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The toxic effects of micro(nano)plastics are long-standing, flourishing and fadeless as a research topic because of its' underlying threats to the ecology and human health. Nevertheless, in most of the existing studies, some model organisms are exposed to micro(nano)plastics at a high concentration unlikely to occur in the real environment, and there is limited data available on the impact of micro(nano)plastics at environmentally relevant concentrations (ERC) on environmental organisms. To gain a better insight into micro(nano)plastic toxicity to the environmental organisms, here we integrate the related publications of micro(nano)plastic research at ERC in the past 10 years using a bibliometric analysis, and focus on the analysis of publication trends, research focuses, collaborations, and research status. In addition, we further analyze the 33 final filtered literature, and elucidate the organismal response to micro(nano)plastics at ERC from the perspective of in vivo toxic effects and mechanisms involved. This paper also puts forward some limitations of the current study and some suggestions for future research. Our study may be of great significance in further understanding the ecotoxicity of micro(nano)plastics.

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The number of studies reporting hormetic responses is rapidly increasing, and quantitative evaluations are needed to improve the understanding of hormetic dose responses. However, there is no standardized methodology to estimate the no-observed-adverse-effect-level (NOAEL) of hormetic dose-response relationships developed using data mined from the published literature. Here, we propose a protocol that can be followed to estimate NOAEL, a process that is illustrated using a specific example. This protocol can be used for maintaining a mutual language (since NOAEL can be defined in different ways), permitting comparisons among different studies, and facilitating cumulative science.

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BACKGROUND: The process of alternative splicing provides a unique mechanism by which eukaryotes are able to produce numerous protein products from the same gene. Heightened variability in the proteome has been thought to potentiate increased behavioral complexity and response flexibility to environmental stimuli, thus contributing to more refined traits on which natural and sexual selection can act. While it has been long known that various forms of environmental stress can negatively affect sexual behavior and reproduction, we know little of how stress can affect the alternative splicing associated with these events, and less still about how splicing may differ between sexes. Using the model of the rock dove (Columba livia), our team previously uncovered sexual dimorphism in the basal and stress-responsive gene transcription of a biological system necessary for facilitating sexual behavior and reproduction, the hypothalamic-pituitary-gonadal (HPG) axis. In this study, we delve further into understanding the mechanistic underpinnings of how changes in the environment can affect reproduction by testing the alternative splicing response of the HPG axis to an external stressor in both sexes. RESULTS: This study reveals dramatic baseline differences in HPG alternative splicing between males and females. However, after subjecting subjects to a restraint stress paradigm, we found a significant reduction in these differences between the sexes. In both stress and control treatments, we identified a higher incidence of splicing activity in the pituitary in both sexes as compared to other tissues. Of these splicing events, the core exon event is the most abundant form of splicing and more frequently occurs in the coding regions of the gene. Overall, we observed less splicing activity in the 3'UTR (untranslated region) end of transcripts than the 5'UTR or coding regions. CONCLUSIONS: Our results provide vital new insight into sex-specific aspects of the stress response on the HPG axis at an unprecedented proximate level. Males and females uniquely respond to stress, yet exhibit splicing patterns suggesting a convergent, optimal splicing landscape for stress response. This information has the potential to inform evolutionary theory as well as the development of highly-specific drug targets for stress-induced reproductive dysfunction.

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Biological feedbacks play a crucial role in determining effects of toxicants, radiation, and other environmental stressors on organisms. Focusing on reactive oxygen species (ROS) that are increasingly recognized as a crucial mediator of many stressor effects, we investigate how feedback strength affects the ability of organisms to control negative effects of exposure. We do this by developing a general theoretical framework for describing effects of a wide range of stressors and species. The framework accounts for positive and negative feedbacks representing cellular processes: (i) production of ROS due to metabolism and the stressor, (ii) ROS reactions with cellular compounds that cause damage, and (iii) cellular control of both ROS and damage. We suggest functional forms that capture generic properties of cellular control mechanisms constituting the feedbacks, assess stability of equilibrium states in the resulting models, and investigate tipping points at which cellular control breaks down causing unregulated increase of ROS and damage. Depending on the chosen functional forms, the models can have zero, one, or two positive steady states; except in one singular case, the steady state with lowest values of ROS and damage is locally stable. We found two types of tipping points: those induced by changes in the parameters (including the stressor intensity), and those induced by the history of exposure, i.e. ROS and damage levels. The relatively simple models effectively describe several patterns of cellular responses to stress, such as the covariation of ROS and damage, the break-down of cellular control leading to explosion of ROS and/or damage, increase in damage even when ROS is (near)-constant, and the effects of exposure history on the ability of the cell to handle additional stress. The models quantify dynamics of cellular control, and could therefore be used to estimate the metabolic costs of stress and help integrate them into models that use energetic considerations to model organism's response to the environment. Although developed with unicellular organisms in mind, our models can be applied to all multicellular organisms that utilize similar feedbacks when dealing with stress.

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