With the development of marine oil industry, oil spill accidents will inevitably occur, further polluting the intertidal zone and causing biological poisoning. The muddy intertidal zone and Boleophthalmus pectinirostris were selected as the research objects to conduct indoor acute exposure experiments within 48 h of crude oil pollution. Statistical analysis was used to reveal the activity changes of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase (GST) in the gills and liver of mudskipper. Then, integrated biomarker response (IBR) indicators were established to comprehensively evaluate the biological toxicity. The results showed that the activities of SOD, CAT and GST in livers were higher than those in gills, and the maximum induction multipliers of SOD, CAT and GPx in livers appeared earlier than those in gills. Both SOD and GPx activities were induced at low pollutant concentrations and inhibited at high pollutant concentrations. For the dose-effect, the change trends of CAT and SOD were roughly inversed. There was substrate competition between GPx and CAT, with opposite trends over time. The activating mechanism of GST was similar to that of GPx, and the activation time was earlier than that of GPx. In terms of dose-effect trends, the IBR showed that the antioxidant enzymes activities in biological tissues were induced by low and inhibited by high pollutant concentrations. Overall, SOD and GPx in gills and CAT and GST in livers of the mudskippers were suitable as representative markers to comprehensively analyze and evaluate the biotoxicity effects of oil pollution in the intertidal zone. The star plots and IBR values obtained after data standardization were consistent with the enzyme activity differences, which can be used as valid supplementary indexes for biotoxicity evaluation. These research findings provide theoretical support for early indicators of biological toxicity after crude oil pollution in intertidal zones.

Pesticides used in agriculture are some of the most common pollutants in the world. This study aimed to investigate the effects of Organophosphorus Pesticides (OPPs) and Organochlorine Pesticides (OCPs) on the families of farmworkers in the southeast of Iran.In the present case-control study, 141 family members of farmworkers (as the case group) and 59 family members of non-farmworkers (as the controls) were recruited. Serum levels of OCPs such as α-HCH, β-HCH, γ-HCH, 2,4-DDE, 4,4-DDE, 2,4-DDT, and 4,4-DDT were determined. In addition, erythrocyte acetylcholinesterase (AChE) activity, malondialdehyde (MDA), total antioxidant capacity (TAC), protein carbonyl (PC), nitric oxide (NO) serum levels, arylesterase activity of paraoxonase 1 (PON-1), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activity were determined in all participants. Furthermore, distance to farmlands, education, crops, type, and the number of consumed fruits were evaluated for each individual separately.The erythrocyte AChE activity and serum activities of GPx, SOD, and PON-1 and TAC levels were significantly decreased, whereas the concentration of MDA, PC, NO, and seven OCPs were significantly increased in the farmworkers’ families as compared to the controls. Spearman correlation and linear regression suggest that OCPs increase the oxidative stress in farmworkers’ family members. Moreover, distance, education, farming precedence, products, and ventilation had significant effects on the OCP levels and increased the odds ratio of OCP levels in farmworkers’ families.With regards to the data obtained in this study, it was revealed that OCPs as illegal pesticides and OPPs were higher than expected in the farmworkers’ family members. Furthermore, exposure to OCPs and OPPs, apart from the other effects on the body, leads to oxidative stress (OS) that may cause serious diseases in the exposed populations.

Glyphosate is the most popular herbicide used worldwide. This study aimed to investigate the adverse effects of glyphosate on the small intestine and gut microbiota in rats. The rats were gavaged with 0, 5, 50, and 500 mg/kg of body weight glyphosate for 35 continuous days. The different segments of the small intestine were sampled to measure indicators of oxidative stress, ion concentrations and inflammatory responses, and fresh feces were collected for microbiota analysis. The results showed that glyphosate exposure decreased the ratio of villus height to crypt depth in the duodenum and jejunum. Decreased activity of antioxidant enzymes (T-SOD, GSH, GSH-Px) and elevated MDA content were observed in different segments of the small intestine. Furthermore, the concentrations of Fe, Cu, Zn and Mg were significantly decreased or increased. In addition, the mRNA expression levels of IL-1β, IL-6, TNF-α, MAPK3, NF-κB, and Caspase-3 were increased after glyphosate exposure. The 16 S rRNA gene sequencing results indicated that glyphosate exposure significantly increased α-diversity and altered bacterial composition. Glyphosate exposure significantly decreased the relative abundance of the phylum Firmicutes and the genus Lactobacillus, but several potentially pathogenic bacteria were enriched. In conclusion, this study provides important insight to reveal the negative influence of glyphosate exposure on the small intestine, and the altered microbial composition may play a vital role in the process.

Trichlorfon is an organic phosphorus pesticide used to control different parasitic infections in aquaculture. The repeated, excessive use of trichlorfon can result in environmental pollution, thus affecting human health. This study aimed to determine the effects of different concentrations of trichlorfon (0, 0.1, 0.5 and 1.0 mg/L) on the intestinal barrier, oxidative stress, inflammatory response and intestinal microbiome of common carp. Trichlorfon exposure significantly reduced the height of intestinal villus and decreased the expression levels of tight junction genes, such as claudin-2, occludin and ZO-1, in common carp. Moreover, the activities of antioxidant enzymes, such as CAT, SOD and GSH-Px, exhibited a decreasing trend with increasing trichlorfon concentrations, while the contents of MDA and ROS elevated in the intestinal tissues of common carp. The mRNA and protein levels of pro-inflammatory cytokines TNF-α and IL-1β were significantly upregulated by trichlorfon exposure. The level of anti-inflammatory cytokine TGF-β was remarkably higher in 1.0 mg/L trichlorfon treatment group compared to control group. In addition, the results demonstrated that trichlorfon exposure could affect the microbiota community composition and decreased the community diversity in the gut of common carp. Notably, the proportions of some probiotic bacteria, namely, Lactobacillus, Bifidobacterium and Akkermansia, were observed to be reduced after trichlorfon exposure. In summary, the findings of this study indicate that exposure to different concentrations of trichlorfon can damage intestinal barrier, induce intestinal oxidative damage, trigger inflammatory reaction and alter gut microbiota structure in common carp.

Heavy metals have been found in increasing concentrations in the aquatic environment. Fishes exposed to such metals have altered gene expression, serum profiles, tissue histology and bioindices that serve as overall health biomarkers. The heavy metals (Ni, Cd, and Cr) accumulated in water and fish tissues, were beyond the permissible limits defined by the Central Pollution Control Board/World Health Organization. Metallothionein (MT) and glutathione peroxidase (GPX) genes expression patterns highlighted the metal-specific exposure of fish. An increased fold change of genes against beta-actin serves as a potential feature for toxicity. Metal toxicity is also reflected by an increased level of digestive enzymes (amylase and lipase) in the serum and alterations in values of reproductive hormones (11-Ketotestosterone and progesterone). Total serum bilirubin attribute to the liver and biliary tract disease in fishes. Histopathological studies show cellular degeneration, breakage, vacuolization signifying the chronic stress.

The increasing consumption of anticancer drugs through single and/or combinatory chemotherapy worldwide raised concern regarding their toxicity burden in coastal zones. The toxicity of a mixture of three compounds involving the drugs cisplatin (CisPt), cyclophosphamide (CP) and tamoxifen (TAM) was determined on the marine polychaete Nereis diversicolor exposed to an increasing range of their concentrations, respectively: Mix A: 0.1 + 10 + 0.1 ng L−1; Mix B: 10 + 100 + 10 ng L−1; Mix C: 100 + 500 + 25 ng L−1; Mix D: 100 + 1000 + 100 ng L−1. Different endpoints were assessed, including disturbance in the burrowing behaviour, neurotoxicity (acetylcholinesterase – AChE activity), antioxidant enzymes (superoxide dismutase – SOD; catalase – CAT; selenium-dependent glutathione peroxidase – Se-GPx and total glutathione peroxidases T-GPx activities), biotransformation metabolism (glutathione-S-transferases - GST), lipid peroxidation (LPO) and genotoxicity (DNA damage). Biological effects of the mixtures of anticancer compounds on N. diversicolor were compared with previous studies about effects on the same biological model under single-drug exposure conducted with the same molecules. Regarding SOD activity, TAM showed an antagonist effect over CisPt and CP in mixtures C and D. In Mix D, there was a synergistic effect of TAM and CisPt that inhibited CAT activity and an additive interaction of CisPt and CP on the Phase II biotransformation enzyme. Drugs in Mix A also suppressed polychaetes' GST activity, although different from the respective single-drug responses, besides able to induce T-GPx activity, that was not sufficient to avoid oxidative damage and mid-grade DNA damage. Due to the absence of burrowing impairment in Mix A, mechanisms involved in neurotoxicity were other than the one driven by AChE alterations. At the intermediary concentrations (Mix B and C), only LPO occurred. Data from drugs individually may not predict the risks provided by mixtures.

Phycoremediation technologies significantly contribute to solving serious problems induced by heavy metals accumulation in the aquatic systems. Here we studied the mechanisms underlying Al stress tolerance in two diazotrophic cyanobacterial species, to identify suitable species for Al phycoremediation. Al uptake as well as the physiological and biochemical responses of Anabaena laxa and Nostoc muscorum to 7 days Al exposure at two different concentrations i.e., mild (100 μM) and high dose (200 μM), were investigated. Our results revealed that A. laxa accumulated more Al, and it could acclimatize to long-term exposure of Al stress. Al induced a dose-dependent decrease in photosynthesis and its related parameters e.g., chlorophyll content (Chl a), phosphoenolpyruvate carboxylase (PEPC) and Ribulose‒1,5‒bisphosphate carboxylase/oxygenase (RuBisCo) activities. The affect was less pronounced in A. laxa than N. muscorum. Moreover, Al stress significantly increased cellular membrane damage as indicated by induced H₂O₂, lipid peroxidation, protein oxidation, and NADPH oxidase activity. However, these increases were lower in A. laxa compared to N. muscorum. To mitigate the impact of Al stress, A. laxa induced its antioxidant defense system by increasing polyphenols, flavonoids, tocopherols and glutathione levels as well as peroxidase (POX), catalase (CAT), glutathione reductase (GR) and glutathione peroxidase (GPX) enzymes activities. On the other hand, the antioxidant increases in N. muscorum were only limited to ascorbate (ASC) cycle. Overall, high biosorption/uptake capacity and efficient antioxidant defense system of A. laxa recommend its feasibility in the treatment of Al contaminated waters/soils.

PM2.5 is becoming a worldwide environmental problem, which profoundly endangers public health, thus progressively capturing public attention this decade. As a fragile target of PM2.5, the underlying mechanisms of endothelial cell damage are still obscure. According to the previous microarray data and signaling pathway analysis, a new form of cell death termed ferroptosis in the current study is proposed following PM2.5 exposure. In order to verify the vital role of ferroptosis in PM2.5-induced endothelial lesion and further understand the potential mechanism involved, intracellular iron content, ROS release and lipid peroxidation, as well as biomarkers of ferroptosis were detected, respectively. As a result, uptake of particles increases cellular iron content and ROS production. Meanwhile, GSH depletion, and the decrease of GSH-Px and NADPH play significant roles in PM2.5-induced endothelial cell ferroptosis. Moreover, significantly changed expression of TFRC, FTL and FTH1 hinted that dysfunction of iron uptake and storage is a major inducer of ferroptosis. Importantly, index monitored above can be partially rescued by lipid peroxidation inhibitor ferrostatin-1 and iron chelator deferoxamine mesylate, which mediated antiferroptosis activity mainly depends on the restoration of antioxidant activity and iron metabolism. In conclusion, our data basically show that PM2.5 enhances ferroptosis sensitivity with increased ferroptotic events in endothelial cells, in which iron overload, lipid peroxidation and redox imbalance act pivotal roles.

Blueberry anthocyanin (BA) have strong health benefits as an active natural antioxidant and perfluorooctanoic acid (PFOA) can result in oxidative stress in animals. In our study, the protective effects of BA against stress induced by PFOA was investigated in the planarian Dugesia japonica using oxidative stress biomarkers, ATP contents, ATPase activity, DNA methylation and mRNA expression. PFOA exposure could resulted in malondialdehyde production. At the same time, treatment with BA decreased the production of malondialdehyde in BA-exposed and co-treatment planarians. PFOA caused activities increase in glutathione peroxidase (GPx), glutathione S-transferase (GST) and activities decrease in glutathione reductase (GR). PFOA exposure decreased the GSH and ATP contents. Additionally, it increased the GSSG contents and ATPase activity. BA administration increased the activities of GPx, GST and GR in BA and co-treatment planarians. Meanwhile BA maintained the contents of ATP, ATPase activity, GSH and GSSG by alleviating PFOA toxicity. Moreover, PFOA and BA increased the contents of 5-methylcytosine and decreased 5-hydroxymethylcytosine in all group. In addition, PFOA and BA treated planarians significantly altered the expression of genes associated with above biochemical parameters. The results showed that the mRNA expression of gpx, Djgst, gr, Djnak and dnmt1 were significantly elevated in all groups. Alterations in the mRNA expression levels indicated a stress response to PFOA exposure and anthocyanin protection. These alterations regulated biomarkers of oxidative stress, energy metabolism and DNA methylation levels in planarians. These results indicate that BA attenuated PFOA-induced oxidative stress, energy metabolism, DNA methylation and gene expression disorders.

Fluralaner is a novel isoxazoline insecticide which shows high insecticidal activity against parasitic, sanitary and agricultural pests, but there is little information about the effect of fluralaner on non-target organisms. This study reports the acute toxicity, bioconcentration, elimination and antioxidant response of fluralaner in zebrafish. All LC50 values of fluralaner to zebrafish were higher than 10 mg L⁻¹ at 24, 48, 72 and 96 h. To study the bioconcentration and elimination, the zebrafish were exposed to sub-lethal concentrations of fluralaner (2.00 and 0.20 mg L⁻¹) for 15 d and then held 6 d in clean water. The results showed medium BCF of fluralaner with values of 12.06 (48 h) and 21.34 (144 h) after exposure to 2.00 and 0.20 mg L⁻¹ fluralaner, respectively. In the elimination process, a concentration of only 0.113 mg kg⁻¹ was found in zebrafish on the 6th day after removal to clean water. After exposure in 2.00 mg L⁻¹ fluralaner, the enzyme activities of SOD, CAT, and GST, GSH-PX, CarE and content of MDA were measured. Only CAT and CarE activities were significantly regulated and the others stayed at a stable level compared to the control group. Meanwhile, transcriptional expression of CYP1C2, CYP1D1, CYP11A were significantly down-regulated at 12 h exposed to 2.00 mg L⁻¹ of fluralaner. Except CYP1D1, others CYPs were up-regulated at different time during exposure periods.Fluralaner and its formulated product (BRAVECTO®) are of low toxicity to zebrafish and are rapidly concentrated in zebrafish and eliminated after exposure in clean water. Antioxidant defense and metabolic systems were involved in the fluralaner-induced toxicity. Among them, the activities of CAT and CarE, and most mRNA expression level of CYPs showed fast response to the sub-lethal concentration of fluralaner, which could be used as a biomarker relevant to the toxicity.