Lead is a metal that exists naturally in the Earth's crust and is a ubiquitous environmental contaminant. The alleviation of lead toxicity is important to keep human health under lead exposure. Biosynthesized selenium nanoparticle (SeNPs) and selenium-enriched Lactobacillus rhamnosus SHA113 (Se-LRS) were developed in this study, and their potentials in alleviating lead-induced injury to the liver and intestinal tract were evaluated in mice by oral administration for 4 weeks. As results, oral intake of lead acetate (150 mg/kg body weight per day) caused more than 50 times and 100 times lead accumulation in blood and the liver, respectively. Liver function was seriously damaged by the lead exposure, which is indicated as the significantly increased lipid accumulation in the liver, enhanced markers of liver function injury in serum, and occurrence of oxidative stress in liver tissues. Serious injury in intestinal tract was also found under lead exposure, as shown by the decrease of intestinal microbiota diversity and occurrence of oxidative stress. Except the lead content in blood and the liver were lowered by 52% and 58%, respectively, oral administration of Se-LRS protected all the other lead-induced injury markers to the normal level. By the comparison with the effects of normal L. rhamnosus SHA113 and the SeNPs isolated from Se-LRS, high protective effects of Se-LRS can be explained as the extremely high efficiency to promote lead excretion via feces by forming insoluble mixture. These findings illustrate the developed selenium-enriched L. rhamnosus can efficiently protect the liver and intestinal tract from injury by lead.

Although Polychlorinated biphenyl (PCB) levels are decreased in the environment, the adverse effects of gestational exposure on the mother and offspring cannot be ignored due to the vulnerability of the fetus. In the present study, pregnant Balb/c mice were administered PCB52 (1 mg/kg BW/day) or corn oil vehicle by gavage until parturition. In the dams, PCB52 caused histopathological changes in the liver, higher serum levels of aminotransferase and alanine aminotransferase, and activated apoptosis and autophagy, suggesting hepatotoxicity. Overexpressed indicators of TLR4 pathway were observed in the liver of PCB52-exposed dams, indicated hepatic inflammation. Moreover, PCB52 exposure weakened the intestinal barrier and triggered inflammatory response, which might contribute to the hepatic inflammation by gut-liver axis. In the pups, prenatal PCB52 exposure affected the sex ratio at birth and reduced birth length and weights. Similar to the dams, prenatal PCB52 exposure induced hepatotoxicity in the pups without gender difference. Consistent with the alteration of gut microbiota, intestinal inflammation was confirmed, accompanying the disruption in the intestinal barrier and the activation of apoptosis and autophagy in the PCB52-exposed pups. Intestinal injury might be responsible for hepatotoxicity at least in part. Taken together, these findings suggested that gestational PCB52 exposure induced hepatic and intestinal injury in both maternal and offspring mice by arousing inflammation.

The intestine is not only the main accumulation organ of microplastics (MPs), but also the intestinal environment is very conductive to the release of additives in MPs. However, the kinetics of release process, influence factors, and the related effects on gut microbiota remain largely unknown. In this study, a mucosal-simulator of the human intestinal microbial ecosystem (M-SHIME) was used to investigate the influence of gut microbiota on the release of phthalates (PAEs) from MPs and the effects of MPs on the intestinal luminal microbiota and mucosal microbiota. We found that di-(2-ethylhexyl) phthalate (DEHP), di-n-butyl phthalate (DBP), and dimethyl phthalate (DMP) were the dominant PAEs released in the gut. Gut microbiota accelerated the release of PAEs, with the time to reach the maximum release was shortened from 7 days to 2 days. Moreover, MPs induced differential effects on luminal microbiota and mucosal microbiota. Compared with mucosal microbiota, the luminal microbiota was more susceptible to the leaching of PAEs from MPs, as evidenced by more microbiota alterations. MPs also inhibited the metabolic activity of intestinal flora based on the reduced production of short chain fatty acids (SCFA). These effects were mainly contributed by the release of PAEs. Acidaminococcus and Morganella were simultaneously correlated to the release of PAEs and the inhibition of metabolic activity of intestinal microbiota and can be used as indicators for the intestinal exposure of MPs and additives.

Nanoplastic is recognized as an emerging environmental pollutant due to the anticipated ubiquitous distribution, increasing concentration in the ocean, and potential adverse health effects. While our understanding of the ecological impacts of nanoplastics is still limited, we benefit from relatively rich toxicological studies on other nanoparticles such as nano metal oxides. However, the similarity and difference in the toxicokinetic and toxicodynamic aspects of plastic and metallic nanoparticles remain largely unknown. In this study, juvenile Pacific white shrimp Litopenaeus vannamei was exposed to two types of nanoparticles at environmentally relative low and high concentrations, i.e., 100 nm polystyrene nanoplastics (nano-PS) and titanium dioxide nanoparticles (nano-TiO₂) via dietary exposure for 28 days. The systematic toxicological evaluation aimed to quantitatively compare the accumulation, excretion, and toxic effects of nano-PS and nano-TiO₂. Our results demonstrated that both nanoparticles were ingested by L. vannamei with lower egestion of nano-TiO₂ than nano-PS. Both nanoparticles inhibited the growth of shrimps, damaged tissue structures of the intestine and hepatopancreas, disrupted expression of immune-related genes, and induced intestinal microbiota dysbiosis. Nano-PS exposure caused proliferative cells in the intestinal tissue, and the disturbance to the intestinal microbes was also more serious than that of nano-TiO₂. The results indicated that the effect of nano-PS on the intestinal tissue of L. vannamei was more severe than that of nano-TiO₂ with the same particle size. The study provides new theoretical basis of the similarity and differences of their toxicity, and highlights the current lack of knowledge on various aspects of absorption, distribution, metabolism, and excretion (ADME) pathways of nanoplastics.

In recent years, pollution of antibiotics and heavy metal has often been reported in organic wastes. Saprophytic insects have been recorded as biological control agents in organic waste management. During organic waste conversion, the intestinal bacteria of the saprophytic insects play an important role in digestion, physiology, immunity and prevention of pathogen colonization. Black soldier fly (BSF) Hermetia illucens has been widely used as saprophytic insects and showed tolerance to sulfonamides (SAs) and cadmium (Cd). Diversity and changes in gut microbiota of black soldier fly larvae (BSFL) were evaluated through 16S rRNA high-throughput sequencing, and a decrease in diversity of gut microbiota along with an increase in SAs stress was recorded. Major members identified were Actinomycetaceae, Enterobacteriaceae, and Enterococcaceae. And fourteen multi-resistance Klebsiella pneumoniae strains were isolated. Two strains BSFL7-B-5 (from middle midgut of 7-day BSFL) and BSFL11-C-1 (from posterior midgut of 11-day BSFL) were found to be low-toxic and multi-resistance. The adsorption rate of SAs in 5 mg/kg solutions by these two strains reached 65.2% and 61.6%, respectively. Adsorption rate of Cd in 20 mg/L solutions was 77.2% for BSFL7-B-5. The strain BSFL11-C-1 showed higher than 70% adsorption rates of Cd in 20, 30 and 40 mg/L solutions. This study revealed that the presence of multi-resistance bacterial strains in the gut of BSFL helped the larvae against SAs or Cd stress. After determining how and where they are used, selected BSFL gut bacterial strains might be utilized in managing SAs or Cd contamination at suitable concentrations in the future.

The present paper reports on the interrelationships of fish, parasites and the bioaccumulation of hazardous organic compounds in the Zemplínska Šírava water reservoir in eastern Slovakia, which is heavily polluted with polychlorinated biphenyls (PCBs). The concentrations of these contaminants were measured in various fish matrices (dorsal and abdominal muscle tissues, hepatopancreas, intestine wall and adipose tissue) of the freshwater bream, Abramis brama (Cyprinidae), and in its intestinal parasite Caryophyllaeus laticeps (Cestoda), which was used for the first time as a model for a PCB bioaccumulation study. Regarding the fish, the highest concentrations of PCBs were found in the intestine, followed by hepatopancreas and muscle tissues. The amounts of PCBs were higher in abdominal muscles than in their dorsal parts. Concentrations of ∑PCBs above the limits set by European regulations were detected in both muscle parts in the fish, confirming the persistent unfavorable conditions in this locality and high risk for biota and humans. Based on bioconcentration factor values (BCFs), PCBs reached much higher levels in cestodes compared to bream matrices. Some significant differences in PCB amounts between infected and uninfected bream were determined. Fulton's condition factor (CF) significantly differed in infected and non-infected fish (p ˂ 0.05), with CF values surprisingly lower in fish free of parasites compared to parasitized fish, which suggests a “mutualistic” relationship between the parasite and its host.

Known as a cause of food poisoning, Bacillus cereus (B. cereus) is widespread in nature. Cereulide, the heat-stable and acid-resistant emetic toxin which is produced by some B. cereus strains, is often associated with foodborne outbreaks, and causes acute emetic toxicity at high dosage exposure. However, the toxicological effect and underlying mechanism caused by chronic low-dose cereulide exposure require to be further addressed. In the study, based on mouse model, cereulide exposure (50 μg/kg body weight) for 28 days induced intestinal inflammation, gut microbiota dysbiosis and food intake reduction. According to the cell models, low dose cereulide exposure disrupted the intestinal barrier function and caused intestinal inflammation, which were resulted from endoplasmic reticulum (ER) stress IRE1/XBP1/CHOP pathway activation to induce cell apoptosis and inflammatory cytokines production. For gut microbiota, cereulide decreased the abundances of Lactobacillus and Oscillospira. Furthermore, cereulide disordered the metabolisms of gut microbiota, which exhibited the inhibitions of butyrate and tryptophan. Interestingly, cereulide exposure also inhibited the tryptophan hydroxylase to produce the serotonin in the gut and brain, which might lead to depression-like food intake reduction. Butyrate supplementation (100 mg/kg body weight) significantly reduced intestinal inflammation and serotonin biosynthesis suppression caused by cereulide in mice. In conclusion, chronic cereulide exposure induced ER stress to cause intestinal inflammation, gut microbiota dysbiosis and serotonin biosynthesis suppression. IRE1 could be the therapeutic target and butyrate supplementation is the potential prevention strategy.

PM₂.₅ has a major impact on the gastrointestinal system, but the specific mechanism behind this action is not fully understood. Current studies have focused on the relationship between PM₂.₅ and intestinal flora disorder, while ignoring the important influence of diet on gut microbes. In this study, SD rats were fed either a normal, high-fat, or high-carbohydrate diet for two months and exposed to PM₂.₅ (7 mg/kg b.w.) by intratracheal instillation. The results showed that the body and kidney weights of the rats in the high-fat diet group were significantly increased relative to those with a normal diet, and changes in the intestinal microbes and metabolites induced by PM₂.₅ were observed. Rats in the high-carbohydrate diet group had a significant response, and the diversity and richness indices of the flora were reduced (p < 0.05); additionally, intestinal Biffidobacterium and Lactobacillus were enriched, while many endogenous metabolites were found. Some amino acids derivatives and long-chain fatty acids were increased (p < 0.05). Both diet structure and PM₂.₅ exposure can affect the composition of gut microbiota, and intestinal metabolites may be associated with cell membrane damage when a high-carbohydrate diet interacts with PM₂.₅. This study considers multiple dietary factors to further supplement the evidence of intestinal damage via PM₂.₅.

The surface modifications of nanoparticles (NPs), are well-recognized parameters that affect the toxicity, while there has no study on toxicity of Al₂O₃ NPs with different surface modification. Therefore, for the first time, this study pays attention to evaluating the toxicity and potential mechanism of pristine Al₂O₃ NPs (p-Al₂O₃), hydrophilic (w-Al₂O₃) and lipophilic (o-Al₂O₃) modifications of Al₂O₃ NPs both in vitro and in vivo. Applied concentrations of 10, 20, 40, 80,100 and 200 μg/mL for 24 h exposure on Caenorhabditis elegans (C. elegans), while 100 μg/mL of Al₂O₃ NPs significantly decreased the survival rate. Using multiple toxicological endpoints, we found that o-Al₂O₃ NPs (100 μg/mL) could induce more severe toxicity than p-Al₂O₃ and w-Al₂O₃ NPs. After uptake by C. elegans, o-Al₂O₃ NPs increased the intestinal permeability, easily swallow and further destroy the intestinal membrane cells. Besides, cytotoxicity evaluation revealed that o-Al₂O₃ NPs (100 μg/mL) are more toxic than p-Al₂O₃ and w-Al₂O₃. Once inside the cell, o-Al₂O₃ NPs could attack mitochondria and induce the over-production of reactive oxygen species (ROS), which destroy the intracellular redox balance and lead to apoptosis. Furthermore, the transcriptome sequencing and RT-qPCR data also demonstrated that the toxicity of o-Al₂O₃ NPs is highly related to the damage of cell membrane and the imbalance of intracellular redox. Generally, our study has offered a comprehensive sight to the adverse effects of different surface modifications of Al₂O₃ NPs on environmental organisms and the possible underlying mechanisms.

The importance of microplastic (MPs) contamination in marine environments is reflected by increasing number of studies in fish species. Some even dedicated to the toxicological effects from the ingestion. Microplastics (MPs) and their trace metal composition were examined in the muscle and intestine of five commercially important fish species (i.e., Sufflamen fraenatus, Heniochus acuminatus, Atropus atropos, Pseudotriacanthus and Leiognathus brevirostris) from Thoothukudi at the Gulf of Mannar coast in south India. The abundance and morphology of MPs (size, shape, and texture) in muscle and intestinal were investigated by micro-Fourier Transform Infrared Spectroscopy (μ-FT-IR) and atomic force microscope (AFM). ICP-OES was used to investigate the adsorption/leaching of trace metals in microplastics in order to assess health risk for adults and children. Particles of 100–250 μm and white color dominated, and the mean abundances (items/100 g) of total MPs were more in Pseudotriacanthus (muscle: 51.2; intestine: 50.1) compared to Heniochus acuminatus (muscle: 9.6; intestine: 15), Leiognathus brevirostris (muscle: 12; intestine: 13.2) and Atropus atropus (muscle: 15.2; intestine: 44.1). Polyethylene (35.3%), polypropylene (27.2%), polyamide (nylon) (22.2%) and fiber (15.3%) represented the MPs present in muscles, and polyamide (nylon) (30.2%), polyethylene (28.1%), polypropylene (25.9%), and fiber (15.8%) composed the intestine MPs. We estimated possible consumption of 121–456 items of MPs/week by adults and about 19–68 items of MPs/week by children by considering the sizes of safe meals. Zn, Cu, Mn and Cr in these fish species reflected influence of the sewage waste. However, the non-carcinogenic risk evaluated through EDI, THQ, HI, and CR did not suggest any immediate health problem for the consumers.