A review focusing on mechanisms and ecological risks of enrichment and propagation of antibiotic resistance genes and mobile genetic elements by microplastic biofilms.

Microplastics (MPs) are emerging ubiquitous pollutants in aquatic environment and have received extensive global attention. In addition to the traditional studies related to the toxicity of MPs and their carrier effects, their unique surface-induced biofilm formation also increases the ecotoxicity potential of MPs from multiple perspectives. In this review, the ecological risks of MPs biofilms were summarized and assessed in detail from several aspects, including the formation and factors affecting the development of MPs biofilms, the selective enrichment and propagation mechanisms of current pollution status of antibiotic resistance genes (ARGs) and mobile genetic elements (MGEs) in MPs biofilms, the dominant bacterial communities in MPs biofilms, as well as the potential risks of ARGs and MGEs transferring from MPs biofilms to aquatic organisms. On this basis, this paper also put forward the inadequacy and prospects of the current research and revealed that the MGEs-mediated ARG propagation on MPs under actual environmental conditions and the ecological risk of the transmission of ARGs and MGEs to aquatic organisms and human beings are hot spots for future research. Relevant research from the perspective of MPs biofilm should be carried out as soon as possible to provide support for the ecological pollution prevention and control of MPs.

Early-Stage High-Concentration Thiacloprid Exposure Induced Persistent Behavioral Alterations in Zebrafish.

As a major neonicotinoid insecticide, thiacloprid (THCP) is frequently detected in aquatic environments worldwide due to its heavy use, posing potential threats to aquatic organisms. In this study, zebrafish (Danio rerio) embryos were exposed to THCP (1, 10, 100, 1000 and 10,000 µg/L) for 5 days and then recovered in THCP-free water for 20 days to investigate the effects of early-stage THCP exposure on the development, antioxidant defense, and neurotransmitter systems of zebrafish, and explore their recovery mechanism. The results show that THCP exposure induced developmental toxicity and oxidative stress in zebrafish. The hypoactivity, behavioral alterations (decreased avoidance and edge preference behaviors) and neurotoxicity were found throughout the exposure-recovery experiments. THCP exposure altered the expression of γ-aminobutyric acid (GABA)- and serotonin (5-HT)-related genes accompanied by the decrease in GABA and 5-HT contents. However, after recovery, GABA content returned to the control level, but 5-HT did not, indicating that only the serotonergic system was persistently disrupted. Overall, our results suggest that the disruption of the serotonergic system and oxidative stress may aggravate neurotoxicity and that the former was the main reason for the depressive-like behavior. This study could help to unravel the mechanisms of the behavioral alterations induced by early-stage THCP exposure in zebrafish.

Melanin interference toxicity or transgenerational toxicity of organic UV filter ethylhexyl salicylate on zebrafish.

With the improvement of human health awareness, the production and usage of sunscreens have increased dramatically, and their active ingredients, organic ultraviolet (UV) filters (OUVFs), have the potential to induce melanin abnormalities in aquatic organisms due to their UV-absorbing properties as they enter the aquatic environment directly with the washing of skin during water activities. In this paper, the melanin interference toxicity or transgenerational toxicity effects of typical OUVFs ethylhexyl salicylate (EHS) on zebrafish (Danio rerio) were investigated based on transcriptomic sequencing technology. Results showed that EHS induced significant enrichment of the melanin-related pathway cAMP signaling pathway in parental skin tissue through UV absorption, with sensitive genes identified as melanocortin 1 receptor, protein kinase A catalytic subunit beta a, calcium/calmodulin-dependent protein kinase II delta 2, adenylate cyclase 1 and G protein subunit alpha I a. qRT-PCR verification results showed that EHS may inhibit the expression of the melanin master regulator microphthalmia-associated transcription factor a (mitfa) and its induced signaling cascade mitf-tyrosinase (tyr)-dopachrome tautomerase (dct)-tyrosinase related protein 1 (tyrp1) by inducing abnormal expression of the above sensitive genes, thereby reducing melanogenesis. After reproduction, the melanin interference effect of EHS on the parents can be carried over to offsprings through maternal inheritance of abnormally expressed mitfa and parental transfer of pollutants, as evidenced by significant enrichment of melanogenesis pathway, abnormal expression of sensitive genes mitfa, tyr, dct and tyrp1b and significant decreases in melanin content and spinal melanin area. These findings revealed the specific melanin interference toxicity of OUVFs with UV-absorbing properties, facilitating a comprehensive ecological risk assessment of OUVFs and providing scientific support for the management of new pollutants.

Thiacloprid-induced hepatotoxicity in zebrafish: Activation of the extrinsic and intrinsic apoptosis pathways regulated by p53 signaling pathway.

Thiacloprid (THCP) is one of the major neonicotinoid insecticides, and its wide use has led to high detection in various media of aquatic environment, posing potential risks to aquatic organisms. This study was focused on the phenotypic responses and mechanisms of toxicity in zebrafish (Danio rerio) upon treatment with waterborne THCP (0.4, 4 and 40 µM) for 21 days in vivo or 412.9 µM for 24 h in vitro. In vivo, we found that THCP induced severe oxidative stress, hepatic abnormalities, leakage of alanine aminotransferase and aspartate aminotransferase and apoptosis. The analysis of RNA-sequencing suggested the activation of the p53 signaling pathway under THCP exposure. The following in vitro study showed that THCP intoxication activated reactive oxygen species (ROS)-dependent p53 signaling pathway and induced hepatotoxicity in the zebrafish liver cells. The addition of p53 inhibitor pifithrin-α (10 µM) exerted protection against of THCP-induced hepatotoxicity by reducing oxidative stress and inhibiting the p53 signaling pathway and apoptosis. Moreover, gene expression analyses indicated that both the extrinsic and intrinsic apoptosis pathways were involved in apoptosis induced by p53 activation. Overall, our results suggest that activation of the p53 signaling pathway is an important mechanism of THCP-induced hepatotoxicity.