The method of air pollution level evaluation of urban landscapes on the basis of D. melanogaster cohort analysis has been suggested. The method implies the binding to the landscape areas of the city. Within each landscape area traps and cultivators for D. melanogaster have been installed in sanitary-protective zones of various enterprises as well as on the background territory with the least level of anthropogenic load serving as the control. Based on specifically elaborated technique for field conditions, the amount of eggs, third instar larvae, pupae and imago has been calculated. Then, using the computer program ImageJ, the square under the curves of cohort survival has been determined which is considered overall cohort viability (OCVD.m). The previously mentioned indicator considers cohort survival at all stages of ontogenesis. In addition, the expressed in percentage indicator of oppression (IO OCVD.m) in relevance to the control OCVD. m affects the level of air pollution of urban landscapes by emissions of various enterprises. The relevance between these indicators is determined by a four-level scale elaborated specifically for the purpose. The method has been tested based on technogenic landscapes of Chernivtsi, Ukraine. The sensitivity of the suggested indicator for a wide range of pollutants has been proved and its ability to respond to different levels of greening of similar enterprises has been shown.

Single-chemical thresholds cannot comprehensively evaluate the risk of chemical mixture exposure in indoor air. Moreover, a large number of researches have focused on short-term and high-concentration co-exposure scenarios related to different species, based on diverse endpoints, which hampers the application and improvement of existing risk evaluation models of chemical mixture exposures. More importantly, current risk evaluation models are not user-friendly for construction practitioners who do not have sufficient toxicological knowledge. Therefore, in this study, an inhalation experiment system and a hazard index (HI) were developed to investigate the risks associated with low-concentration and long-term inhalation exposure scenarios of formaldehyde and benzene, individually and combined, based on Drosophila melanogaster mortality. The results showed that the system exhibited good reproducibility in providing stable exposure concentrations during D. melanogaster life cycle. Furthermore, in a range of experimental concentrations, the interaction between formaldehyde and benzene was additive or synergistic, which was concentration- and ratio-dependent. This study is of great significance in harmonising and providing toxicity data under long-term and low-concentration exposure scenarios, which is beneficial for establishing a new user-friendly risk evaluation model for indoor chemical mixture exposures. It should be noted that the proposed HI value could indicate the hazard degrees of long-term inhalation exposures of formaldehyde and benzene, individually and combined, to D. melanogaster. However, the applicability of this index requires further experiments to evaluate the exposure risks of other volatile organic compounds (VOCs) to D. melanogaster.

With the rapid development of science and technology, 5G technology will be widely used, and biosafety concerns about the effects of 5G radiofrequency radiation on health have been raised. Drosophila melanogaster was selected as the model organism for our study, in which a 3.5 GHz radiofrequency radiation (RF-EMR) environment was simulated at intensities of 0.1 W/m², 1 W/m², and 10 W/m². The activity of parent male and offspring (F1) male flies was measured using a Drosophila activity monitoring system under short-term and long-term 3.5 GHz RF-EMR exposure. Core genes associated with heat stress, the circadian clock and neurotransmitters were detected by QRT-PCR technology, and the contents of GABA and glutamate were detected by UPLC-MS. The results show that short-term RF-EMR exposure increased the activity level and reduced the sleep duration while long-term RF-EMR exposure reduced the activity level and increased the sleep duration of F1 male flies. Under long-term RF-EMR, the expression of heat stress response-related hsp22, hsp26 and hsp70 genes was increased, the expression of circadian clock-related per, cyc, clk, cry, and tim genes was altered, the content of GABA and glutamate was reduced, and the expression levels of synthesis, transport and receptor genes were altered. In conclusion, long-term RF-EMR exposure enhances the heat stress response of offspring flies and then affects the expression of circadian clock and neurotransmitter genes, which leads to decreased activity, prolonged sleep duration, and improved sleep quality.

Bis(2-ethylhexyl) phthalate (DEHP) is the most common plasticizer. Previous studies have shown DEHP treatment accelerates neurological degeneration, suggesting that DEHP may impact retinal sensitivity to light, neurotransmission, and copulation behaviors. Although its neurotoxicity and antifertility properties have been studied, whether DEHP exposure disrupts vision and how DEHP influences neuromuscular junction (NMJ) have not been reported yet. Moreover, the impact of DEHP on insect courtship behavior is still elusive. Fruit flies (Drosophila melanogaster) were treated with series concentrations of DEHP and observed for lifespan, motor function, electroretinogram (ERG), electrophysiology of neuromuscular junction (NMJ), courtship behaviors, and relevant gene expression. Our results confirmed the DEHP toxicity on lifespan and capacity of motor function and updated its effect on copulation behaviors. Additionally, we report for the first time that DEHP exposure may harm vision by affecting the synaptic signaling between the photoreceptor and the laminar neurons. Further, DEHP treatment altered both spontaneous and evoked neurotransmission properties. Noteworthy, the effect of DEHP exposure on the copulation behavior is sex-dependent, and we proposed potential mechanisms for future investigation.

Early life environmental influences such as exposure to cigarette smoke (CS) can disturb molecular processes of lung development and thereby increase the risk for later development of chronic respiratory diseases. Among the latter, asthma and chronic obstructive pulmonary disease (COPD) are the most common. The airway epithelium plays a key role in their disease pathophysiology but how CS exposure in early life influences airway developmental pathways and epithelial stress responses or survival is poorly understood. Using Drosophila melanogaster larvae as a model for early life, we demonstrate that CS enters the entire larval airway system, where it activates cyp18a1 which is homologues to human CYP1A1 to metabolize CS-derived polycyclic aromatic hydrocarbons and further induces heat shock protein 70. RNASeq studies of isolated airways showed that CS dysregulates pathways involved in oxidative stress response, innate immune response, xenobiotic and glutathione metabolic processes as well as developmental processes (BMP, FGF signaling) in both sexes, while other pathways were exclusive to females or males. Glutathione S-transferase genes were further validated by qPCR showing upregulation of gstD4, gstD5 and gstD8 in respiratory tracts of females, while gstD8 was downregulated and gstD5 unchanged in males. ROS levels were increased in airways after CS. Exposure to CS further resulted in higher larval mortality, lower larval-pupal transition, and hatching rates in males only as compared to air-exposed controls. Taken together, early life CS induces airway epithelial stress responses and dysregulates pathways involved in the fly's branching morphogenesis as well as in mammalian lung development. CS further affected fitness and development in a highly sex-specific manner.

With the rapidly increasing popularity of 5G mobile technology, the effect of radiofrequency radiation on human health has caused public concern. This study explores the effects of a simulated 3.5 GHz radiofrequency electromagnetic radiation (RF-EMF) environment on the development and microbiome of flies under intensities of 0.1 W/m², 1 W/m² and 10 W/m². We found that the pupation percentages in the first 3 days and eclosion rate in the first 2 days were increased under exposure to RF-EMF, and the mean development time was shortened. In a study on third-instar larvae, the expression levels of the heat shock protein genes hsp22, hsp26 and hsp70 and humoral immune system genes AttC, TotC and TotA were all significantly increased. In the oxidative stress system, DuoX gene expression was decreased, sod2 and cat gene expression levels were increased, and SOD and CAT enzyme activity also showed a significant increase. According to the 16S rDNA results, the diversity and species abundance of the microbial community decreased significantly, and according to the functional prediction analysis, the genera Acetobacter and Lactobacillus were significantly increased. In conclusion, 3.5 GHz RF-EMF may enhance thermal stress, oxidative stress and humoral immunity, cause changes in the microbial community, and regulate the insulin/TOR and ecdysteroid signalling pathways to promote fly development.

Deciphering the potential mechanism of chemical-induced toxicity enables us to alleviate the cellular and organismal dysfunction. The environmental presence of nonylphenol (endocrine disruptor) has a major health concern due to its widespread usage in our day-to-day life. The current study establishes a novel functional link among nonylphenol-induced oxidative stress, Heat shock protein 27 (Hsp27, member of stress protein family), and Ecdysone receptor (EcR, a nuclear receptor), which eventually coordinates the nonylphenol-induced sub-cellular and organismal level toxicity in a genetically tractable model Drosophila melanogaster. Drosophila larvae exposed to nonylphenol (0.05, 0.5 and 5.0 μg/mL) showed a significant decrease in Hsp27 and EcR mRNA levels in the midgut. In concurrence, reactive oxygen species (ROS) levels were increased with a corresponding decline in glutathione (GSH) level and Thioredoxin reductase (TrxR) activity. Increased lipid peroxidation (LPO), protein carbonyl (PC) contents, and cell death were also observed in a correlation with the nonylphenol concentrations. Sub-cellular toxicity poses a negative organismal response, which was evident by delayed larval development and reduced Drosophila emergence. Subsequently, a positive genetic correlation (p < 0.001) between EcR and Hsp27 revealed that nonylphenol-dependent EcR reduction is a possible link for the downregulation of Hsp27. Further, Hsp27 overexpression in midgut cells showed a reduction in nonylphenol-induced intracellular ROS, LPO, PC content, and cell death through the TrxR mediated regenerative pathway and reduced GSH level improving the organismal response to the nonylphenol exposure. Altogether, the study elucidates the potential EcR-Hsp27 molecular interactions in mitigating the nonylphenol-induced cellular and organismal toxicity.

The analysis of lipid disruption in invertebrates is limited by our poor knowledge of their lipidomes and of the associated metabolic pathways. For example, the mechanism by which exposure of the crustacean Daphnia magna to tributyltin, juvenoids, or bisphenol A increase the accumulation of storage lipids into lipid droplets is largely unknown/presently unclear. Here we analyze transcriptome changes subsequent to this lipid accumulation effect induced by either the pesticide pyriproxyfen (a juvenoid agonist), the plasticizer bisphenol A, or the antifouling agent tributyltin. Changes in the whole transcriptome were assessed after 8 and 24 h of exposure, the period showing the greatest variation in storage lipid accumulation. The three compounds affected similarly to a total of 1388 genes (965 overexpressed and 423 underexpressed transcripts), but only after 24 h of exposure. In addition, 225 transcripts became up-regulated in samples exposed to tributyltin for both 8 h and 24 h. Using D. melanogaster functional annotation, we determined that upregulated genes were enriched in members of KEGG modules implicated in fatty acid, glycerophospholipid, and glycerolipid metabolic pathways, as well as in genes related to membrane constituents and to chitin and cuticle metabolic pathways. Conversely, down-regulated genes appeared mainly related to visual perception and to oocyte development signaling pathways. Many tributyltin specifically upregulated genes were related to neuro-active ligand receptor interaction signaling pathways. These changes were consistent with the phetotypic effects reported in this and in previous studies that exposure of D. magna to the tested compounds increased lipid accumulation and reduced egg quantity and quality.

Continuous exposure to low levels of toxic substances can be associated with delayed physical disturbances, which can be preceded by changes in enzyme activities and gene expression. Thus, understanding changes in the transcriptional profile could help in recognition of early molecular events involved in the toxicity mechanism of toxicants. Vinylcyclohexene (VCH) and methylmercury (MeHg⁺) are xenobiotics, which do not present a completely elucidated mechanism of toxicity. Metabolites of both compounds have some overlapping chemical properties that involve moderate to high affinity for thiol and selenol groups. In this work, we characterized by deep-sequencing transcriptomic approach the effects of VCH and MeHg⁺ on the mRNA transcriptional profile of adults fruit flies (Drosophila melanogaster) after individual and concomitant exposure to VCH and MeHg⁺. The flies were separated into four groups: control, VCH, MeHg⁺, and VCH + MeHg⁺. After individual exposure, VCH deregulated 38 genes (of which the majority was up-regulated), whereas MeHg⁺ altered 26 genes (i.e., 14 down-regulated). VCH and MeHg⁺ co-exposure changed 72 genes with a high number of genes down-regulated. Together, the results suggest that although the compounds could have some similar protein targets (e.g., sulfhydryl-containing proteins), the transcriptional profile after individual exposures and co-exposure were completely different.

Insecticide resistance is a major challenge in successful insect pest control as the insects have the ability to develop resistance to various widely used insecticides. Butene-fipronil is a novel compound with high toxicity to insects and less toxicity to the non-target organisms. In the present study, the effect of butene-fipronil alone and in combination with three enzyme inhibitors, piperonyl butoxide (PBO), diethyl maleate (DEM), and triphenyl phosphate (TPP), was carried out on larvae and adults of Drosophilia melanogaster. Our results indicated that the co-toxicity indices of butene-fipronil + PBO, butene-fipronil + TPP, and butene-fipronil + DEM mixtures were 437.3, 335.0, and 210.3, respectively, in the second-instar larvae, while 186.6, 256.2, and 238.5, respectively, in the adults, indicating synergistic effects. Interestingly, butene-fipronil increased the expression of CYP28A5 in the larvae; CYP9F2, CYP304A1, CYP28A5, and CYP318A1 in the female adults; and CYP303A1 and CYP28A5 in the male adults. Furthermore, high-level expression of Est-7 was observed in the female adults compared to larvae and male adults. Our results suggest that there is no difference in butene-fipronil metabolism in larvae and male and female adults of D. melanogaster.