Microplastics in the marine environment: Current trends in environmental pollution and mechanisms of toxicological profile

Potential human health risks due to environmental exposure to nano- and microplastics and knowledge gaps: A scoping review.

To obtain a global view of functional interactions among genes in a metazoan genome, we computationally integrated interactome data, gene expression data, phenotype data, and functional annotation data from three model organisms—Saccharomyces cerevisiae, Caenorhabditis elegans, and Drosophila melanogaster—and predicted genome-wide genetic interactions in C. elegans. The resulting genetic interaction network (consisting of 18,183 interactions) provides a framework for system-level understanding of gene functions. We experimentally tested the predicted interactions for two human disease-related genes and identified 14 new modifiers.

Supporting Online Material for Genome-wide Prediction of C. elegans Genetic Interactions

Micro- and nanoplastics are generated from plastics and have negative impacts on the environment due to their high level of fragmentation. They can originate from various sources such as fragments, fibers and foams. The large proportion of the waste and resistance to degradation means micro- and nanoplastics have become a serious global environmental problem, but there are few studies on their potential toxicity for human health. In this review, we discussed routes of exposure and the potential effects of micro- and nanoplastics to human health. Human beings could mainly be exposed to micro- and nanoplastics orally and by inhalation. The possible toxic effects of plastic particles are due to the potential toxicity of plastics themselves, and their combined toxicity with leachable additives and adsorbed contaminants. The potential risks for human health focused on their gastrointestinal toxicity and liver toxicity. The toxic mechanisms could involve oxidative stress, inflammatory reactions and metabolism disorders. More studies are needed to carry out and explore the potential toxicological mechanisms of micro- and nanoplastics and evaluate the combined toxicity of their adsorbed contaminants.

Potential health impact of environmental micro- and nanoplastics pollution

Uptake of nanopolystyrene particles induces distinct metabolic profiles and toxic effects in Caenorhabditis elegans.

Using acs-22 mutant Caenorhabditis elegans to detect the toxicity of nanopolystyrene particles.

Nanopolystyrene particles have been widely used in many fields. However, the molecular responses of organisms to nanopolystyrene particles at predicted environmentally relevant concentrations are still largely unclear. Caenorhabditis elegans is employed herein to investigate the molecular response of p38 mitogen-activated protein kinase (MAPK) signaling to nanoplastic particles (1 µg L-1 ) and the underlying molecular mechanism. In wild-type nematodes, prolonged exposure (from L1-larvae to adult day 3) to nanopolystyrene particles increases the expression of pmk-1 encoding a p38 MAPK. Mutation of pmk-1 induces a susceptibility to nanopolystyrene toxicity, suggesting that the p38 MAPK signaling mediates a protective response to nanopolystyrene particles. PMK-1 functions in the intestine to act upstream of two transcriptional factors (ATF-7 and SKN-1), which can further act upstream of XBP-1, a key regulator of endoplasmic reticulum unfolded protein response (ER UPR), to regulate the response to nanopolystyrene particles. PMK-1, ATF-7, SKN-1, and XBP-1 are all required for the induction of intestinal ER UPR in nematodes exposed to nanopolystyrene particles. Therefore, the intestinal p38 MAPK signaling may mediate a protective response to nanopolystyrene particles by activating XBP-1-mediated ER UPR. The results herein highlight the importance of molecular response in the intestine of organisms to nanopolystyrene particles.

Kangni Xu

Papers

Using acs-22 mutant Caenorhabditis elegans to detect the toxicity of nanopolystyrene particles.

Activation of p38 MAPK Signaling-Mediated Endoplasmic Reticulum Unfolded Protein Response by Nanopolystyrene Particles.