The induction of oxidative stress in plants grown on crude oil-contaminated soils was investigated using a diesel contaminated soils model. Twelve cassava stems were grown in four garden pots containing different amounts of diesel oil as contaminants: 150 ppm, 300 ppm, 600 ppm and control (0 ppm). The growth of the plants was monitored for 12 weeks, after which chlorophyll contents, total proteins, lipid peroxidation and activities of catalase, glutathione, and superoxide dismutase (antioxidant enzymes) were determined from the leaves. Significant decreases (p<0.05) were observed in the antioxidant enzymes (67-86%), total proteins (79%) and total chlorophyll content (67%) in the cassava grown on diesel contaminated soil (600 ppm) compared to the control. Consequently, there were significant increase (p<0.05) in the leaf ratio and malondialdehyde (a marker for lipid peroxidation) 0.1909 ± 04 and 1.77 ± 0.34, when compared to the control 0.1530 ± 08 sq.cm/g and 0.10±0.01 µmol/mg protein respectively. It was thus concluded that stunted growth of plants and their death in diesel or crude oil contaminated soil could be traced to oxidative stress.

Oxytetracycline (OTC) and Cu are prevalent in aquatic ecosystems and their pollution are issues of serious concern. The present working hypothesis is that the toxicity of Cu and OTC mixture on physiological activity of fish was different from single OTC and Cu alone. The present study indicated that, compared to single OTC or Cu alone, Cu+OTC mixture reduced growth performance and feed utilization of grass carp, escalated the contents of Cu, OTC and TG, increased lipogenesis, induced oxidative stress, damaged the mitochondrial structure and functions and inhibited the lipolysis in the liver tissues and hepatocytes of grass carp. Cu+OTC co-treatment significantly increased the mRNA abundances and protein expression of Nrf2. Moreover, we found that Cu+OTC mixture-induced oxidative stress promoted Nrf2 recruitment to the SREBP-1 promoter and increased SREBP-1-mediated lipogenesis; Nrf2 sited at the crossroads of oxidative stress and lipid metabolism, and mediated the regulation of oxidative stress and lipid metabolism. Our findings clearly indicated that OTC and Cu mixture differed in environmental risks from single antibiotic or metal element itself, and thus posed different toxicological responses to aquatic animals. Moreover, our findings suggested that Nrf2 functioned as an important antioxidant regulator linking oxidative stress to lipogenic metabolism, and thus elucidated a novel regulatory mechanism for lipid metabolism.

Nuclear factor-erythroid 2-related factor-2 (Nrf2) is an important modulator of cellular responses against Cd in mammalian cells. However, whether such modulation is conserved in Marsupenaeus japonicas remains unknown.In our study, the shrimps were injected with dsRNA targeting Nrf2 at 4 μg g⁻¹ body weight (b.w.) or sulforaphane (SFN) at 5 μg g⁻¹ b.w., and then were exposed to 40 mg L⁻¹ CdCl₂ for 48 h. After Nrf2 knockdown, the Cd content increased, but decreased in the SFN group. This suggested that Nrf2 could promote Cd excretion. A terminal deoxynulceotidyl transferase nick-end-labeling (TUNEL) assay revealed that the Nrf2 knockdown increased the number of apoptotic cells in M. japonicas, while SFN decreased the number of apoptotic cells. After Nrf2 knockdown, the total antioxidant capacity (T-AOC), superoxide dismutase (Sod) activity, and related gene expression decreased significantly, while the malondialdehyde (MDA) content increased remarkably. By contrast, SFN injection alleviated the oxidative stress, as evidenced by increased T-AOC, Sod activity, sod mRNA expression and a reduced MDA content. Similarly, detoxification related enzyme activities (ethoxyresorufin O-deethylase and glutathione-S-transferase (GST)) and their corresponding gene expressions (cyp3a (cytochrome P450 family 3 subfamily A) and gst) were suppressed in the ds-Nrf2 injection group, while they were elevated in the SFN group. In addition, ds-Nrf2 activated mitochondrial apoptotic pathway, as evidenced the mRNA and protein levels of caspase-3, Bcl2 associated X protein (Bax), and p53, while SFN treatment suppressed them. These results displayed that in M. japonicus Cd-induced cellular oxidative damage probably acts via the Nrf2 pathway.

As drug abuse has become increasingly serious, carbamazepine (CBZ) is discharged into the aquatic environment with municipal sewage, causing potential harm to aquatic organisms. Here, we utilized zebrafish, an aquatic vertebrate model, to comprehensively evaluate the hepatotoxicity of CBZ. The larvae were exposed to 0.07, 0.13, and 0.26 mmol/L CBZ from 72 hpf to 144 hpf, and the adults were exposed to 0.025, 0.05, and 0.1 mmol/L CBZ for 28 days. The substantial changes were observed in the size and histopathology of livers, indicating that CBZ induced severe hepatoxicity in the larvae and adults. Oil red O staining demonstrated CBZ exposure caused severe lipid accumulation in the livers of both larvae and adults. Furthermore, CBZ exposure facilitated hepatocyte apoptosis through TUNEL staining, which was caused by rising ROS content. Subsequently, down-regulation of genes related to the Wnt pathway in exposure groups indicated that CBZ inhibited the development of liver via the Wnt/β-catenin signaling pathway. In conclusion, CBZ induced severe hepatotoxicity by promoting lipid accumulation, generating excessive ROS production, and inhibiting the Wnt/β-catenin signaling pathway in zebrafish. The results reveal the occurrence of CBZ-induced hepatotoxicity in zebrafish and clarify its mechanism of action, which potentially illustrate environmental concerns associated with CBZ exposure.

Four most concerned heavy metal pollutants, arsenic, cadmium, lead, and mercury may share common mechanisms to induce metabolic syndrome (MetS). However, recent studies exploring the relationships between MetS and metal exposure presented inconsistent findings. We aimed to clarify the relationship between heavy metal exposure biomarkers and MetS using a meta-analysis and systematic review approach. Literature search was conducted in international and the Chinese national databases up to June 2020. Of selected studies, we extracted the relevant data and evaluated the quality of each study’s methodology. We then calculated the pooled effect sizes (ESs), standardized mean differences (SMDs), and their 95% confidence intervals (CIs) using a random-effect meta-analysis approach followed by stratification analyses for control of potential confounders. Involving 55,536 participants, the included 22 articles covered 52 observational studies reporting ESs and/or metal concentrations on specific metal and gender. Our results show that participants with MetS had significantly higher levels of heavy metal exposure [pooled ES = 1.16, 95% CI: 1.09, 1.23; n = 42, heterogeneity I² = 75.6%; and SMD = 0.22, 95% CI: 0.15, 0.29; n = 32, I² = 94.2%] than those without MetS. Pooled ESs in the subgroups stratified by arsenic, cadmium, lead, and mercury were 1.04 (95% CI: 0.97, 1.10; n = 8, I² = 61.0%), 1.10 (0.95, 1.27; 11, 45.0%), 1.21 (1.00, 1.48; 12, 82.9%), and 1.26 (1.06, 1.48; 11, 67.7%), respectively. Pooled ESs in the subgroups stratified by blood, urine, and the other specimen were 1.22 (95% CI: 1.08, 1.38; n = 26, I² = 75.8%), 1.06 (1.00, 1.13; 14, 58.1%), and 2.41 (1.30, 4.43; 2, 0.0%), respectively. In conclusion, heavy metal exposure was positively associated with MetS. Further studies are warranted to examine the effects of individual metals and their interaction on the relationship between MetS and heavy metals.

We tested antioxidant responses of the green microalga Pseudokirchneriella subcapitata exposed to different concentrations of the three antibiotics erythromycin (ETM), ciprofloxacin (CPF) and sulfamethoxazole (SMZ). Measurements included the level of lipid peroxidation, the total antioxidative capacity and three major antioxidant mechanisms: the ascorbate–glutathione cycle, the xanthophyll cycle and the enzyme activities of catalase (CAT), superoxide dismutase (SOD), guaiacol glutathione peroxidase (GPX) and glutathione-S-transferase (GST). Three antibiotics significantly affect the antioxidant system of P. subcapitata, but in different ways the alga was more tolerant to CPF and SMZ exposures than to ETM exposure. ETM caused reductions in AsA and GSH biosynthesis, ascorbate–glutathione cycle, xanthophylls cycle and antioxidant enzyme activities. The toxicity of CPF seems to be mainly overcome via induction of the ascorbate–glutathione cycle and CAT, SOD and GPX activities, while the toxicity of SMZ on the photosynthetic apparatus is predominantly reduced by the xanthophyll cycle and GST activity.

The main intent of the current research was to appraise if combined application of hydrogen sulfide (H₂S, 0.2 mM) and silicon (Si 2.0 mM) could improve tolerance of tomato plants to arsenic (As as sodium hydrogen arsenate heptahydrate, 0.2 mM) stress. Plant growth, chlorophylls (Chl), PSII maximum efficiency (Fv/Fm), H₂S concentration and L-cysteine desulfhydrase activity were found to be suppressed, but leaf and root As, leaf proline content, phytochelatins, malondialdehyde (MDA) and H₂O₂ as well as the activity of lipoxygenase (LOX) increased under As stress. H₂S and Si supplied together or alone enhanced the concentrations of key antioxidant biomolecules such as ascorbic acid, and reduced glutathione and the activities of key antioxidant system enzymes including catalase (CAT), superoxide dismutase (SOD), dehydroascorbate reductase (DHAR), glutathione reductase (GR), and glutathione S-transferase (GST). In comparison with individual application of H₂S or Si, the joint supplementation of both had better effect in improving growth and key biochemical processes, and reducing tissue As content, suggesting a putative collaborative role of both molecules in improving tolerance to As-toxicity in tomato plants.

Due to the large-scale outbreak of Corona Virus Disease (2019), amounts of disinfecting agents was regularly used in public environments and their potential toxicity towards organisms needed to be appreciated. Thus, one mostly used cationic disinfectant, benzalkonium chlorides (BAC(C12)), was selected to assess its potential toxicity one common cyanobacteria Microcystis aeruginosa (M. aeruginosa) in this study. The aims were to explore the toxic effect and mechanism of BAC (C12) on M. aeruginosa growth within 96 h via morphological, physiological, and the relative and absolute quantification (iTRAQ)-based quantitative proteomics variations. The results found that BAC(C12) significantly inhibited cell density of M. aeruginosa at concentrations from 1 mg/L to 10 mg/L, and the 96-h EC₅₀ value was identified to be 3.61 mg/L. Under EC₅₀ concentration, BAC(C12) depressed the photosynthesis activities of M. aeruginosa exhibited by 36% decline of the maximum quantum yield for primary photochemistry (Fv/Fm) value and denaturation of photosynthetic organelle, caused oxidative stress response displayed by the increase of three indexes including superoxide dismutase (SOD), malondialdehyde (MDA), and the intracellular reactive oxygen species (ROS), and destroyed the integrity of cell membranes demonstrated by TEM images and the increase of ex-cellular substances. Then, the iTRAQ-based proteomic analysis demonstrated that BAC(C12) depressed photosynthesis activities through inhibiting the expressions of photosynthetic protein and photosynthetic electron transport related proteins. The suppression of electron transport also led to the increase of superoxide radicals and then posed oxidative stress on cell. Meantime, the 63.63% ascent of extracellular microcystin production of M. aeruginosa was observed, attributing to the high expression of microcystin synthesis proteins and the damage of cell membrane. In sum, BAC(C12) exposure inhibited the growth of M. aeruginosa mainly by depressing photosynthesis, inducing oxidative stress, and breaking the cell membrane. And, it enhanced the release of microcystin from the cyanobacterial cells via up-regulating the microcystin synthesis proteins and inducing the membrane damage, which could enlarge its toxicity to aquatic species.

Cadmium (Cd) in the food chain poses a serious hazard to human health. Therefore, a greenhouse hydroponic experiment was conducted to examine the potential of exogenously strigolactone GR24 in lessening Cd toxicity and to investigate its physiological mechanisms in the two barley genotypes, W6nk2 (Cd-sensitive) and Zhenong8 (Cd-tolerant). Exogenous application of 1 μM GR24 (strigol analogue) reduced the suppression of growth caused by 10 μM Cd, lowered plant Cd contents, increased the contents of other nutrient elements, protected chlorophyll, sustained photosynthesis, and markedly reduced Cd-induced H₂O₂ and malondialdehyde accumulation in barley. Furthermore, exogenous GR24 markedly increased NO contents and nitric oxide synthase activity in the Cd-sensitive genotype, W6nk2, effectively alleviating the Cd-induced repression of the activities of superoxide dismutase and peroxidase, increasing reduced glutathione (GSH) and ascorbic acid (AsA) pools and activities of AsA-GSH cycle including ascorbate peroxidase, glutathione peroxidase, glutathione reductase, dehydroascorbate reductase and monodehydroascorbate reductase. The findings of the present study indicate that GR24 could be a candidate for Cd detoxification by decreasing Cd contents, balancing nutrient elements, and protecting barley plants from toxic oxidation via indirectly eliminating reactive oxygen species (ROS), consequently contributing to reducing the potential risk of Cd pollution.

Microplastics (MPs) pollution frequently co-occur with Microcystis-dominated blooms in freshwaters, but MPs effects on toxigenic Microcystis growth and effect mechanisms remained poorly understood. This study used 0.5 μm-size polyethylene (PE) and polyvinyl chloride (PVC) to explore dose- and time-dependent effects of single and combined MPs (i.e., PE + PVC) on toxigenic Microcystis growth and cellular responses during 16 day-test. Results showed that Microcystis growth and cellular responses depended on exposure time, MPs dose and type. MPs elicited hormesis effect in early stage at low dose (5 mg/L), while increasingly inhibited growth with rising PVC or PE + PVC dose but declining PE dose (5, 10, 50 mg/L) in mid-late stage, with stress intensity of PE + PVC > PVC > PE. Further analyses revealed unobvious cell damage under MPs stress, largely because antioxidases were increasingly activated as MPs stress enhanced. Unicellular MCs release ability during mid stage almost coincided with total/bound amount and each fraction of ex-poly and ex-pro trends under MPs stress. Significant positive relationship existed between MCs release ability and ex-poly/ex-pro fractions and total amount of Microcystis cells along mid-late stage under MPs stress, validating that ex-poly/ex-pro production was regulated as a result of MCs release. Besides, unicellular MCs production ability was generally positively correlated with soluble, tightly-bound and total ex-poly and ex-pro at late stage. These suggested that cellular antioxidants, MCs production/release ability and ex-poly/ex-pro production of Microcystis could be coupled to exert integrated defense against MPs stress to protect surviving cells in Microcystis population. These findings are crucial for acquiring the fate of Microcystis-dominated blooms co-occurring with MPs pollution, and reasonably assessing and managing involved eco-risks.