In the study, the effects of dimethyl phthalate (DMP) on the antioxidant defense capacity and immune functions of human erythrocytes were experimentally explored. DMP affected the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) and the contents of glutathione (GSH) and malondialdehyde (MDA) in erythrocytes, thus impairing the function of antioxidant defense system of erythrocytes. When DMP concentration increased from 0 to 28 μmol L⁻¹, the SOD and GPX activities were increased firstly and then gradually decreased. When DMP concentration was below 20 μmol L⁻¹, the relative activity of SOD was enhanced by DMP and the effect was known as hormesis. The relative activity of GPX was also increased when the concentration of DMP was below 12 μmol L⁻¹. The CAT activity was more significantly inhibited by DMP than the activities of SOD and GPX, whereas the relative GSH content was increased by DMP. MDA levels were significantly changed after the exposure to DMP (0–24 μmol L⁻¹). The experimental results of the activity of SOD and CAT, and the content of MDA also suggested that DMP could inhibit the immune functions of red blood cells (RBCs), which were further proved by the decrease of two indicators (RBC-C₃b and RBC-IC) due to the destruction of C₃b receptor with immune adherence function on erythrocyte membrane. The study provides a deep understanding of the toxicity of DMP on erythrocytes.

Di(2-ethylhexyl) phthalate (DEHP), as a widely used plasticizer, is reported to have widespread environmental and global health hazards. Trace amounts of phthalates in the environment are sufficient to disrupt ecological balance and affect human health. However, DEHP-induced splenic toxicity remains in an unknown state. Therefore, to explore the mechanism of DEHP-induced splenic toxicity, male quail were employed with 0, 250, 500 and 750 mg/kg body weight DEHP by daily gastric perfusion for 45 days. Notably, splenic corpuscular border and cell gap enlargement were observed in the spleen tissue of DEHP-exposed quail under the histopathological analysis. Furthermore, DEHP induced dysregulation of oxidative stress markers by increasing malondialdehyde (MDA) content and decreasing superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activities. Low concentration of DEHP (≤250 mg/kg) exposure suppressed nuclear factor-E2-related factor 2 (Nrf2) signaling pathway, while high concentration of DEHP (≥500 mg/kg) exposure activated Nrf2-mediated defense response. DEHP induced splenic oxidative stress via interfering Nrf2 signal pathway and altering the transcription of its downstream genes. In conclusion, this study suggested that DEHP induced splenic toxicity.

T-2 toxin is an unavoidable contaminant in human food, animal feeds, and agricultural products. T-2 toxin has been found to impair male reproductive function. But, few data is available that reveals the reproductive toxicity mechanism. In the study, male Kunming mice were orally administrated with T-2 toxin at the doses of 0, 0.5, 1 or 2 mg/kg body weight for 28 days. The body and reproductive organs weight, the concentration, malformation rate and ultrastructure of sperm in cauda epididymis were detected. Oxidative stress biomarkers and apoptosis were also measured in testes. Histological change of testes was performed by H&E and TUNEL staining. T-2 toxin down-regulated body and reproductive organs (testis, epididymis and seminal vesicle) weight, sperm concentration, increased sperm malformation rate and damaged the ultrastructure of sperm and structure of testes. T-2 toxin treatment increased the reactive oxygen species (ROS) and malondialdehyde content, while, decreased the total anti-oxidation capacity (T-AOC) and the superoxide dismutase activity in testes. T-2 toxin exposure increased the TUNEL-positive germ cells, the activities and mRNA expressions of caspase-3, caspase-8 and caspase-9, the mRNA expression of Bax, and inhibited the Bcl-2 mRNA expression. Furthermore, the expressions of caspase-3, caspase-8 caspase-9 and Bax were positively correlated with ROS level, but negatively correlated with T-AOC in testis. In summary, T-2 toxin caused spermatogenesis disorder associated with the germ cell apoptosis medicated by oxidative stress, impairing the male reproductive function.

The present study investigated the physiological responses, photosynthetic activity, and microbial community structure of leaf-associated biofilms on the microphyte Vallisneria natans during a harmful algal bloom. Results of the physiological and photosynthetic indices (Fᵥ/Fₘ ratios [maximum quantum yield of photosystem II (PSII)]; malondialdehyde content; total chlorophyll; and activities of superoxide dismutase, catalase and peroxidase) indicated that algal blooms could cause inhibition of photosynthesis, oxidative stress and an antioxidant system stress response in Vallisneria natans leaf-associated biofilms. Multifractal analysis suggested that allelochemicals or algal organic matter released by cyanobacteria could reduce the surface roughness of the leaf. Microbial diversity analysis of the biofilms showed that algal blooms slightly altered the microbial community structure while the richness and evenness of the microbial composition remained stable. This study provided useful information to better understand the adverse effects of algal blooms on submerged macrophytes.

Harmful algal blooms have emerged as a worldwide issue. After concentrations of herbicides entering water, herbicides in water may pose ecological effects on them. The present study investigates the toxicity and environmental behavior of the herbicides, napropamide and acetochlor as enantiomers and as racemates on Microcystis aeruginosa which is the main specie known to produce hepatotoxins. S-napropamide/acetochlor are degraded faster than their corresponding isomer R-napropamide/acetochlor, with the latter more prone to accumulate in algal cells. Moreover, all the enantiomers did not undergo measurable racemization in the medium and algal cells. S-napropamide/acetochlor exhibited much higher toxicity than R-napropamide/acetochlor, with the S-enantiomer inducing a much greater production of antioxidant defense enzymes (superoxide dismutase (SOD) and malondialdehyde (MDA)) and microcystins (MC). SOD and MC increased after treatment with the herbicides and these increases were dependent on the exposure time, whereas MDA showed no apparent change. The information provided in this work will be useful for understanding the toxicity mechanism and environmental behaviors of different amide herbicides (napropamide and acetochlor) in aquatic environments at the enantiomeric level. Additionally, analysis of chiral herbicides in aquatic system needs more attention to aide in the environmental assessment of chiral herbicides.

Recent studies have demonstrated the occurrence of microplastic fibers (MFs) in soil environments. To determine whether MFs are harmful for soil biota, we evaluated toxic effects on terrestrial snails (Achatina fulica) after 28 d exposure to polyethylene terephthalate MFs at concentrations of 0.01–0.71 g kg−1 (dry soil weight). Digestion kinetics experiments on 24 snails showed that MFs can be ingested and excreted within 48 h. We found the appearance of cracks and deterioration on the surface of MFs after depuration by the digestive system. Prolonged exposure to 40 snails showed that 0.14–0.71 g kg−1 MFs caused an average reduction of 24.7–34.9% food intake and 46.6–69.7% excretion. 0.71 g kg−1 MFs induced significant villi damage in the gastrointestinal walls of 40% snails, but did not influence the histology of the liver and kidney. Moreover, 0.71 g kg−1 MFs exposure reduced glutathione peroxidase (59.3 ± 13.8%) and total antioxidant capacity (36.7 ± 8.5%), but elevated malondialdehyde level (58.0 ± 6.4%) in the liver, which indicates oxidative stress is involved in the toxic mechanism. Our results suggest that MFs have adverse impacts on the fitness of soil organisms, and highlight the ecological risks of microplastic pollution in terrestrial ecosystems.

In wheat production areas of China, soil lead (Pb) pollution is generally accompanied by cadmium (Cd) pollution and it is of considerable significance in repairing the Cd and Pb co-contaminated soils for safe agronomic production. Organosilicon fertilizer (OSiF) is a new type of silicon (Si) fertilizer that can effectively alleviate heavy metal toxicity in plants, but the mechanisms on its heavy metal detoxification are poorly understood. A soil pot experiment was conducted to evaluate and compare the effects of two OSiFs (OSiFA and OSiFB) and an inorganic silicon fertilizer (InOSiF) on wheat heavy metal uptake and biochemical parameters in a Cd and Pb co-contaminated soil. The results demonstrated that OSiFA, OSiFB and InOSiF could alleviate the Cd and Pb toxicity of wheat, as indicated by increasing wheat grain yield by 65%, 45% and 22%, respectively. The Si fertilizers enhanced leaf gas exchange attributes and chlorophyll content, whereas diminished the oxidative damage, as indicated by a lower level of hydrogen peroxide (H2O2) and malondialdehyde (MDA) content, and lower activity of superoxide dismutase (SOD) and catalase (CAT) activity, as compared with control. Adding OSiFA, OSiFB and InOSiF increased Si uptake in roots and shoots, thus reducing Cd and Pb accumulation in the wheat shoot, bran and flour, especially, flour Cd contents by 17%, 10% and 31% respectively, flour Pb contents by 74%, 53% and 48% respectively. Also, Si fertilizers application decreased the health risk index (HRI) of both Cd and Pb. The grey correlation degrees of OSiFA, OSiFB and InOSiF are 0.72, 0.77 and 0.61, respectively, indicating that the effects of OSiFs on detoxifying Cd and Pb could be better than that of InOSiF in wheat. Thus, the use of OSiFs might be a feasible approach to reduce Cd and Pb entry into the human body through crops.

Concentrations of atmospheric carbon dioxide have been continuously increasing, and more investigations are needed in regard to the responses of various plants to the corresponding climatic conditions. In particular, potential variations in phytoremediation efficiency induced by global warming have rarely been investigated. Objective of this research was to evaluate the changes in phytoremediation efficiency of Noccaea caerulescens exposed to different concentrations of CO2. The concentrations of CO2 in the elevated CO2 treatments were adjusted to 550 ± 50 ppm to match the level of atmospheric CO2 predicted in 2050–2070. Compared to ambient controls (400 ppm), biomass yields and metal concentrations of N. caerulescens increased under elevated CO2 conditions, thus indicating that the phytoremediation efficiency of the species could increase in higher CO2 environment. In addition, water soluble and exchangeable Pb and Cu concentrations in soils decreased under elevated CO2 conditions, which reduced the leaching risks of the metals. The concentrations of malondialdehyde (MDA) of N. caerulescens decreased to different degrees with the increased CO2 concentrations. The overall findings suggested that elevations in CO2 can reduce the oxidative damage caused by metals in this species. The phytoremediation efficiency of N. caerulescens grown in multiple metal-enriched soils could be enhanced with global warming.

Insecticide ethiprole, the alternative of fipronil which has been restricted in many countries, may contaminant water bodies through surface runoff after agricultural application, however, the aquatic toxicity and environmental behavior of ethiprole is still unknown. In this study, five metabolites of ethiprole (ethiprole sulfone, ethiprole sulfide, ethiprole amide, desethylsulfinyl ethiprole and ethiprole sulfone amide) were synthesized and their toxic effects on photosynthetic pigment and antioxidase in aquatic plant Chlorella pyrenoidosa (C. pyrenoidosa) were evaluated on an enantiomeric level. Besides, the accumulation and metabolism of rac-ethiprole and its enantiomers in algae suspension and algae were studied. Ethiprole sulfide was found to be more toxic than ethiprole, with the 96h EC₅₀ value seven times lower than ethiprole. Enantioselective toxicity was observed with R-ethiprole more toxic than S-ethiprole. The contents of chlorophyll were significantly reduced by all the chemicals at higher concentrations, and the levels of protein, malondialdehyde (MDA) and the activity of antioxidant defense enzymes were dose-dependent. The half-life of rac-ethiprole in algae suspension was 13.6 days and ethiprole amide was the major metabolite. However, ethiprole sulfide was the main metabolite in algae, suggesting different metabolic pathways in algae suspension and algae. Enantioselective metabolism in algae suspension was found with S-ethiprole metabolized faster than R-ethiprole. The preferentially accumulated and metabolized of R-ethiprole in algae was observed and C. pyrenoidosa had limited capacity to convert one enantiomer into the other. These findings indicated the toxicity of ethiprole to C. pyrenoidosa is lower than fipronil. The individual enantiomers of chiral pollutants and their metabolites should be considered in risk assessments.

Arsenic (As) present in water is a nonignorable environmental issue, even at low concentrations (≤150 μg L⁻¹). To evaluate the toxic effect of low concentrations of As, zebrafish at early life stage were exposed to 0, 25, 50, 75, or 150 μg L⁻¹ AsIII for 120 h. Our results indicated that low concentration of AsIII decreased zebrafish larvae’s survival rate to 85%, 89% and 86% at 50, 75 and 150 μg L⁻¹. Furthermore, low concentrations of AsIII exposure caused oxidative stress (elevated superoxide dismutase (SOD) activity and influenced the mRNA transcriptional levels of Cu/ZnSOD and MnSOD) and damage (increased malondialdehyde levels). Meanwhile, zebrafish larvae regulated the mRNA transcription of metallothionein and heat shock protein 70 to alleviate toxicity caused by AsIII. These results revealed lower concentrations (≤150 μg L⁻¹) of AsIII had a detriment effect on the survival of fish at early life stage, moreover, oxidative stress caused by AsIII posed potential risk for the zebrafish. This study provides novel insight into low concentration AsIII-induced toxicity in zebrafish.