RESUMEN
The translocation and accumulation patterns of polycyclic aromatic hydrocarbons (PAHs) in the soil-crop system have important implications for the fate of PAHs and human health. This study summarized the concentrations of 16 priority PAHs in the soils and various parts of mature winter wheat in China, sourced from a screening of previous literature in English and Chinese databases. The study analyzes the distribution characteristics, transfer patterns, and human health risks of PAHs in sites studied in Shaanxi, Henan, and Shandong provinces. The results showed that the concentrations of Σ16 PAHs in the rhizosphere soil of wheat ranged from 10.30 to 893.68 ng/g, in descending order of Shaanxi > Henan > average > Shandong. In sites with mild to moderate contamination (200 < Σ16 PAHs < 600 ng/g; i.e., Henan and Shaanxi), the concentration of Σ16 PAHs in the roots was higher than that in the stems or the grains, while in contamination-free sites (Σ16 PAHs < 200 ng/g; i.e., Shandong), the highest concentration of Σ16 PAHs was found in the stems. Generally, the concentrations of PAHs increased in the order of roots-stems-grains. The predominant PAHs in each part of wheat were 2- or 3-ring compounds, with five- or six-ring PAHs being more prevalent in wheat from Shanghe, Shandong. The bioaccumulation factors of different wheat parts from Shaanxi and Henan were consistently smaller than 1, and low- and medium-ring (2-4 rings) PAHs had bigger bioconcentration factors than high-ring (5-6 rings) PAHs. However, the accumulation of PAHs in the aboveground parts of wheat was larger than that in the underground parts of the Shandong sites. The linear regression relationship between the octanol-water partition coefficient and root concentration factor (RCF) of PAHs reflected that low and medium-ring PAHs were more easily absorbed by wheat roots than high-ring PAHs in Shaanxi and Henan. Our assessment of the health risks of oral wheat intake in adults and children by the incremental lifetime cancer risk (ILCR) model found a potential carcinogenic risk for both age groups in each province, with higher risks in adults than in children.
Asunto(s)
Hidrocarburos Policíclicos Aromáticos , Contaminantes del Suelo , Adulto , Niño , Humanos , Hidrocarburos Policíclicos Aromáticos/análisis , Suelo , Triticum , Ecosistema , Monitoreo del Ambiente , Contaminantes del Suelo/análisis , China , Medición de RiesgoRESUMEN
Lonicera japonica polysaccharides (LJPs) exhibit anti-aging effect in nematodes. Here, we further studied the function of LJPs on aging-related disorders in D-galactose (D-gal)-induced ICR mice. Four groups of mice including the control group, the D-gal-treated group, the intervening groups with low and high dose of LJPs (50 and 100 mg/kg/day) were raised for 8 weeks. The results showed that intragastric administration with LJPs improved the organ indexes of D-gal-treated mice. Moreover, LJPs improved the activity of superoxide dismutase (SOD), catalase (CAT) as well as glutathione peroxidase (GSH-Px) and decreased the malondialdehyde (MDA) level in serum, liver and brain. Meanwhile, LJPs restored the content of acetylcholinesterase (AChE) in the brain. Further, LJPs reversed the liver tissue damages in aging mice. Mechanistically, LJPs alleviate oxidative stress at least partially through regulating Nrf2 signaling. Additionally, LJPs restored the gut microbiota composition of D-gal-treated mice by adjusting the Firmicutes/Bacteroidetes ratio at the phylum level and upregulating the relative abundances of Lactobacillaceae and Bifidobacteriacesa. Notably, the KEGG pathways involved in hazardous substances degradation and flavone and flavonol biosynthesis were significantly enhanced by LJPs treatment. Overall, our study uncovers the role of LJPs in modulating oxidative stress and gut microbiota in the D-gal-induced aging mice.
Asunto(s)
Microbioma Gastrointestinal , Lonicera , Ratones , Animales , Antioxidantes/farmacología , Galactosa/farmacología , Ratones Endogámicos ICR , Acetilcolinesterasa/metabolismo , Estrés Oxidativo , Polisacáridos/farmacología , Superóxido Dismutasa/metabolismo , Malondialdehído/metabolismoRESUMEN
Static magnetic fields (SMFs) exhibit numerous biological effects and regulate the proliferation and differentiation of several adult stem cells. However, the role of SMFs in the self-renewal maintenance and developmental potential of pluripotent embryonic stem cells (ESCs) remains largely uninvestigated. Here, we show that SMFs promote the expression of the core pluripotent markers Sox2 and SSEA-1. Furthermore, SMFs facilitate the differentiation of ESCs into cardiomyocytes and skeletal muscle cells. Consistently, transcriptome analysis reveals that muscle lineage differentiation and skeletal system specification of ESCs are remarkably strengthened by SMF stimuli. Additionally, when treated with SMFs, C2C12 myoblasts exhibit an increased proliferation rate, improved expression of skeletal muscle markers and elevated myogenic differentiation capacity compared with control cells. Together, our data show that SMFs effectively promote muscle cell generation from pluripotent stem cells and myoblasts. The noninvasive and convenient physical stimuli can be used to increase the production of muscle cells in regenerative medicine and the manufacture of cultured meat in cellular agriculture.
Asunto(s)
Mioblastos , Células Madre Pluripotentes , Células Madre Pluripotentes/metabolismo , Fibras Musculares Esqueléticas/metabolismo , Músculo Esquelético/metabolismo , Campos MagnéticosRESUMEN
Pluripotent embryonic stem cells (ESCs) can self-renew indefinitely and are able to differentiate into all three embryonic germ layers. Synaptosomal-associated protein 29 (Snap29) is implicated in numerous intracellular membrane trafficking pathways, including autophagy, which is involved in the maintenance of ESC pluripotency. However, the function of Snap29 in the self-renewal and differentiation of ESCs remains elusive. Here, we show that Snap29 depletion via CRISPR/Cas does not impair the self-renewal and expression of pluripotency-associated factors in mouse ESCs. However, Snap29 deficiency enhances the differentiation of ESCs into cardiomyocytes, as indicated by heart-like beating cells. Furthermore, transcriptome analysis reveals that Snap29 depletion significantly decreased the expression of numerous genes required for germ layer differentiation. Interestingly, Snap29 deficiency does not cause autophagy blockage in ESCs, which might be rescued by the SNAP family member Snap47. Our data show that Snap29 is dispensable for self-renewal maintenance, but required for the proper differentiation of mouse ESCs.