This study presents the synthesis of highly active BiPO 4 /AgI/BC composite photocatalysts via a green, simple, and low-cost ambient temperature precipitation method. The electron transfer rate and visible-light responsiveness can be effectively enhanced by utilizing BiPO 4 compounded with the semiconductor AgI, which has a narrow bandgap and good visible-light responsiveness. Additionally, the introduction of biocarbon (BC) enhances the absorption and separation of photogenerated electrons and holes under visible light. Notably, the synthesized BP-AgI 0.6 -BC 5 % could remove 99.16 % and 99.7 % of EE2 and E2, respectively, at a concentration of 3 mg/L after 40 min of light exposure. The capture experiments and electron paramagnetic resonance spectroscopy reveal that the main active substance in the system is ·O 2 - , with BC playing a crucial role in enhancing the ·O 2 - concentration in the system. The findings from phytotoxicity and antimicrobial tests reveal that BP-AgI 0.6 -BC 5 % can efficiently degrade pollutants, producing degradation products that are substantially less toxic than the original pollutants. Moreover, it can remove more than 99.99 % of E. coli under both dark and light conditions, demonstrating excellent antimicrobial performance. Additionally, the photocatalytic mechanism and degradation pathway were examined in this study. Notably, the composite photocatalysts synthesized in this study achieved efficient degradation of EE2 and E2 under visible light conditions while exhibiting efficient bactericidal function. Furthermore, the room-temperature preparation method is conducive to industrial-scale production, highlighting a better prospect for practical applications.
Summary Novosphingobium sp. ES2-1 is an efficient 17 β -estradiol (E2)-degrading bacterium, which can convert E2 to estrone (E1), then to 4-hydroxyestrone (4-OH-E1) for subsequent oxidative cracking. In this study, the molecular bases for this process were elucidated. Two novel monooxygenase systems EstP and EstO were shown to catalyse the oxygenation of E1 and 4-OH-E1, respectively. EstP was a three-component cytochrome P450 monooxygenase system consisting of EstP1 (P450 monooxygenase), EstP2 (ferredoxin) and EstP3 (ferredoxin reductase). Ultraperformance liquid chromatography-high resolution mass spectrometry (UPLC-HRMS) analysis revealed that EstP catalysed the 4-hydroxylation of E1 to produce 4-OH-E1. The resultant 4-OH-E1 was further oxidized by a two-component monooxygenase system EstO consisting of EstO1 (flavin-dependent monooxygenases) and EstO2 (flavin reductase). UPLC-HRMS combined with 1 H-nuclear magnetic resonance analysis demonstrated that EstO catalysed the breakage of C9-C10 to yield a ring B-cleavage product. In addition, the oxygenase component genes estP1 and estO1 exhibited contrary inductive behaviours when exposed to different steroids, suggesting that EstP1-mediated 4-hydroxylation was E2-specific, whereas EstO1-mediated monooxygenation might be involved in the degradation of testosterone, androstenedione, progesterone and pregnenolone. This also implied that the mechanisms of the catabolism of different steroids by the same microorganism might be partially interlinked.
Zhaoyun Zong,Jing Liu,Ning Wang,Changmei Yang,Qingtao Wang,Wenhao Zhang,Yuling Chen,Xiaohui Liu,Haiteng Deng
Liver fibrosis is a reversible wound-healing response to acute or chronic liver injury that can progress to cirrhosis and liver cancer. Finding new strategies for prevention and management of liver fibrosis is urgently needed. It is known that hepatic stellate cell (HSC) is the primary source of extracellular matrix that drives liver fibrosis progression. Herein, we carried out a comprehensive secretome profiling to identify NMN-induced changes in secretory proteins and found that NMN suppressed the secretion of profibrotic protein and oxidoreductase in activated HSC (LX-2) cells, while real-time quantitative PCR analysis revealed that NMN downregulated profibrotic gene expression, resulting in HSC inactivation. Next, we demonstrated that nicotinamide mononucleotide (NMN) reduced the accumulation of liver extracellular matrix in thioacetamide (TAA) and carbon tetrachloride (CCl 4 ) induced mouse models for liver fibrosis. Furthermore, we determined that NMN inhibited oxidation-mediated 15-PGDH degradation to promote prostaglandin E 2 degradation and suppress HSC activation. In summary, our results propose that NMN supplementation is a new therapeutic approach for liver fibrosis prevention.
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