Mechanism of polyethylene and biodegradable microplastic aging effects on soil organic carbon fractions in different land-use types.

Microplastics (MPs) are widely present in terrestrial ecosystems, but knowledge about the aging characteristics of MPs in different land-use types and their impact on soil organic carbon fractions is still limited. Polyethylene (PE) and biodegradable MPs (Poly propylene carbonate and Polybutylene adipate terephthalate synthetic material (PPC + PBAT, Bio)), at 0 %, 0.03 %, and 0.3 % (w/w) dosages, were added to grassland, farmland, and facility soils for eight-week incubation. The aging degree of MPs was explored by quantifying the carbonyl index (CI). Soil organic C fractions such as SOC, particulate organic carbon (POC), mineral-associated organic carbon (MAOC), and microbial-derived C were analyzed. MPs underwent rapid aging after incubation, and the CI value for 0.03 % PE-MPs increased from 0.05 to 0.27 (farmland) and 0.26 (facility) (p < 0.05). The aging degree of 0.03 % and 0.3 % Bio-MPs was most significant in grassland, with CI decreasing by 46.6 % and 69.0 %, respectively. The CI of MPs were negatively correlated with their dosage. The 0.03 % and 0.3 % PE-MPs decreased soil organic carbon (SOC) content by 7.4 % and 8.2 % in grassland, and 3.0 % and 6.0 % in the facility (p < 0.05). POC content of farmland and facility soil was negatively correlated with PE-MPs' CI (p < 0.05). The 0.03 % PE and Bio-MPs decreased fungal necromass C (FNC) by 0.40 and 0.05 g kg-1 in grassland and 0.48 and 0.21 g kg-1 in farmland. Besides, the dosage of MPs regulated FNC content through soil pH, nutrients, and extracellular enzyme activity, either directly or indirectly, ultimately affecting the soil C pool. Therefore, this study demonstrates that MPs strongly affect SOC dynamics by influencing soil microbial enzyme activity and fungal necromass.

MiR-146a affects the alteration in myeloid differentiation induced by hydroquinone in human CD34+ hematopoietic progenitor cells and HL-60 cells.

The MiR-146a/TRAF6/NF-κB axis is important for the regulation of hematopoiesis and the immune system. To identify the key axis that regulates benzene-induced hematotoxicity or even leukemia, we investigated miR-146a expression in human CD34+ hematopoietic progenitor cells (HPCs) and human acute promyelocytic leukemia cells (HL-60) during the differentiation process. By performing a colony formation assay and flow cytometry on cells in the differentiation process after hydroquinone treatment, we found that hydroquinone induced a marked reduction of differentiation toward myeloid cells and immune cells in CD34+ cells (5 days exposure) as well as in HL-60 cells (3 h exposure). Further study using real-time PCR and western blot showed that the impaired myeloid differentiation was accompanied by the up-regulation of miR-146a and the down-regulation of TRAF6 and NF-κB. Using the miR-146a-5p inhibitor to suppress miR-146a expression could relieve the inhibitory effect on myeloid differentiation induced by hydroquinone to a certain extent. At the same time, the level of TRAF6 protein, as well as the phosphorylated IκBα protein which indicates NF-κB transcriptional activity was restored to the same levels as the control group. These results suggested that hydroquinone induced a dysregulation of miR-146a and its downstream NF-κB transcriptional factor pathway, which might be an early event in the generation of benzene-induced differentiation disturbance and subsequent leukemogenesis.