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.

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.

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.

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.

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.

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.

PM₂.₅ exposure is an emerging environmental concern and severe health insult closely related to psychological conditions such as anxiety and depression in adolescence. Adolescence is a critical period for neural system development characterized by continuous brain maturation, especially in the prefrontal cortex. The etiology of these adolescent conditions may derive from fetal origin, probably attributed to the adverse effects induced by intrauterine environmental exposure. Anxiety- and depression-like behavior can be induced by gestational exposure to PM₂.₅ in mice offspring which act as a useful model system. Recent studies show that B-vitamin may alleviate PM₂.₅-induced hippocampal neuroinflammation- and function-related spatial memory impairment in adolescent mice offspring. However, cortical damage and related neurobehavioral defects induced by gestational PM₂.₅ exposure, as well as the potential reversibility by interventions in mice offspring require to be elucidated. Here, we aimed to investigate whether B-vitamin would protect mice offspring from the adverse effects derived from gestational exposure to urban PM₂.₅ on cortical areas to which anxiety and depression are closely related. Pregnant mice were divided into three groups: control group (treated with PBS alone), model group (treated with both PM₂.₅ and PBS), and intervention group (treated with both PM₂.₅ and B-vitamin), respectively. The mice offspring were then applied to comprehensive neurobehavioral, ultrastructural, biochemical, and molecular biological analyses. Interestingly, we observed that gestational PM₂.₅ exposure led to neurobehavioral defects including anxiety- and depression-like behavior. In addition, neuroinflammation, oxidative damage, increased apoptosis, and caspase-1-mediated inflammasome activation in the prefrontal cortex were observed. Notably, both behavioral and molecular changes could be significantly alleviated by B-vitamin treatment. In summary, our results suggest that the anxiety- and depression-like behavior induced by gestational PM₂.₅ exposure in mice offspring can be ameliorated by B-vitamin supplementation, probably through the suppression of apoptosis, oxidative damage, neuroinflammation, and caspase-1-mediated inflammasome activation.

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.

The roles that ozone and nitric oxide (NO), the chief O3 precursor, play in the antioxidative balance and inducible volatile emissions of lima bean were assessed. Exposure to O3 inhibited APX, CAT, and GR, decreased GSH content and induced emissions of (E)-β-ocimene, limonene, 1,8-cineole, linalool, (E)-4,8-dimethyl-1,3,7-nonatriene (E)-DMNT, 2-butanone and nonanal. O3 did not induce emissions of (E)-β-caryophyllene and appeared to reduce the antioxidative capacity of plants to a greater extent than NO and NO followed by O3 (NO/O3) treatments. There were significant differences in emissions of (E)-β-ocimene and linalool between NO/O3 treated plants and controls, but no differences in antioxidant concentrations. A model to explain the relationships between the ascorbate–glutathione cycle and O3 and NO inducible volatiles was proposed. Our findings suggest that prior exposure to NO modulates the oxidative effect of ozone by the process of cross-tolerance, which might regulate the antioxidative system and induction of volatile organic compounds.

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.