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.

Numerous studies reported that BPA could cause oxidative damage to different tissues in rats/mice. This study aimed to perform a systematic review and meta-analysis of BPA exposure on oxidative damage in rats/mice. A comprehensive literature search was conducted using PubMed, Embase, and Web of Science databases from their inception date until July 18, 2020. 20 eligible articles were included in this study. The results showed that BPA could significantly increase the level of MDA (SMD, 16.88; 95%CI, 12.06–21.71), but there was a significant reduction in the contents of antioxidants, such as GR (−10.46, −13.91 ∼ −7.02), CAT (−8.48, −11.66 ∼ −5.30), GPx (−9.37, −11.95 ∼ −6.80), GST (−7.59, −14.51 ∼ −0.67), GSH (−10.64, −13.96 ~ −7.33), and SOD (−6.48, −8.37 ∼ −4.58) in rats/mice. Our study provided clear evidence that BPA exposure could significantly induce oxidative damage in rats/mice. And we also found that the degree of oxidative damage was related to BPA dose, target tissue, intervention means, and exposure duration of BPA.

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.

Experimental studies have suggested perfluoroalkyl substances (PFASs) as mammary toxicants, but few studies evaluated the prospective associations of PFASs with breast cancer risk. We performed a case-cohort study within the Dongfeng-Tongji cohort, including incident breast cancer cases (n = 226) and a random sub-cohort (n = 990). Baseline plasma concentrations of four perfluorinated carboxylic acids (PFCAs) [perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), and perfluoroheptanoic acid (PFHpA)] and two perfluorinated sulfonic acids (PFSAs) [perfluorooctane sulfonic acid (PFOS) and perfluorohexane sulfonic acid (PFHxS)] were measured. Barlow-weighted Cox regression models revealed that each 1-unit increase in ln-transformed PFOA and PFHpA was associated with a separate 35% and 20% elevated incident risk of breast cancer [HR(95%CI) = 1.35(1.03, 1.78) and 1.20(1.02, 1.40), respectively], which were also significant among postmenopausal females [HR(95%CI) = 1.34(1.01, 1.77) and 1.23 (1.02, 1.48), respectively]. Quantile g-computation analysis observed a 19% increased incident risk of breast cancer along with each simultaneous quartile increase in all ln-transformed PFCA concentrations [HR(95%CI) = 1.19(1.01, 1.41)], with PFOA accounting for 56% of the positive effect. Our findings firstly revealed the impact of short-chain PFHpA on increased incident risk of breast cancer, suggested exposure to PFASs as a risk factor for breast cancer, and shed light on breast cancer prevention by regulating PFASs as a chemical class.

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.