Bisphenol A (BPA) is pervasive in the environment, and exposure to BPA may increase the incidence of noncommunicable diseases like autoimmune diseases and cancer. Although BPA causes immunological problems at the cellular level, no system-level research has been conducted on this. Hence, in this study, we aimed to gain a better understanding of the biological response to BPA exposure and its association with immunological disorders. For that, we explored the transcriptome and the proteomic modifications at the systems and cellular levels following BPA exposure. Our integrated multi-omics data showed the alteration of the T cell receptor (TCR) signaling pathway at both levels. The proportion of enlarged T cells increased with upregulation of CD69, a surface marker of early T cell activation, even though the number of T cells reduced after BPA exposure. Additionally, on BPA exposure, the levels of pLCK and pSRC increased in T cells, while that of pLAT decreased. Following BPA exposure, we investigated cytokine profiles and discovered that chitinase 3 Like 1 and matrix metalloproteinase 9 were enriched in T cells. These results indicated that T cells were hyperactivated by CD69 stimulation, and phosphorylation of SRC accelerated on BPA exposure. Hence, alteration in the TCR signaling pathway during development and differentiation due to BPA exposure could lead to insufficient and hasty activation of TCR signaling in T cells, which could modify cytokine profiles, leading to increased environmental susceptibility to chronic inflammation or diseases, increasing the chance of autoimmune diseases and cancer. This study enhances our understanding of the effects of environmental perturbations on immunosuppression at molecular, cellular, and systematic levels following pubertal BPA exposure, and may help develop better predictive, preventative, and therapeutic techniques.

Mycotoxins are increasingly considered as micropollutants in the environment. Fumonisins, as one of the most important mycotoxins, cause potential health threats to humans and animals due to their ubiquitous contamination on cereals, fruit, vegetables and other environmental samples around the world. However, the contribution of fumonisins to the interaction of fungi with plant hosts is not still fully understood. Here, we investigated the effect of fumonisin B1 (FB1) on the infection of Fusarium proliferatum on banana fruit and the underlying mechanisms from the host perspective. Our results found that FB1 treatment increased the aggressiveness of F. proliferatum on banana fruit and inhibited the defense ability of banana fruit via decreasing phenylalanine ammonia lyase (PAL), β-1,3-glucanase (GLU) and chitinase (CHI) activities. Meanwhile, FB1 accelerated cell death, indicated by higher relative conductivity, MDA content and higher transcripts of cell death-related genes. FB1 treatment resulted in higher hydrogen peroxide (H₂O₂) content possibly due to MaRBOHs induction. These consequences accelerated the ROS-dependent cell death, which subsequently result in reduction of disease resistance of banana fruit. Additionally, energy metabolism and MaDORN1s-mediated eATP signaling might involve in FB1-meidiated suppression of banana defense responses. Collectively, results of the current study indicated that FB1 contamination triggered the cell death of banana peel, subsequently instigating the invasion and growth of F. proliferatum on banana fruit. In summary, for the first time, we demonstrated a previously unidentified role of fumonisins as a potential virulence factor of F. proliferatum in modulating fruit defense response, which provides new insight on the biological roles of fumonisins.

Thifluzamide is widely used in treatment of rice diseases and has potential toxicity on aquatic organism. Although previous studies have focused on the toxic effect of thifluzamide in zebrafish, no consistent conclusions have been reached. To help to elucidate the toxic mechanism, qualities of liver and mitochondria were evaluated. The global changes in the transcriptome of zebrafish after exposure to thifluzamide were measured. Based on this, the expression and activities of chitinase and succinate dehydrogenase (SDH) were further assayed. And the targeted site of thifluzamide in zebrafish was confirmed by dock study and co-exposure study. Here we report that developmental inhibition was observed along with presence of liver and mitochondrial damage. The expression of SDHa-d and genes related to mitochondrial DNA (mtDNA) replicate and mitochondrial complexes were significantly altered. And, as the top differentially expressed genes, the expression of chia.1-6 did show apparent changes, but differences of chitinase activity between exposure groups and the controls did not reach significance. In line with that, dock study showed that the binding potentials of thifluzamide toward zebrafish chitinase and SDH exhibited in the following order: SDH> chitinase. And sdhb-sdhc-sdhd (Qp site) showed the highest binding activity toward thifluzamide. The joint exposure (thifluzamide + Q10) significantly improved the survival of zebrafish compared with single thifluzamide exposure. These results indicate that SDH, especially Qp-site, may be the target of thifluzamide in zebrafish and inhibition of SDH activity may be at least in partial responsible for the toxicity of thifluzamide in zebrafish. In addition, the antagonistic effect of Q10 on thifluzamide toxicity in zebrafish suggests that Q10 may be a useful adjunct to detoxification.

Recent studies have demonstrated the ability of mealworm (Tenebrio molitor) for plastic degradation. This study is focused on changes in microbiome structure depending on diets. Microbial community obtained from oat and cellulose diet formed similar group, two kinds of polyethylene formed another group, while polystyrene diet showed the highest dissimilarity. The highest relative abundance of bacteria colonizing gut was in PE-oxodegradable feeding, nevertheless all applied diets were higher in comparison to oat. Dominant phyla consisted of Proteobacteria, Bacteroides, Firmicutes and Actinobacteria, however after PS feeding frequency in Planctomycetes and Nitrospirae increased. The unique bacteria characteristic for cellulose diet belonged to Selenomonas, while Pantoea were characteristic for both polyethylene diets, Lactococcus and Elizabethkingia were unique for each plastic diet, and potential diazotropic bacteria were characteristic for polystyrene diet (Agrobacterium, Nitrosomonas, Nitrospira).Enzymatic similarity between oatmeal and cellulose diets, was shown. All three plastics diet resulted in different activity in both, digestive tract and bacteria. The enzymes with the highest activity were included phosphatases, esterases, leucine arylamidase, β-galactosidase, β-glucuronidase, α-glucosidase, β-glucosidase, chitinase, α-mannosidase and α-fucosidase. The activity of digestive tract was stronger than cultured gut bacteria. In addition to known polyethylene degradation methods, larvae may degrade polyethylene with esterase, cellulose and oatmeal waste activity is related with the activity of sugar-degrading enzymes, degradation of polystyrene with anaerobic processes and diazotrophs.

Different extraction methods have been proposed to study the ingestion of microplastics by marine organisms, including enzymatic digestion. While mussels have been the focus of research, crustaceans' enzymatic digestion has received little attention. An overlooked source of information for microplastic research is analysis of long-term time-series biotic samples. These collections are invaluable for the detection and monitoring of changes in ecosystems, especially those caused by anthropogenic factors. Here, crustacean larvae collected in two periods, 1985 and 2020, in the central North Sea were used to develop and optimise an effective and gentle enzymatic digestion method suitable for microplastic research. Sequential breakdown of these chitinaceous samples via a mechanical and surfactant (Sodium Dodecyl Sulphate 1% v/v) pre-treatment, followed by proteinase K (100 mU/mL) and chitinase (50 mU/mL) digestion, efficiently removed >96% of biomass of 1985 and 2020 samples. The optimised method was effective without interfering with the identification of naturally weathered microplastics via FTIR Spectroscopy.

Low-density polyethylene (LDPE) is made from the monomer, ethylene. It is mainly used as food packing material and is difficult to recycle. Thus, we attempted to identify the fungal compositions from a plastic disposal site and use them to degrade LDPE. We identified five isolates as belonging to Rhizopus spp. and Aspergillus spp. according to their morphologies. The fungal isolates were tested using a biodegradation assay with LDPE-supplemented growth medium. Among the five fungal isolates identified, strain A effectively degraded LDPE as evidenced by its increased biomass and greater reduction of the LDPE weight (60%). PCR amplification of the 18S rRNA from genomic DNA isolation of this strain revealed that the strain had 96% similarity to Rhizopus oryzae according to BLAST searches. As an LDPE-degrading fungus, the sequence was submitted to GenBank under the accession number MT259131. Fourier-transform infrared spectroscopy and scanning electron microscopy analysis provided evidence for the functional group and morphological changes in the LDPE. We further substantiated its ability to degrade plastic by docking the LDPE and polyethylene terephthalate (PET) substrates with the chitinase enzyme from Rhizopus oryzae and a control enzyme. The docking scores for the chitinase enzyme (AAP57213) were − 7.0 kJ/mol for LDPE and − 6.7 kJ/mol for PET. The docking score for the control was − 5.5 kJ/mol. These results suggest that degradation of LDPE and PET helps with societal recycling of plastic waste.

Crustacean shell waste disposal is considered as biggest problem in seafood processing centers. Incineration and landfilling are the commonest ways of disposal of the waste which causes environmental pollution. Microbial bio-conversion is one of the promising approaches to minimize the wastes by utilizing the same for deriving different value added metabolites. In this perspective, chitinase- and protease-producing bacterial strains were isolated from shrimp culture pond, and the potent isolate was subsequently identified as Alcaligenes faecalis SK10. Fermentative optimization of the production of chitinase (85.42 U/ml), protease (58.57 U/ml), and their catalytic products, viz., N-acetylamino sugar (84 μg/ml) and free amino acids (112 μg/ml), were carried out by utilizing shrimp and crab shell powder as principal substrate. The fermented hydrolysate (FH) was subsequently applied to evaluate its potential to be a candidate fertilizer for the growth of leguminous plant Pisum sativum and Cicer arietinum, and the results were compared with chitin, chitosan, and commercial biofertilizer amended group. The results revealed that FH have paramount potential to improve plants morpho-physiological parameters like stem and root length, chlorophyll, cellular RNA, protein content, and soil physico-chemical parameters like total nitrogen, magnesium, calcium, phosphorus, and potassium significantly (p < 0.05). Moreover, the application of FH also selectively encouraged the growth of free-living nitrogen-fixing bacteria, Rhizobium, phosphate-solubilizing bacteria in the soil by 4.82- and 5.27-, 5.57- and 4.71, and 7.64- and 6.92-fold, respectively, in the rhizosphere of P. sativum and C. arietinum, which collectively is a good sign for an ideal biofertilizer. Co-supplementation of FH with commercial PGPR-biofertilizer significantly influenced the morpho-physiological attributes of plant and physico-chemical and microbial attributes of soil. The study validated proficient and sustainable utilization of fermented hydrolysate of waste crustacean shell as biofertilizer.

Several studies have reported the toxicological implications of exposure to petroleum hydrocarbon fumes in animal models. There is little documentation on the effect of such exposure on oxidative stress levels and immune response. To our knowledge, no documentation of M1 polarization in macrophages in gasoline station male attendants. Therefore, this study aimed to evaluate the harmful effects of gasoline vapors in 62 male attendants (16–70 years) compared to 29 age- and sex-matched–unexposed controls. The attendants were recruited from Damietta governorate gasoline stations. Gasoline exposure induced a significant increase in tumor necrosis factor-α (TNF-α) level (p < 0.05) as well as a slight but non-significant increase in the activity of acidic mammalian chitinase (AMCase) (p > 0.05). Further TNF-α/AMCase ratio was significantly increased (p < 0.01) in sera of the attendants when compared to those of the healthy controls. Also, the total leucocytic and lymphocytic counts were significantly increased (p < 0.01 and p < 0.001, respectively). On contrary, neutrophils to lymphocytes ratio (NLR) and platelets to lymphocytes ratio (PLR) were significantly decreased (p < 0.05 and p < 0.001, respectively). In addition, significant reduction in hemoglobin (Hb) concentration, plasma glutathione reduced form (GSH), and catalase, as well as superoxide dismutase (SOD) activities in red blood cells were observed in the exposed attendants. As a result, malondialdehyde (MDA), nitric oxide (NO) levels, and NO/AMCase ratio were significantly increased (p < 0.05). In conclusion, this study inferred that prolonged gasoline exposure can mediate immune activation, especially M1 macrophages polarization, possibly via oxidative stress-mediated mechanism.

The endocrine system of crustaceans regulates the molt cycle with ecdysteroid hormones, mainly the 20-hydroxyecdysone (20-HE). Moreover, the molt process requires the action of chitinolytic enzymes (e.g., chitinase, chitobiase) to break down the old cuticle. However, endocrine disrupting compounds (EDC) are capable of altering their normal functioning. Glyphosate-based herbicides (GBH), such as Roundup®, the most widely used herbicides, are found in freshwater environments and have been considered EDC for many aquatic organisms. Therefore, this study examined the effects of environmentally relevant GBH concentrations (0.0065, 0.065, and 0.28 mg L⁻¹) on the 20-HE concentration and chitobiase activity in the decapod prawn Macrobrachium potiuna exposed for 14 days. Additionally, lipid peroxidation, a biomarker of membrane lipid degradation, was evaluated in hepatopancreas to assess cellular damage. Results showed that GBH decreased the 20-HE concentration in females at the two highest concentrations tested, while an increase was observed in males exposed to the highest GBH concentration. In addition, GBH also decreased chitobiase activity in males (all concentrations) and females (the two highest concentrations). Finally, GBH caused increased lipid peroxidation in males, indicating cellular damage in the hepatopancreas. In conclusion, this work suggests that GBH is an EDC for crustaceans by disrupting molting, which could lead to altered reproduction and thus population dynamics. Graphical abstract Decrease in the 20-HE concentration and chitobiase activity in muscle of males and females of the freshwater prawn Macrobrachium potiuna exposed to the herbicide Roundup® for 14 days