The use of artificial lighting to illuminate the night has provided substantial benefits to humankind. It has also disrupted natural daily, seasonal, and lunar light cycles as experienced by a diversity of organisms, and hence it has also altered cues for the timings of many biological activities. Here we review the evidence for impacts of artificial nighttime lighting on these timings. Although the examples are scattered, concerning a wide variety of species and environments, the breadth of such impacts is compelling. Indeed, it seems reasonable to conclude that the vast majority of impacts of artificial nighttime lighting stem from effects on biological timings. This adds support to arguments that artificial nighttime lighting has a quite pervasive and marked impact on ecological systems, that the rapid expansion in the global extent of both direct illuminance and skyglow is thus of significant concern, and that a widespread implementation of mitigation measures is required.

Impacts of Artificial Light at Night on Biological Timings

Natural light cycles are being eroded over large areas of the globe by the direct emissions and sky brightening that result from sources of artificial night-time light. This is predicted to affect wild organisms, particularly because of the central role that light regimes play in determining the timing of biological activity. Although many empirical studies have reported such effects, these have focused on particular species or local communities and have thus been unable to provide a general evaluation of the overall frequency and strength of these impacts. Using a new database of published studies, we show that exposure to artificial light at night induces strong responses for physiological measures, daily activity patterns and life history traits. We found particularly strong responses with regards to hormone levels, the onset of daily activity in diurnal species and life history traits, such as the number of offspring, predation, cognition and seafinding (in turtles). So far, few studies have focused on the impact of artificial light at night on ecosystem functions. The breadth and often strength of biological impacts we reveal highlight the need for outdoor artificial night-time lighting to be limited to the places and forms-such as timing, intensity and spectrum-where it is genuinely required by the people using it to minimize ecological impacts.

A meta-analysis of biological impacts of artificial light at night

Artificial night lighting is expanding globally, but its ecological consequences remain little understood. Animals often use changes in day length as a cue to time seasonal behaviour. Artificial night lighting may influence the perception of day length, and may thus affect both circadian and circannual rhythms. Over a 3.5 month period, from winter to breeding, we recorded daily singing activity of six common songbird species in 12 woodland sites, half of which were affected by street lighting. We previously reported on analyses suggesting that artificial night lighting affects the daily timing of singing in five species. The main aim of this study was to investigate whether the presence of artificial night lighting is also associated with the seasonal occurrence of dawn and dusk singing. We found that in four species dawn and dusk singing developed earlier in the year at sites exposed to light pollution. We also examined the effects of weather conditions and found that rain and low temperatures negatively affected the occurrence of dawn and dusk singing. Our results support the hypothesis that artificial night lighting alters natural seasonal rhythms, independently of other effects of urbanization. The fitness consequences of the observed changes in seasonal timing of behaviour remain unknown.

https://royalsocietypublishing.org/doi/pdf/10.1098/rstb.2014.0126

Light pollution alters the phenology of dawn and dusk singing in common European songbirds

Early life exposure to artificial light at night affects the physiological condition: An experimental study on the ecophysiology of free-living nestling songbirds.

The fundamental change in nocturnal landscapes due to the increasing use of artificial light at night (ALAN) is recognized as being detrimental to the environment and raises important regulatory questions as to whether and how it should be regulated based on the manifold risks to the environment. Here, we present the results of an analysis of the current legal obligations on ALAN in context with a systematic review of adverse effects. The legal analysis includes the relevant aspects of European and German environmental law, specifically nature conservation and immission control. The review represents the results of 303 studies indicating significant disturbances of organisms and landscapes. We discuss the conditions for prohibitions by environmental laws and whether protection gaps persist and, hence, whether specific legislation for light pollution is necessary. While protection is predominantly provided for species with special protection status that reveal avoidance behavior of artificially lit landscapes and associated habitat loss, adverse effects on species and landscapes without special protection status are often unaddressed by existing regulations. Legislative shortcomings are caused by difficulties in proving adverse effect on the population level, detecting lighting malpractice, and applying the law to ALAN-related situations. Measures to reduce ALAN-induced environmental impacts are highlighted. We discuss whether an obligation to implement such measures is favorable for environmental protection and how regulations can be implemented.

https://www.mdpi.com/2071-1050/12/6/2551/pdf

Working with Inadequate Tools: Legislative Shortcomings in Protection against Ecological Effects of Artificial Light at Night

Differences in the reproductive hormone rhythm of tree sparrows (Passer montanus) from urban and rural sites in Beijing: the effect of anthropogenic light sources.

Mechanical loading promotes bone formation and osteocytes are a major mechanosensory cell in the bone. Both Piezo1 channels and connexin 43 hemichannels (Cx43 HCs) in osteocytes are important players in mechanotransduction and anabolic function by mechanical loading. However, the mechanism underlying mechanotransduction involving Piezo1 channels and Cx43 HCs in osteocytes and bone remains unknown.We showed that, like mechanical loading, Piezo1 specific agonist Yoda1 was able to increase intracellular Ca2+ signaling and activate Cx43 HCs, while Yoda1 antagonist Dooku1 inhibited Ca2+ and Cx43 HC activation induced by both mechanical loading and Yoda1. Moreover, the intracellular Ca2+ signal activated by Yoda1 was reduced by the inhibition of Cx43 HCs and pannexin1 (Panx1) channels, as well as ATP-P2X receptor signaling. Piezo1 and Cx43 HCs were co-localized on the osteocyte cell surface, and Yoda1-activated PI3K-Akt signaling regulated the opening of Cx43 HCs. Furthermore, Cx43 HCs opening by mechanical loading on tibias was ablated by inhibition of Piezo1 activation in vivo.We demonstrated that upon mechanical stress, increased intracellular Ca2+ activated by Piezo1 regulates the opening of HCs through PI3K-Akt and opened Cx43 HCs, along with Panx1 channels, and ATP-P2X signaling sustain the intracellular Ca2+ signal, leading to bone anabolic function. 

/pdf/mechanosensitive-piezo1-calcium-channel-activates-connexin-1jrhnbz7.pdf

Mechanosensitive piezo1 calcium channel activates connexin 43 hemichannels through PI3K signaling pathway in bone

Engineered beige adipose tissues could be used for screening therapeutic strategies or as a direct treatment for obesity and metabolic disease. Microvascular fragments are vessel structures that can be directly isolated from adipose tissue and may contain cells capable of differentiation into thermogenic, or beige, adipocytes. In this study, culture conditions were investigated to engineer three-dimensional, vascularized functional beige adipose tissue using microvascular fragments isolated from both healthy animals and a model of type II diabetes (T2D). Vascularized beige adipose tissues were engineered and exhibited increased expression of beige adipose markers, enhanced function, and improved cellular respiration. While microvascular fragments isolated from both lean and diabetic models were able to generate functional tissues, differences were observed in regard to vessel assembly and tissue function. This study introduces an approach that could be employed to engineer vascularized beige adipose tissues from a single, potentially autologous source of cells.

https://journals.sagepub.com/doi/pdf/10.1177/20417314221109337

Engineering Functional Vascularized Beige Adipose Tissue from Microvascular Fragments of Models of Healthy and Type II Diabetes Conditions

TNFα-induced protein 1 (TNFAIP1) serve a role in neurovascular disease. However, the potential role and molecular mechanism of TNFAIP1 in cerebral ischemia-reperfusion (I/R) remains elusive. In the present study, reverse transcription-quantitative PCR and western blotting were used to assess TNFAIP1 mRNA and protein expression levels in PC12 cells. Furthermore, using Cell Counting Kit-8, flow cytometry and western blotting, cell viability and apoptosis were evaluated. Oxidative stress was evaluated using DCFH-DA staining and ELISA was used for assessment of inflammatory factors. Expression of components in the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway and ferroptosis were assessed using western blotting analysis and an iron assay kit. TNFAIP1 expression was significantly upregulated in oxygen glucose deprivation and reperfusion (OGD/R)-injured PC12 cells. However, knocking down TNFAIP1 expression restored PC12 cell viability and decreased apoptosis following OGD/R-challenge. Furthermore, TNFAIP1 silencing significantly suppressed OGD/R-induced oxidative stress and inflammatory damage in PC12 cells. TNFAIP1 knockdown inhibited ferroptosis via activation of the Nrf2 signaling pathway in OGD/R-injured PC12 cells. Erastin treatment reversed the beneficial effects of TNFAIP1 knockdown on PC12 cell viability, apoptosis alleviation, oxidative stress and inflammation following OGD/R treatment. These results suggested that TNFAIP1 knockdown could alleviate OGD/R-induced neuronal cell damage by suppressing Nrf2-mediated ferroptosis, which might lay the foundation for the investigation of targeted-therapy for cerebral I/R injury in clinic.

/pdf/downregulation-of-tnfaip1-alleviates-ogd-r-induced-neuronal-3vgr91bf.pdf

Downregulation of TNFAIP1 alleviates OGD/R‑induced neuronal damage by suppressing Nrf2/GPX4‑mediated ferroptosis

Oxidative stress is a major risk factor that causes osteocyte cell death and bone loss. Prior studies primarily focus on the function of cell surface expressed Cx43 channels. Here, we reported a new role of mitochondrial Cx43 (mtCx43) and hemichannels (HCs) in modulating mitochondria homeostasis and function in bone osteocytes under oxidative stress. In osteocyte MLO-Y4 cells, the translocation of Cx43 to mitochondria was increased under H2O2-induced oxidative stress. H2O2 increased the mtCx43 level accompanied by elevated mitochondrial Cx43 HC activity determined by dye uptake assay. Cx43 knockdown (KD) by CRISPR-Cas9 lentivirus system resulted in impairment of mitochondrial function, primarily manifested as decreased ATP production. Cx43 KD had reduced intracellular reactive oxidative species (ROS) levels and mitochondrial membrane potential. Additionally, live-cell imaging results demonstrated that the proton flux was dependent upon mtCx43 HCs because its activity was specifically inhibited by an antibody targeting Cx43 C-terminus. The co-localization and interaction of mtCx43 and ATP synthase subunit F (ATP5J2) were confirmed by fluorescence resonance energy transfer (FRET) and a protein pull-down assay. Together, our study suggests that mtCx43 hemichannels regulate mitochondrial ATP generation by mediating K+, H+, and ATP transfer across the mitochondrial inner membrane and the interaction with mitochondrial ATP synthase, leading to enhancing the protection capacity of osteocytes against oxidative insults.

Jingruo Zhang

Papers

Differences in the reproductive hormone rhythm of tree sparrows (Passer montanus) from urban and rural sites in Beijing: the effect of anthropogenic light sources.

Mechanosensitive piezo1 calcium channel activates connexin 43 hemichannels through PI3K signaling pathway in bone

Engineering Functional Vascularized Beige Adipose Tissue from Microvascular Fragments of Models of Healthy and Type II Diabetes Conditions

Downregulation of TNFAIP1 alleviates OGD/R‑induced neuronal damage by suppressing Nrf2/GPX4‑mediated ferroptosis

Connexin 43 hemichannels regulate mitochondrial ATP generation, mobilization, and mitochondrial homeostasis against oxidative stress