Insight into microplastics in the aquatic ecosystem: Properties, sources, threats and mitigation strategies.

Globally recognized as emergent contaminants, microplastics (MPs) are prevalent in aquaculture habitats and subject to intense management. Aquaculture systems are at risk of microplastic contamination due to various channels, which worsens the worldwide microplastic pollution problem. Organic contaminants in the environment can be absorbed by and interact with microplastic, increasing their toxicity and making treatment more challenging. There are two primary sources of microplastics: (1) the direct release of primary microplastics and (2) the fragmentation of plastic materials resulting in secondary microplastics. Freshwater, atmospheric and marine environments are also responsible for the successful migration of microplastics. Until now, microplastic pollution and its effects on aquaculture habitats remain insufficient. This article aims to provide a comprehensive review of the impact of microplastics on aquatic ecosystems. It highlights the sources and distribution of microplastics, their physical and chemical properties, and the potential ecological consequences they pose to marine and freshwater environments. The paper also examines the current scientific knowledge on the mechanisms by which microplastics affect aquatic organisms and ecosystems. By synthesizing existing research, this review underscores the urgent need for effective mitigation strategies and further investigation to safeguard the health and sustainability of aquatic ecosystems.

Correction: Khan et al. Anticancer Function and ROS-Mediated Multi-Targeting Anticancer Mechanisms of Copper (II) 2-hydroxy-1-naphthaldehyde Complexes. Molecules 2019, 24, 2544.

Due to the previous incorrect characterization of compound C1, the authors wish to make the following corrections to this paper [...].

Synthesis of a series of novel In(III) 2,6-diacetylpyridine bis(thiosemicarbazide) complexes: structure, anticancer function and mechanism.

The anticancer function and anticancer mechanism of indium (In) complexes still remain mysterious to date. Furthermore, it is greatly challenging to design a multi-functional metal agent that not only kills cancer cells but also inhibits their invasion and metastasis. Thus, to develop novel next-generation anticancer metal agents, we designed and synthesized a series of novel In(iii) 2,6-diacetylpyridine bis(thiosemicarbazide) complexes (C1-C4) for the first time and then investigated their structure-activity relationships with human urinary bladder cancer (T-24) cells. In particular, C4 not only showed higher cytotoxicity to cancer cells and less toxicity toward normal cells relative to cisplatin but also inhibited cell invasion and metastasis of T-24 cells. Interestingly, C4 acted against T-24 cells exhibiting multiple mechanisms: (1) arresting the S-phase of cell cycle via regulation of cytokine kinases, (2) activating the mitochondrial-mediated apoptosis, endoplasmic reticulum-stress-mediated cell death, PERK and c-Jun N-terminal kinase 1 (JNK) cell signaling pathways, and (3) inhibiting the expression of telomerase via the regulation of c-myc and h-TERT proteins. Our results suggested that C4 may be developed as a potential multi-functional and multi-targeting anticancer candidate.

Developing a binuclear multi-target Bi(III) complex by optimizing 2-acetyl-3-ethylpyrazine thiosemicarbazides.

On the one hand, the multi-target agents have been promising for overcoming the deficiency of the single targeted anticancer metal agents, on the other hand, bismuth (Bi) complexes have shown significant antiproliferative activity and minimal side effects. Therefore, to develop the next-generation anticancer metal agents, we designed and synthesized four novel binuclear Bi(III) complexes by modifying the N-4 position of a series of 2-Acetyl-3-ethylpyrazine thiosemicarbazides, and then investigated their structure-activity relationships to human cancer cell lines, obtaining a lead Bi drug (C4) with significant antiproliferative activity to human bladder cancer cells (T24). C4 arrested the cell cycle in the S-phase by regulation of cyclin and cyclin-dependent kinases, and exerted a chemotherapeutic effect via multi-target mechanism including the activation of apoptotic and autophagic cell signaling pathways. Besides, C4 effectively inhibited metastasis of T24 cell. Our results suggested that C4 can be developed as a potential multi-target anticancer candidate.

Anticancer Function and ROS-Mediated Multi-Targeting Anticancer Mechanisms of Copper (II) 2-hydroxy-1-naphthaldehyde Complexes.

Multi-targeting of oncoproteins by a single molecule represents an effectual, rational, and an alternative approach to target therapy. We carried out a systematic study to reveal the mechanisms of action of newly synthesized Cu2+ compounds of 2-naphthalenol and 1-(((2-pyridinylmethyl)imino)methyl)- (C1 and C2). The antiproliferative activity of the as-synthesized complexes in three human cancer cell lines indicates their potential as multi-targeted antitumor agents. Relatively, C1 and C2 showed better efficacy in vitro relative to Cisplatin and presented promising levels of toxicity against A-549 cells. On the whole, the Cu2+ complexes exhibited chemotherapeutic effects by generating reactive oxygen species (ROS) and arresting the cell cycle in the G0/G1 phase by competent regulation of cyclin and cyclin-dependent kinases. Fascinatingly, the Cu2+ complexes were shown to activate the apoptotic and autophagic pathways in A-549 cells. These complexes effectively induced endoplasmic reticulum stress-mediated apoptosis, inhibited topoisomerase-1, and damaged cancer DNA through a ROS-mediated mechanism. The synthesized Cu2+ complexes established ROS-mediated targeting of multiple cell signaling pathways as a fabulous route for the inhibition of cancer cell growth.