Microplastics in marine ecosystems: A comprehensive review of biological and ecological implications and its mitigation approach using nanotechnology for the sustainable environment.

Microplastic contamination has rapidly become a serious environmental issue, threatening marine ecosystems and human health. This review aims to not only understand the distribution, impacts, and transfer mechanisms of microplastic contamination but also to explore potential solutions for mitigating its widespread impact. This review encompasses the categorisation, origins, and worldwide prevalence of microplastics and methodically navigates the complicated structure of microplastics. Understanding the sources of minute plastic particles infiltrating water bodies worldwide is critical for successful removal. The presence and accumulation of microplastics has far reaching negative impacts on various marine creatures, eventually extending its implications to human health. Microplastics are known to affect the metabolic activities and the survival of microbial communities, phytoplankton, zooplankton, and fauna present in marine environments. Moreover, these microplastics cause developmental abnormalities, endocrine disruption, and several metabolic disorders in humans. These microplastics accumulates in aquatic environments through trophic transfer mechanisms and biomagnification, thereby disrupting the delicate balance of these ecosystems. The review also addresses the tactics for minimising the widespread impact of microplastics by suggesting practical alternatives. These include increasing public awareness, fostering international cooperation, developing novel cleanup solutions, and encouraging the use of environment-friendly materials. In conclusion, this review examines the sources and prevalence of microplastic contamination in marine environment, its impacts on living organisms and ecosystems. It also proposes various sustainable strategies to mitigate the problem of microplastics pollution. Also, the current challenges associated with the mitigation of these pollutants have been discussed and addressing these challenges require immediate and collective action for restoring the balance in marine ecosystems.

Developmental toxicity and neurobehavioral effects of sodium selenite and selenium nanoparticles on zebrafish embryos.

Selenium, a trace mineral, is essential for several physiological processes in humans and animals. It is an antioxidant vital for the immunological response, DNA synthesis, thyroid hormone metabolism, and antioxidant defense enzymes. Zebrafish embryos and larvae were exposed to different concentrations of sodium selenite (SodSe) and selenium nanoparticles (SeNs) at various developmental stages. The study evaluated the impact of SodSe and SeNs on larvae survival, hatching rate, and morphological abnormalities. Also, acridine orange staining was used to analyze the apoptotic cell death, and behavioral tests were conducted to assess anxiety-like behaviors. The results showed that both SodSe and SeNs influence the development and neurobehavior of zebrafish larvae in a concentration-dependent manner. SodSe at high concentration causes low survival rates, delayed hatching, and increased morphological defects in zebrafish larvae. In addition, exposure to SodSe resulted in elevated apoptosis in different larval tissues. Zebrafish larvae treated with SodSe and SeNs exhibited anxiety-like behaviour, increased thigmotaxis, less exploratory behaviour, and less swimming patterns. The nerve conductions and stimuli responses evaluated through acetylcholine esterase (AChE) and cortisol assays, revealed a decrease in the activity in a dose-dependent manner of SodSe and SeNs. Interestingly, the effects of SeNs were lower even at higher concentrations when compared with SodSe at lower concentrations on zebrafish embryos. This shows that SeNs synthesized through biological methods may be less toxic and may have lower effect on the development and neurobehavior of zebrafish larvae. Thus, our study confirms the cytotoxic and neurobehavioral effects of SodSe and suggests the use of SeNs at lower concentration to provide insights into better understanding of developmental stages and metabolic pathways in zebrafish larvae.

Biological Activities of Selenium Nanoparticles Synthesized from Camellia sinensis (L) Kuntze Leaves.

Selenium in the form of selenoproteins is formed through a unique translocation recoding pathway and plays a vital role in human metabolism. Selenium nanoparticles (SeNPs) when synthesized using green synthesis from plant extract offer more advantages than physical and chemical methods. Previous studies have synthesized selenium nanoparticles from green tea and white tea; here, we report the synthesis of selenium nanoparticles from Camillia sinensis (L) Kuntze leaves (black tea) by green synthesis. Moreover, we have tested the antimicrobial and antioxidant activity of the plant extract, SeNPs, and combination of plant extract and SeNPs which have not been previously studied. The antimicrobial efficacy of SeNPs was tested against Klebsiella pneumonia, Candida albicans, and Staphylococcus aureus. They showed inhibitory effects against these organisms individually and in combination with Camellia sinensis leaf extract. The antioxidant properties of SeNPs were checked using FRAP and DPPH assays, where high radical scavenging activity was exhibited by SeNPs and in combination with the plant extract. Furthermore, synthesized SeNPs were examined for cytotoxicity tolerance against Vero cells and their IC50 values determine that plant-mediated SeNPs showed high cytotoxicity at minimal concentrations. If explored further, the reducing, capping, and stabilizing capabilities of SeNPs may demonstrate other inhibitory effects and could be explored for understanding the role of selenium in cellular metabolism.

Hypoxia alters expression of zebrafish microtubule-associated protein tau (mapta, maptb) gene transcripts.

BACKGROUND: Microtubule-associated protein tau (MAPT) is abundant in neurons and functions in assembly and stabilization of microtubules to maintain cytoskeletal structure. Human MAPT transcripts undergo alternative splicing to produce 3R and 4R isoforms normally present at approximately equal levels in the adult brain. Imbalance of the 3R-4R isoform ratio can affect microtubule binding and assembly and may promote tau hyperphosphorylation and neurofibrillary tangle formation as seen in neurodegenerative diseases such as frontotemporal dementia (FTD) and Alzheimer's disease (AD). Conditions involving hypoxia such as cerebral ischemia and stroke can promote similar tau pathology but whether hypoxic conditions cause changes in MAPT isoform formation has not been widely explored. We previously identified two paralogues (co-orthologues) of MAPT in zebrafish, mapta and maptb. RESULTS: In this study we assess the splicing of transcripts of these genes in adult zebrafish brain under hypoxic conditions. We find hypoxia causes increases in particular mapta and maptb transcript isoforms, particularly the 6R and 4R isoforms of mapta and maptb respectively. Expression of the zebrafish orthologue of human TRA2B, tra2b, that encodes a protein binding to MAPT transcripts and regulating splicing, was reduced under hypoxic conditions, similar to observations in AD brain. CONCLUSION: Overall, our findings indicate that hypoxia can alter splicing of zebrafish MAPT co-orthologues promoting formation of longer transcripts and possibly generating Mapt proteins more prone to hyperphosphorylation. This supports the use of zebrafish to provide insight into the mechanisms regulating MAPT transcript splicing under conditions that promote neuronal dysfunction and degeneration.

Identification and expression analysis of the zebrafish orthologues of the mammalian MAP1LC3 gene family.

Autophagy is the principle pathway within cells involved in clearing damaged proteins and organelles. Therefore autophagy is necessary to maintain the turnover balance of peptides and homoeostasis. Autophagy occurs at basal levels under normal conditions but can be upregulated by chemical inducers or stress conditions. The zebrafish (Danio rerio) serves as a versatile tool to understand the functions of genes implicated in autophagy. We report the identification of the zebrafish orthologues of mammalian genes MAP1LC3A (map1lc3a) and MAP1LC3B (map1lc3b) by phylogenetic and conserved synteny analysis and we examine their expression during embryonic development. The zebrafish map1lc3a and map1lc3b genes both show maternally contributed transcripts in early embryogenesis. However, levels of map1lc3a transcript steadily increase until at least 120h post-fertilisation while the levels of map1lc3b show a more variable pattern across developmental time. We have also validated the LC3I ratio/LC3I immunoblot autophagy assay in the presence of chloroquine (a lysosomal proteolysis inhibitor). We found that the LC3II/LC3I ratio is significantly increased in the presence of sodium azide with chloroquine supporting that hypoxia induces autophagy in zebrafish. This was supported by our qPCR assay that showed increased map1lc3a transcript levels in the presence of sodium azide. In contrast, levels of map1lc3b transcripts were reduced in the presence of rapamycin but the decrease in the presence of sodium azide did not reach statistical significance. Our study supports the use of zebrafish for analysing the interplay between hypoxia, development and autophagy.