The oxidative dissolution of arsenopyrite (FeAsS) is a significant source of arsenic contamination in nature. Activated biochar (AC), a widely used environmental remediation agent, is prevalent in ecosystems and participated in various geochemical processes of arsenic and iron-containing sulfide minerals. However, the impact of AC-arsenopyrite association on reactive oxidation species (ROS) generation and its contribution to As transformation were rarely explored. Here, ROS formation and the redox conversion of As during the interaction between AC and arsenopyrite were investigated. AC-mediated arsenopyrite oxidation was a two-stage process. At stage I, the heterogeneous electron transfer from arsenopyrite facilitated O₂ reduction on AC, enhancing arsenopyrite dissolution and ROS formation. TBA, PBQ and catalase inhibited 86.40 %, 79.39 % and 49.66 % of As(III) oxidation, respectively, indicating indicated that HO˙, (O₂^•)^- and H₂O₂ were responsible for As(III) oxidation. However, at stage II, the mobility of As was highly restricted, especially increasing AC addition. Besides adsorption, AC retained appreciable As through catalyzing insoluble ferric arsenate formation and growth by promoting Fe(II) and As(III) oxidation and functioning as nuclei. These findings deepen our understanding of the coupling behavior of AC-arsenopyrite and its influence on geochemical cycling of arsenic in mined surroundings, which has important implications for mitigating arsenic pollution.

2024-11-01·Animal Reproduction Science

Inhibition of testicular development by suppressing neonatal LH rise in male domestic pigs

Article

作者: Park, ChanJin ; Hess, Rex A ; Soto-Heras, Sandra ; Bunnell, Mary ; de França, Luiz Renato ; Chai, Katie ; Oh, Ji-Eun ; Hess, Rex A. ; Lin, Po-Ching ; Reinacher, Lindsey ; Zhou, Sherry ; Ko, CheMyong

The neonatal increase in circulating luteinizing hormone (LH) is crucial for testicular development. In male pigs, blood LH levels start to increase approximately 1 week after birth and return to basal level by 5-6 weeks of age. This study tested the hypothesis that neonatal treatment with a combination of estrogens and androgens suppresses LH secretion and thereby inhibits testicular development. On Day 1 after birth, piglets received a slow-release implant containing estradiol (E₂, 8-40 mg) and trenbolone acetate (TBA, 40-200 mg) or remained intact. At 4 weeks of age, mean serum LH concentrations were ∼ 7 ng/mL in untreated males, whereas pigs with implants had serum LH concentrations < 1 ng/mL. Despite this reduction, LH was still detected in the pituitary glands of treated pigs. Interestingly, neonatal castration also lowered circulating LH, highlighting the importance of testis physiology in the early establishment of the reproductive axis. The higher dose (20 mg E2 + 100 mg TBA) inhibited testis function more effectively, as evidenced by lower circulating testosterone concentrations compared to intact pigs. Furthermore, E2 + TBA treatment had a lasting impact on testicular growth, resulting in smaller testes at 26 weeks of age and the presence of immature Leydig cells. Overall, neonatal E2 + TBA treatment suppressed the postnatal LH rise and testicular growth until market age, offering a potential non-surgical alternative to castration in male pigs.

2024-11-01·Pesticide Biochemistry and Physiology

Transcriptomics reveals the mechanism of terbuthylazine-induced nephrotoxicity in chickens: Insights from AMPK/p53-mediated apoptosis perspective

Article

作者: Yang, Qingwen ; Ao, Da ; Lv, Yongzhi ; Liu, Xuesong

As a commonly used pesticide, the widespread use of terbuthylazine (TBA) may cause toxic effects in animals and human. However, the nephrotoxicity induced by TBA is unclear. Here, we explored the mechanism of TBA-induced nephrotoxicity through transcriptomics and molecular biology techniques in broilers. Pathologic analysis showed that TBA could cause renal cell vacuolation and fibrosis in broilers. Additionally, transcriptomic analysis showed that TBA can cause significant changes in the expression of some apoptosis-related genes, and GO and KEGG analysis also found that TBA can significantly change the functions of apoptosis pathway and AMPK signaling pathway in kidney. Subsequently, the protein expression levels of Bax, Bak-1, FADD, and cleaved Caspase-3/Caspase-3 were elevated significantly and the number of TUNEL-positive cells was increased markedly in kidney under TBA exposure. Meanwhile, we also found that TBA could activate AMPK/p53 pathway, as evidenced by the upregulated levels of AMPKα1 phosphorylation and protein expression of p53. Therefore, our results suggested that TBA could induce apoptosis via AMPK/p53 pathway in kidney. These findings identified the nephrotoxic mechanism of TBA through transcriptomics, providing a new insight into TBA toxicology.

100 项与 TBA 相关的药物交易

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