Domestic laundry and microfiber pollution: Exploring fiber shedding from consumer apparel textiles.

Synthetic fibers are increasingly seen to dominate microplastic pollution profiles in aquatic environments, with evidence pointing to textiles as a potentially important source. However, the loss of microfibers from textiles during laundry is poorly understood. We evaluated microfiber release from a variety of synthetic and natural consumer apparel textile samples (n = 37), with different material types, constructions, and treatments during five consecutive domestic laundry cycles.

Pervasive distribution of polyester fibres in the Arctic Ocean is driven by Atlantic inputs.

Microplastics are increasingly recognized as ubiquitous global contaminants, but questions linger regarding their source, transport and fate. We document the widespread distribution of microplastics in near-surface seawater from 71 stations across the European and North American Arctic - including the North Pole. We also characterize samples to a depth of 1,015 m in the Beaufort Sea.

Using flow cytometry to detect haemic neoplasia in mussels (Mytilus trossulus) from the Pacific Coast of Southern British Columbia, Canada.

Flow cytometry was investigated as an alternative to visual haemocytology for potentially higher-throughput and less subjective detection of neoplasia in Mytilus trossulus. In contrast to previous studies of ploidy in the Mytilus spp. complex, distinct tetra- and pentaploidal neoplastic cells were rare and a wide range of aneuploidy peaks from 1.

Variations in p53-like cDNA sequence are correlated with mussel haemic neoplasia: A potential molecular-level tool for biomonitoring.

Several bivalve species, including mussels (Mytilus spp.) and clams (Mya spp.), are susceptible to a leukemia-like disease called haemic neoplasia that has been known to decimate whole populations.

Paradoxical impact of antioxidants on post-Amadori glycoxidation: Counterintuitive increase in the yields of pentosidine and Nepsilon-carboxymethyllysine using a novel multifunctional pyridoxamine derivative.

The inhibition of post-Amadori advanced glycation end product (AGE) formation by three different classes of AGE inhibitors, carbonyl group traps, chelators, and radical-trapping antioxidants, challenge the current paradigms that: 1) AGE inhibitors will not increase the formation of any AGE product, 2) transition metal ions are required for oxidative formation of AGE, and 3) screening AGE inhibitors only in systems containing transition metal ions represents a valid estimate of potential in vivo mechanisms. This work also introduces a novel multifunctional AGE inhibitor, 6-dimethylaminopyridoxamine (dmaPM), designed to function as a combined carbonyl trap, metal ion chelator, and radical-trapping antioxidant. Other AGE inhibitors including pyridoxamine, aminoguanidine, o-phenylenediamine, dipyridoxylamine, and diethylenetriaminepentaacetic acid were also examined.