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A highly specific, high throughput-amenable bacterial biosensor for chemically induced cellular oxidation was developed using constitutively expressed redox-sensitive green fluorescent protein roGFP2 in E. coli (E. coli-roGFP2). Disulfide formation between two key cysteine residues of roGFP2 was assessed using a double-wavelength ratiometric approach. This study demonstrates that only a few minutes were required to detect oxidation using E. coli-roGFP2, in contrast to conventional bacterial oxidative stress sensors. Cellular oxidation induced by hydrogen peroxide, menadione, sodium selenite, zinc pyrithione, triphenyltin and naphthalene became detectable after 10 seconds and reached the maxima between 80 to 210 seconds, contrary to Cd2+, Cu2+, Pb2+, Zn2+ and sodium arsenite, which induced the oxidation maximum immediately. The lowest observable effect concentrations (in ppm) were determined as 1.0 x 10−7 (arsenite), 1.0 x 10−4 (naphthalene), 1.0 x 10−4 (Cu2+), 3.8 x 10−4 (H2O2), 1.0 x 10−3 (Cd2+), 1.0 x 10−3 (Zn2+), 1.0 x 10−2 (menadione), 1.0 (triphenyltin), 1.56 (zinc pyrithione), 3.1 (selenite) and 6.3 (Pb2+), respectively. Heavy metal-induced oxidation showed unclear response patterns, whereas concentration-dependent sigmoid curves were observed for other compounds. In vivo GSH content and in vitro roGFP2 oxidation assays together with E. coli-roGFP2 results suggest that roGFP2 is sensitive to redox potential change and thiol modification induced by environmental stressors. Based on redox-sensitive technology, E. coli-roGFP2 provides a fast comprehensive detection system for toxicants that induce cellular oxidation.

In heavily urbanized world saturated with environmental pollutants, road traffic noise stands out as a significant factor contributing to widespread public health issues. It contributes in the development of a diverse range of non-communicable diseases, such as cardiovascular diseases, metabolic dysregulation, cognitive impairment, and neurodegenerative disorders. Although the exact mechanisms behind these non-auditory health effects remain unclear, the noise reaction model centres on the stress response to noise. When exposed to noise, the body activates the hypothalamic–pituitary–adrenal axis and the sympathetic nervous system, leading to the secretion of stress hormones like catecholamines and cortisol. Prolonged exposure to noise-induced stress results in chronic inflammation and oxidative stress. This review underscores the role of inflammation and oxidative stress in the progression of noise-induced vascular dysfunction, disruption of the circadian rhythm, accelerated aging, neuroinflammation, and changes in microbiome. Additionally, our focus is on understanding the interconnected nature of these health outcomes: These interconnected factors create a cascade effect, contributing to the accumulation of multiple risk factors that ultimately lead to severe adverse health effects.

• Microclimatic effects (light, temperature) are often neglected in phenological studies and little information is known about the impact of resource availability (nutrient and water) on tree’s phenological cycles. • Here we experimentally studied spring and autumn phenology in four temperate trees in response to changes in bud albedo (white-painted vs black-painted buds), light conditions (nonshaded vs c. 70% shaded), water availability (irrigated, control and reduced precipitation) and nutrients (low vs high availability). • We found that higher bud albedo or shade delayed budburst (up to +12 d), indicating that temperature is sensed locally within each bud. Leaf senescence was delayed by high nutrient availability (up to +7 d) and shade conditions (up to +39 d) in all species, except oak. Autumn phenological responses to summer droughts depended on species, with a delay for cherry (+7 d) and an advance for beech (−7 d). • The strong phenological effects of bud albedo and light exposure reveal an important role of microclimatic variation on phenology. In addition to the temperature and photoperiod effects, our results suggest a tight interplay between source and sink processes in regulating the end of the seasonal vegetation cycle, which can be largely influenced by resource availability (light, water and nutrients).

Integrating the effects of multiple stressors and predicting their consequences for the species’ survival and distribution is an important problem in ecological physiology. This review applies the concept of energy-limited tolerance to stress to develop bioenergetic markers that can assist in integrating the effects of multiple stressors and distinguishing between the moderate stress compatible with long-term survival of populations and bioenergetically unsustainable extreme stress. These markers reflect the progressive decline of the aerobic scope of an organism (defined as the fraction of the energy flux and metabolic power supporting this flux available after the basal maintenance costs of an organism are met) with increasing levels of the environmental stress. During the exposure to moderate stress (i.e., in the pejus range of the environmental conditions), the aerobic scope is positive but reduced compared with the optimum conditions. The reduction of the metabolic scope can be due to the (1) elevated costs of basal metabolism, (2) activation of the mechanisms for protection and damage repair, (3) reduced assimilation of food, and/or (4) stress-induced impacts on the aerobic pathways producing ATP. This leads to suboptimal growth and reproductive rates in the pejus range of environmental conditions and is commonly observed in food-limited and energy-limited wild populations. The tolerance windows of the organisms are delimited by the pessimum range(s) of environmental conditions in which the aerobic scope of the organism disappears (so that all available energy and metabolic capacity are used in support of basal metabolism), energy resources are depleted, and partial anaerobiosis and/or metabolic rate depression set in. The habitats where environmental conditions remain in the pessimum zone long enough to prevent consistent growth and reproduction often coincide with the species’ distributional limits. Thus, focus on the bioenergetic effects of environmental stressors and their immediate consequences for fitness provides a suitable framework for integrating physiology and functional ecology and can assist in understanding the driving forces and limitations of environmental adaptation and improving assessment of ecological risk as well as environmental management in field populations facing multiple stressors.

The Global Burden of Disease Study identified cardiovascular risk factors as leading causes of global deaths and life years lost. Endothelial dysfunction represents a pathomechanism that is associated with most of these risk factors and stressors, and represents an early (subclinical) marker/predictor of atherosclerosis. Oxidative stress is a trigger of endothelial dysfunction and it is a hall-mark of cardiovascular diseases and of the risk factors/stressors that are responsible for their initiation. Endothelial function is largely based on endothelial nitric oxide synthase (eNOS) function and activity. Likewise, oxidative stress can lead to the loss of eNOS activity or even “uncoupling” of the enzyme by adverse regulation of well-defined “redox switches” in eNOS itself or up-/down-stream signaling molecules. Of note, not only eNOS function and activity in the endothelium are essential for vascular integrity and homeostasis, but also eNOS in perivascular adipose tissue plays an important role for these processes. Accordingly, eNOS protein represents an attractive therapeutic target that, so far, was not pharmacologically exploited. With our present work, we want to provide an overview on recent advances and future therapeutic strategies that could be used to target eNOS activity and function in cardiovascular (and other) diseases, including life style changes and epigenetic modulations. We highlight the redox-regulatory mechanisms in eNOS function and up- and down-stream signaling pathways (e.g., tetrahydrobiopterin metabolism and soluble guanylyl cyclase/cGMP pathway) and their potential pharmacological exploitation.

Low-oxygen areas are expanding in the oceans as a result of climate change. Work carried out during the past two decades suggests that, in addition to impairing basic physiological functions, hypoxia can also affect fish behaviour. Given that many fish species are known to school, and that schooling is advantageous for their survival, the effect of hypoxia on schooling behaviour may have important ecological consequences. Here, we review the effects of hypoxia on school structure and dynamics, together with the mechanisms that cause an increase in school volume and that ultimately lead to school disruption. Furthermore, the effect of hypoxia generates a number of trade-offs in terms of schooling positions and school structure. Field observations have found that large schools of fish can exacerbate hypoxic conditions, with potential consequences for school structure and size. Therefore, previous models that predict the maximum size attainable by fish schools in relation to oxygen levels are also reviewed. Finally, we suggest that studies on the effect of hypoxia on schooling need to be integrated with those on temperature and ocean acidifications within a framework aimed at increasing our ability to predict the effect of multiple stressors of climate change on fish behaviour. This article is part of the themed issue ‘Physiological determinants of social behaviour in animals’.

Population response to global change will depend on responses to a multivariate set of changes in abiotic habitat characteristics and biotic interactions. Organismal biologists seeking to make ecological inferences about the impacts of global change by studying physiological performance have traditionally performed carefully controlled experimental studies that examine one variable at a time. Those studies, while of high value, may not lead to accurate predictions of organismal responses in the natural habitat, where organisms experience concomitant changes in multiple environmental factors. The symposium “Physiological Responses to Simultaneous Shifts in Multiple Environmental Stressors: Relevance in a Changing World” focused on physiological studies in which multiple environmental variables were simultaneously examined and brought together an international group of early-career and established speakers with unique perspectives on studies of multistressors. In doing so, the objective of the symposium was to frame the necessary next steps for increasing predictive capacity of organismal responses to environmental shifts in the natural habitat, establish novel collaborations among researchers actively investigating physiological responses to a multivariate environment, and broaden the number of researchers conducting such studies.

Summary There is growing need for reliable biomarkers of the physiological stress response in basic ecological investigations and conservation‐specific applications. One effect of stress hormone secretion is the alteration of circulating leucocytes, specifically an increase in the heterophil : lymphocyte ratio (HLR). There have been numerous studies and reviews of the relationship between the stress response and HLR, yet the data have not been systematically analysed across studies. Here, we performed meta‐analyses of studies in which paired values of plasma corticosterone (CORT) and HLR were available to investigate the relationship between these parameters. Specifically, we analysed CORT and HLR as baseline measures between treatment (or ‘stressed’ populations) and control (or ‘reference’ populations). Additionally, we investigated the relationship within CORT and HLR to identify temporal patterns of the response as a result of the duration of the stressor. Across studies, we identified that CORT and HLR are significantly elevated in populations subjected to environmentally stressful conditions. While not significantly different, CORT tended to be more elevated than HLR in the stressed populations. We found that there is a significant, negative relationship between CORT and the temporal duration of environmental stress. Additionally, we found a significant break point in this response at 85 days of stress duration, above which there is not a clear relationship between CORT and duration. This indicates that the CORT response to environmental stress attenuates. We found a small but positive significant relationship between HLR and temporal duration of environmental stress. This suggests that the elevation of HLR in response to environmental stress does not decrease over time. Our data identified that data gaps of wild populations of species exist and that more studies pairing physiological stress responses will further our understanding of how populations respond to environmental challenges. We found that CORT and HLR responded differently to stress, depending on captivity status, whether the study population was the domestic chicken, and the sex of the study population. Lay Summary

Background Poor sleep is known to adversely affect hospital patients’ recovery and rehabilitation. The aim of the study was to investigate the perceived duration and quality of patient sleep and identify any environmental factors associated with patient-reported poor sleep in hospital. Method A cross-sectional study was conducted involving 15 clinical units within a 672-bed tertiary-referral hospital in Australia. Semi-structured interviews to determine perceptions of sleep quantity and quality and factors that disturb nocturnal sleep were conducted with patients and nursing staff. Environmental noise, light and temperature were monitored overnight, with concurrent logging of noise sources by observers. Results Patients reported a mean reduction in hospital sleep duration, compared to home, of 1.8 h (5.3 vs. 7.1 h; p  < 0.001). The proportions of patients reporting their sleep quality to be poor/very poor, fair and of good quality were 41.6, 34.2 and 24.2% respectively. Patients reported poorer sleep quality than nurses ( p  < 0.05). Patients, nurses and observers all reported the main factors associated with poor sleep as clinical care interventions (34.3%) and environmental noise (32.1%). Noise levels in all 15 clinical areas exceeded WHO recommended levels of < 30 dB [A] by 36.7 to 82.6%, with peak noise levels of 51.3 to 103.3 dB (A). Conclusion Hospital in-patients are exposed to factors which reduce the duration and quality of their sleep. These extrinsic factors are potentially modifiable through behaviour change and reconfiguration of the clinical environment. The findings from this study provided the foundation for a quality improvement project currently underway to improve patients’ sleep.

Over the past several decades, coral reefs have faced a multitude of environmental stressors, resulting in major bleaching events all over the globe. Chemical stressors remain highly understudied in regards to their impact on the health of reef-building corals. Per- and polyfluoroalkyl substances (PFAS) are an expanding class of industrial chemicals that have high persistence in the environment, with many suspected adverse health impacts in vertebrate and invertebrate species. Unfortunately, there are little ecotoxicological data demonstrating possible impacts of PFAS on scleractinian corals with symbiotic algae, and there is no relevant literature that investigates their impact on coral larvae. Coral larvae are at high risk for PFAS exposure as they spend a prolonged period of dispersal drifting through the surface water prior to metamorphosis/settlement. The purpose of this study was to assess the impact of acute perfluorooctanesulfonic acid (PFOS) exposure on symbiotic and aposymbiotic Acropora aff. tenuis larvae to better understand possible ecosystem level impacts of PFAS exposure on coral reefs. Impacts to symbiont acquisition, metamorphosis, and lipidome of the larvae were investigated. Exposure to as low as 1 mg/L PFOS for 24-h decreased symbiont uptake in A. aff. tenuis larvae (p < 0.05). Further research is necessary to understand possible impacts of PFOS on metamorphosis of coral larvae. Additionally, significant alterations to the lipidome were detected following exposure to approximately 1.0 mg/L and approximately 6.7 mg/L PFOS in symbiotic A. aff. tenuis larvae, though no impact was detected in aposymbiotic A. tenuis larvae. Future research is needed to understand the impact of PFAS on the symbiotic relationship between the algae and corals as well PFAS impacts on free living Symbiodiniaceae. Graphical abstract