Mohammad Sadiq Nikzad,Jiangbing Qiu,Guixiang Wang,Xue Wang,Natnael Sisay Demo,Aifeng Li
The increasing prevalence of harmful algal blooms (HABs), specifically those resulted by toxigenic Alexandrium spp., notably threats human health and aquatic ecosystem. Metal organic frameworks (MOFs), particularly copper- and zinc-based MOFs have emerged as promising materials to control HABs. However, their application safety needs to be assessed because of poor knowledge of their ecotoxicity to marine organisms. In this study, the toxicity of Cu-MOF and Zn-MOF was evaluated to Oryzias melastigma at embryonic and adult stages. The Cu-MOF exhibited a concentration-dependent mortality and hatching rate at concentrations ≥ 2.0 mg L −1 . The Zn-MOF exhibited similar effects when the exposure doses ≥ 80 mg L −1 . Additionally, adult fish after exposure to Cu-MOF showed significant mortality rate at higher concentrations (≥ 4.0 mg L −1 ), beside elevated oxidative stress markers. In contrast, Zn-MOF did not show mortality and oxidative stress although bioaccumulation of Zn 2 + occurred in tissues. Based on the safety assessment of MOFs to marine medaka, the dosages for application of Cu-MOF (≤ 1.0 mg L −1 ) and Zn-MOF (≤ 20 mg L −1 ) are safe for controlling A. minutum -forming HABs. This study hints that the application of MOFs in mitigation of HABs should be carefully evaluated to balance their benefits in contrast to ecological risks.
Chuan Liang,Yang Chen,Yunzhe Ling,Peirun Li,Jiahao Liu,Xuantian Li,Yanhua Xu,Zhiying Liu
Non-steroidal anti-inflammatory drugs (NSAIDs), though designed to target specific molecular pathways, pose significant environmental risks to non-target organisms, particularly marine fish. This study investigated the toxicity mechanisms and adaptive responses to diclofenac (DCF) and meloxicam (MEX) during the early life stages (ELS) of Oryzias melastigma at environmentally relevant concentrations over a 31-day period. Mechanistic investigations of sub-lethal effects were conducted using Enzyme-Linked Immunosorbent Assay (ELISA), RNA sequencing (RNA-Seq) and quantitative PCR (qPCR). The results revealed that cyclooxygenase (COX) inhibition disrupted the renin-angiotensin system, leading to an accumulation of angiotensin II and cardiovascular developmental defects. Additionally, downregulation of the pla2 gene reduced substrates essential for COX enzyme activity, exacerbating the effects. Although NSAIDs are known to affect the digestive system, no significant effects on developmental factors were observed. RNA-Seq and qPCR analyses revealed an adaptive upregulation of key genes, including ace2 and cyp7a1 , involved in cardiovascular and metabolic regulation. Furthermore, 16S rRNA sequencing identified shifts in the microbial community, particularly in g_Rubritalea and g_Sphingomonas genera. Both the upregulated genes and the altered microbial taxa likely played a role in mitigating toxic effects and promoting homeostasis. Moreover, molecular docking suggested that MEX exhibited stronger sub-lethal effects than DCF, likely due to its higher binding affinity to COX. These findings provide valuable insights into NSAID toxicity mechanisms in marine fish, highlighting the importance of adaptive responses in countering environmental stress and underscoring the long-term ecological risks of chronic NSAID exposure.
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