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.

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.

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.

Previous in vitro studies have indicated that 2,3,3′,4,4′,5-hexachlorobiphenyl (PCB 156) may be a new contributor to metabolic disruption and may further cause the occurrence of nonalcoholic fatty liver disease (NAFLD). However, no study has clarified the specific contributions of PCB 156 to NAFLD progression by constructing an in vivo model. Herein, we evaluated the effects of PCB 156 treatment (55 mg/kg, i.p.) on the livers of C57BL/6 mice fed a control diet (CD) or a high-fat diet (HFD). The results showed that PCB 156 administration increased intra-abdominal fat mass, hepatic lipid levels and dyslipidemia in the CD-fed group and aggravated NAFLD in HFD-fed group. By using transcriptomics studies and biological methods, we found that the genes expression involved in lipid metabolism pathways, such as lipogenesis, lipid accumulation and lipid β-oxidation, was greatly altered in liver tissues exposed to PCB 156. In addition, the cytochrome P450 pathway, peroxisome proliferator-activated receptors (PPARs) and the glutathione metabolism pathway were significantly activated following exposure to PCB 156. Furthermore, PCB 156 exposure increased serum transaminase levels and lipid peroxidation, and the redox-related genes were significantly dysregulated in liver tissue. In conclusion, our data suggested that PCB 156 could promote NAFLD development by altering the expression of genes related to lipid metabolism and inducing oxidative stress.

Exposure to air pollutants has been associated with respiratory and cardiovascular mortality, but the underlying molecular mechanisms remain inadequately understood. We aimed to examine molecular-level inflammatory and oxidative stress responses to personal air pollutant exposure. Fifty-three healthy adults aged 22–52 were measured three times for their blood inflammatory cytokines and urinary malondialdehyde (MDA, an oxidative stress biomarker) within 2 consecutive months. Pollutant concentrations monitored indoors and outdoors were combined with the time-activity data to calculate personal O₃, PM₂.₅, NO₂, and SO₂ exposures averaged over 12 h, 24 h, 1 week, and 2 weeks, respectively, prior to biospecimen collection. Inflammatory cytokines and MDA were associated with pollutant exposures using linear mixed-effects models controlling for various covariates. After adjusting for a co-pollutant, we found that concentrations of proinflammatory cytokines were significantly and negatively associated with 12-h O₃ exposures and significantly but positively associated with 2-week O₃ exposures. We also found significant and positive associations of proinflammatory cytokines with 12-h and 24-h NO₂ exposures, respectively. However, we did not find clear associations of PM₂.₅ and SO₂ exposure with proinflammatory cytokines and with MDA. The removal of an O₃-generating electrostatic precipitator in the mechanical ventilation systems of the offices and residences of the subjects was associated with significant decreases in IL-1β, IL-2, IL-6, IL-8, IL-17A, and TNF-α. These findings suggest that exposure to O₃ for different time durations may affect systemic inflammatory responses in different ways.

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.

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.

The aquatic ecosystem is seriously damaged because of the heavy use of pesticides and antibiotics. Fish is the indispensable link between environmental pollution and human health. However, the toxic effects of environment-related concentrations of pesticides and antibiotics in fish have not been thoroughly studied. In this study, grass carps exposed to cypermethrin (CMN, 0.651 μg/L) or/and sulfamethoxazole (SMZ, 0.3 μg/L) for 42 days caused oxidative stress, apoptosis and immunodeficiency in the spleen of grass carps. CMN or/and SMZ exposure led to oxidative damage (consumption of antioxidant enzymes (superoxide dismutase and catalase)) and lipid peroxidation (accumulation of malondialdehyde), induced apoptosis (increases in TUNEL index, Bax/bcl-2, p53, puma and Caspase family expression). In addition, the levels of immunoglobulin M (IgM), complement 3 (C3) were significantly decreased in all treatment groups, which trend was also found in C-reactive protein in CMN and MIX group, and lysozyme in MIX group. Transcription of almost all genes involved in the Toll-like receptors (TLR) signaling pathway was up-regulated under CMN or/and SMZ exposure. However, when subsequently attacked by Aeromonas hydrophila for 2 days, the TLR pathway was inhibited in spleens of all treatment groups accompanied by higher mortality. Overall, the environmentally relevant concentration of CMN and SMZ damages the immune system, triggering oxidative stress and apoptosis in carps. And by affecting the conduction of TLR signaling pathway, CMN or/and SMZ exposure inhibits the innate immune response of fish and reducing their disease resistance. This study highlights the importance of rational and regulated use of these pesticides and antibiotics.

Lead, a pervasive environmental hazard worldwide, causes a wide range of physiological and biochemical destruction, including metabolic dysfunction. Grape seed proanthocyanidin extract (GSPE) is a natural production with potential metabolic regulation in liver. This study was performed to investigate the protective role of GSPE against lead-induced metabolic dysfunction in liver and elucidate the potential molecular mechanism of this event. Wistar rats received GSPE (200 mg/kg) daily with or without lead acetate (PbA, 0.5 g/L) exposure for 56 d. According to biochemical and histopathologic analysis, GSPE attenuated lead-induced metabolic dysfunction, oxidative stress, and liver dysfunction. Liver gene expression profiling was assessed by RNA sequencing and validated by qRT-PCR. Expression of some genes in peroxisome proliferator-activated receptor alpha (PPARα) signaling pathway was significantly suppressed in PbA group and revived in PbA + GSPE group, which was manifested by Gene Ontology analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis and validated by western blot analysis. This study supports that dietary GSPE ameliorates lead-induced fatty acids metabolic disturbance in rat liver associated with PPARα signaling pathway, and suggests that dietary GSPE may be a protector against lead-induced metabolic dysfunction and liver injury, providing a novel therapy to protect liver against lead exposure.