A new concern raised from algal bloom: Organic chloramines in chlorination.

Algal blooms have become a significant challenge in water treatment all over the world. In chlorination of drinking water, algal organic matter (AOM) leads to the formation of organic chloramines. The objectives of this review are to comprehensively summarize and discuss the up-to-date researches on AOM-derived organic chloramines and their chemical activities and toxicity, thereby drawing attention to the potentially chemical and hygienic risks of organic chloramines. The predominant algal species in water sources varied with location and season. AOM from cyanobacteria, green algae, and diatoms are composed of diverse composition. AOM-derived amino acids take a low portion of the precursors of organic chloramines. Both experimental kinetic data and quantum chemical calculation demonstrate the preferential formation of organic chloramines in the chlorination of model compounds (amino acids and peptides). Organic chloramines are persistent in water and can transform into dichloro- and trichloro-organic chloramines, unknown low-molecular-weight organic chloramines, and nitrogenous disinfection byproducts with the excess of free chlorine. The active chlorine (Cl+) in organic chloramines can lead to the formation of chlorinated phenolic compounds. Organic chloramines influence the generation and species of radicals and subsequent products in UV disinfection. Theoretical predictions and toxicological tests suggest that organic chloramines may cause oxidative or toxic pressure to bacteria or cells. Overall, organic chloramines, as one group of high-molecular-weight disinfection byproducts, have relatively long lifetimes, moderate chemical activities, and high hygienic risks to the public. Future perspectives of organic chloramines are suggested in terms of quantitative detection methods, the precursors from various predominant algal species, chemical activities of organic chloramines, and toxicity/impact.

GSTP1 is a negative regulator of MAVS in the antiviral signaling against SVCV infection.

Glutathione S-transferase P1 (GSTP1), the most ubiquitous member of the GST superfamily, plays vital roles in the detoxification, antioxidant defense, and modulation of inflammatory responses. However, limited studies have been conducted on the function of GSTP1 in antiviral innate immunity. In this study, we have cloned the homolog of GSTP1 in triploid hybrid crucian carp (3nGSTP1) and investigated its regulatory role in the interferon signaling pathway. The open reading frame of 3nGSTP1 is composed of 627 nucleotides, encoding 209 amino acids. In response to spring viremia of carp virus (SVCV) infection, the mRNA level of 3nGSTP1 was up-regulated in the liver, kidney, and caudal fin cell lines (3 nF C) of triploid fish. The knockdown of 3nGSTP1 in 3 nF C improved host cell's antiviral capacity and attenuated SVCV replication. Additionally, overexpression of 3nGSTP1 inhibited the activation of IFN promoters induced by SVCV infection, poly (I:C) stimulation, or the RLR signaling factors. The co-immunoprecipitation assays further revealed that 3nGSTP1 interacts with 3nMAVS. In addition, 3nGSTP1 dose-dependently inhibited 3nMAVS-mediated antiviral activity and reduced 3nMAVS protein level. Mechanistically, 3nGSTP1 promoted ubiquitin-proteasome degradation of MAVS by promoting its K48-linked polyubiquitination. To conclude, our results indicate that GSTP1 acts as a novel inhibitor of MAVS, which negatively regulates the IFN signaling.

TRIM25 negatively regulates IKKε-mediated interferon signaling in black carp.

IKKε plays an important role in the activation of IRF3/IRF7 and the production of interferon (IFN), however, its regulation remains obscure in human. E3 ligase TRIM25 has been reported to manipulate the K63-linked ubiquitination of RIG-I, leading to the activation of RIG-I/IFN signaling. To elucidate the role of TRIM25 in teleost, a TRIM25 homolog (bcTRIM25) was cloned and characterized from black carp (Mylopharyngodon piceus). bcTRIM25 contains 653 amino acids, possessing conservative RING, B-box and SPRY domain, which is highly expressed in muscle, spleen and skin. bcTRIM25 knock-down enhanced the antiviral ability of host cells. bcTRIM25 over-expression alone in EPC cells attenuated bcIFNa promoter transcription in the reporter assays and impeded PKR and MX1 expression in qRT-PCR. Interestingly, co-IP assays indicated that bcTRIM25 interacted with bcIKKε and the induced bcIFNa promoter transcription by bcIKKε was notably hindered by bcTRIM25. Furthermore, bcIKKε-induced expression of interferon stimulated genes (ISGs) and antiviral activity were dampened by bcTRIM25. Further exploration showed that bcTRIM25 visibly enhanced the ubiquitination of bcIKKε but significantly attenuated the phosphorylation of bcIKKε. Thus, our data demonstrate for the first time in vertebrate that TRIM25 negatively regulates IKKε through enhancing its ubiquitination, which sheds a light on the regulation of IKKε/IFN signaling.