cyclosilicate should be explored further, as no data exists to assess properly its capacity to optimize dosing of RAASi, contrarily as it occurs with patiromer. More research is also necessary to discern between benefits of binding potassium among all type of hyperkalemic patients, for example, patients with DM who may need treatment for proteinuria, patients with early hypertension, etc. https://www.crd.york.ac.uk/PROSPERO/, identifier: CRD42020185614, CRD42020185558, CRD42020191430.
PubMed: 34490289
DOI: 10.3389/fmed.2021.686729