Microplastics are widely identified in aquatic environments, but their impacts on phytoplankton have not been extensively studied. Here, the responses of Chlorella pyrenoidosa under polystyrene (PS) ...microplastics exposure were studied across its whole growth period, with microplastic sizes of 0.1 and 1.0 μm and 3 concentration gradients each, which covered (10 and 50 mg/L) and exceeded (100 mg/L) its environmental concentrations, respectively. PS microplastics caused dose-dependent adverse effects on Chlorella pyrenoidosa growth from the lag to the earlier logarithmic phases, but exhibited slight difference in the maximal inhibition ratio (approximately 38%) with respect to the two microplastic sizes. In addition to the reduced photosynthetic activity of Chlorella pyrenoidosa, unclear pyrenoids, distorted thylakoids and damaged cell membrane were observed, attributing to the physical damage and oxidative stress caused by microplastics. However, from the end of the logarithmic to the stationary phase, Chlorella pyrenoidosa could reduce the adverse effects of microplastics jointly through cell wall thickening, algae homo-aggregation and algae-microplastics hetero-aggregation, hence triggering an increase of algal photosynthetic activity and its growth, and cell structures turned to normal. Our study confirmed that PS microplastics can impair but then enhance algae growth, which will be helpful in understanding the ecological risks of microplastics.
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•Effects of PS microplastics on algae were studied over its entire growth period.•PS microplastics caused depression but then stimulation of algal growth.•Physical damage and oxidative stress are involved in depression of algal growth.
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•Arbuscular mycorrhiza fungi are likely fatty acid auxotrophs.•Plants maintain an arbuscular mycorrhiza (AM)-specific lipid biosynthesis pathway.•Independent experimental approaches ...show lipid transfer from plants to AM fungi.•Lipid scavenging from hosts evolved multiple times in interorganismic interactions.
Arbuscular mycorrhiza (AM) is a widespread symbiosis between most land plants and fungi of the Glomeromycotina, which has existed for more than 400million years. AM fungi (AMF) improve plant nutrition with mineral nutrients and conversely, their growth and development is fueled by organic carbon supplied from their host. Recent studies demonstrated independently and with different experimental approaches that lipids are transferred from plants to fungi in addition to sugars, and that AMF are dependent on this lipid supply because they lack genes encoding fatty acid synthase I subunits. Dependence on host lipids or lipid parasitism occur in a range of interorganismic associations with participants from almost all kingdoms. Thus, these phenomena seem rather common in mutualistic and parasitic interactions.
The identification of disease-causing mutations has in recent years progressed immensely due to whole genome sequencing approaches using patient material. The task accordingly is shifting from gene ...identification to functional analysis of putative disease-causing genes, preferably in an in vivo setting which also allows testing of drug candidates or biotherapeutics in whole animal disease models. In this review, we highlight the advances made in the field of bone diseases using small laboratory fish, focusing on zebrafish and medaka. We particularly highlight those human conditions where teleost models are available.
•Both mitochondrial dysfunction and neuroinflammation contribute significantly to neurodegenerative diseases.•Multiple inflammatory mediators are known to affect in mitochondrial energy metabolism ...and mitochondrial dynamics.•In turn, mitochondrial dysfunction can promote inflammation.
Experimental evidence supports an intricate association between inflammation and mitochondrial dysfunction as main contributors of neurological diseases. Inflammatory mediators produced by activated microglia and infiltrated immune cells trigger intracellular signalling cascades that can alter cellular mitochondrial metabolism. Cytokines, particularly tumor necrosis factor-alpha, impede mitochondrial oxidative phosphorylation and associated ATP production and instigate mitochondrial reactive oxygen species production. This culminates in mitochondrial membrane permeabilization, altered mitochondrial dynamics and might ultimately result in cell death. When severely injured mitochondria are not appropriately removed by mitophagy they can release their contents into the cytosol and extracellular environment and thereby amplify the inflammatory process. Here we provide a comprehensive overview on how inflammatory mediators impair mitochondrial metabolism and discuss how defective mitochondria can elicit and potentiate an inflammatory response.
Cadmium (Cd) is a toxic heavy metal that accumulates in living systems. Exposure can occur occupationally or environmentally. Workers within the electroplating, battery production, and pigment ...industries are at the highest risk for exposure and have been reported to have increased levels of Cd in their blood and urine. Environmental exposure can be the result of anthropogenic activities or smoking. Cd has a long half-life and bio accumulates in plants, invertebrates, and vertebrates. The toxic effects following exposure include growth retardation and organ system toxicity, with kidney and liver toxicity most reported with in higher organisms. At the molecular level, Cd leads to the production of reactive oxygen species, DNA damage, and inhibition of DNA repair. This article gives a brief overview of the correlations between exposure to cadmium occupationally and environmentally and levels measured in blood and urine. It also examines the bioaccumulation of cadmium in aquatic invertebrates and vertebrates indicating that accumulation varies not only by location but also within and between various species.
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•Exposure to cadmium can occur occupationally of environmentally.•Cadmium exposure can be measured using blood and urine samples.•Cadmium bio accumulates in vertebrate and aquatic invertebrate organisms.•Free cadmium can accumulates aquatic organisms leading to biotransfer into vertebrates.•Cadmium exposure leads to ROS production and DNA damage.
Fibroblasts are diverse mesenchymal cells that participate in tissue homeostasis and disease by producing complex extracellular matrix and creating signaling niches through biophysical and ...biochemical cues. Transcriptionally and functionally heterogeneous across and within organs, fibroblasts encode regional positional information and maintain distinct cellular progeny. We summarize their development, lineages, functions, and contributions to fibrosis in four fibroblast-rich organs: skin, lung, skeletal muscle, and heart. We propose that fibroblasts are uniquely poised for tissue repair by easily reentering the cell cycle and exhibiting a reversible plasticity in phenotype and cell fate. These properties, when activated aberrantly, drive fibrotic disorders in humans.
A detailed mechanistic, molecular, and functional view of the commonalities and organ-specific features of fibroblasts in health and disease is just beginning to emerge.
•ROS is both a trigger and an effector of NLRP3 inflammasome activation.•Ca2+ influx is upstream of NLRP3 inflammasome activation.•ADP-ribose (ADPR) activates TRPM2 under ROS in the NLRP3 ...pathway.•ADPR and Ca2+ co-activate TRPM2.•There exist drastic differences in TRPM2’s structure and function during evolution.
The NLRP3 inflammasome is an innate immune platform that senses various pathogens and sterile insults. NLRP3 stimulation leads to activation of caspase-1, the secretion of pro-inflammatory cytokines and an inflammatory cell death called pyroptosis. Effectors of the NLRP3 inflammasome efficiently drive an immune response, not only providing protection in physiological settings but also promoting pathology when over activated. Generation of reactive oxygen species (ROS) and intracellular calcium mobilization can activate the NLRP3 inflammasome. Recent studies suggest that TRPM2 is a calcium-permeable cation channel mediating ROS-dependent NLRP3 activation. Here, we review the role of TRPM2 in NLRP3 inflammasome activation and provide an update on new functional and structural discoveries. Understanding the molecular mechanism of TRPM2 dependent NLRP3 inflammasome activation will shed lights on this complex pathway and help the developing of therapeutic strategies.
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