The present study investigates the influence of an organophosphorus pesticide, namely Dimethoate, and cadmium on biomarkers of the green alga, Spirogyra sp., in a 14-day experiment. For so doing, it has exposed Spirogyra sp. to 0.0, 100, 200, and 400 mg L-1 of Dimethoate and/or 1 mg L-1 of cadmium chloride (CdCl2) to observe a reduction in chlorophyll a and b level in Spirogyra sp., exposed to 200 and 400 mg L-1 of Dimethoate as well as algae treated with cadmium alone or in combination with Dimethoate. Levels of malondialdehyde (MDA) and total antioxidant in cells, as well as the activity of ascorbate peroxidase (APX) soar in Spirogyra sp., exposed to Dimethoate and/or cadmium (alone or simultaneously). Also Spirogyra’sexposure to cadmium and/or Dimethoate significantly increases catalase (CAT) activity. However, levels of carotenoids in Spirogyra sp., treated with both cadmium and Dimethoate, decline significantly, with no significant change found in catalase activity of Spirogyra sp., exposed to 100 and 200 mg L-1 of Dimethoate, in comparison to the control group. However, CAT activity rises significantly in Spirogyra sp., treated with 400 mg L-1 of Dimethoate. Cadmium can cause cytotoxicity in 1 mg L-1 concentration of the green algae(Spirogyra sp.). On the whole, investigating the biological and biochemical markers in Spirogyra sp., exposed to different concentrations of Dimethoate, has revealed some concentration-dependent toxicity. Furthermore, Dimethoate can synergistically increase toxicity and bioavailability of cadmium in Spirogyra sp.

This study aimed at evaluating the interactive effects of acetaminophen (AC; 400 mg kg−1) and silicon dioxide nanomaterial (nano-SiO2;3 mg kg−1) on soil-grown barley. After 14 days of growth, plant growth, evaluated in terms of fresh and dry weight, was greatly inhibited by AC, independently of being or not co-treated with nano-SiO2. Plants growing under high levels of AC did not show any increase in malondialdehyde (MDA) nor thiols contents, though levels of superoxide anion (O2.-) and hydrogen peroxide (H2O2) were increased in leaves and roots, respectively. When plants were co-treated with nano-SiO2, reactive oxygen species (ROS) content remained unchanged, but lipid peroxidation (LP) was diminished and the thiol redox network was up-regulated in roots. The evaluation of the response of the antioxidant system showed that AC affected both non-enzymatic and enzymatic components in an organ-specific manner: proline levels and superoxide dismutase (SOD) activity were enhanced, whilst catalase (CAT) activity decreased in leaves; ascorbate content and CAT activity were diminished in roots. In response to the nano-SiO2 co-treatment, this pattern was not vastly altered, despite for ascorbate peroxidase (APX), whose activity was greatly enhanced in both organs. Overall, combining biometric, biochemical and molecular approaches, this study revealed that, although AC impaired plant growth and development, it did not trigger a harsh oxidative stress condition. Maybe by this reason, the ameliorating potential of nano-SiO2 was not so evident; yet, nano-SiO2 was able to reduce LP and to stimulate thiol content and APX activity, possibly as a defense mechanism against AC-induced stress.

Several monitoring studies have shown that benzoylecgonine (BE) is the main illicit drug residue commonly measured in the aquatic system worldwide. Few studies have investigated the potential toxicity of this molecule towards invertebrate and vertebrate aquatic non-target organisms focusing on effects at low levels of the biological organization, but no one has assessed the consequences at higher ones. Thus, the present study was aimed at investigating the toxicity of a 48-h exposure to two concentrations of BE, similar to those found in aquatic ecosystems (0.5 μg/L and 1.0 μg/L), on the cladoceran Daphnia magna at different levels of the ecological hierarchy. We relied on a multi-level approach focusing on the effects at biochemical/biomolecular (biomarkers), individual (swimming activity) and population (reproduction) levels. We measured the amount of reactive oxygen species and of the activity of antioxidant (SOD, CAT, and GPx) and detoxifying (GST) enzymes to assess if BE exposure can alter the oxidative status of D. magna specimens, while the lipid peroxidation (TBARS) was measured as a marker of oxidative damage. Moreover, we also measured the acetylcholinesterase (AChE) activity because it is strictly related to behavioral changes in aquatic organisms. Changes in swimming behavior were investigated by a video tracking analysis, while the consequences on reproduction were assessed by a chronic toxicity test. Our results showed that BE concentrations similar to those found in aquatic ecosystems induced oxidative stress and inhibited AChE activity, affecting swimming behavior and the reproduction of Daphnia magna individuals.

Polybrominated diphenyl ethers (PBDEs) are toxic chemicals widely distributed in the environment, but few studies are available on their potential toxicity to rice at metabolic level. Therefore we exposed ten rice (Oryza sativa) varieties to 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47), a predominant congener of PBDEs, in hydroponic solutions with different concentrations. Two varieties that showed different biological effects to BDE-47, YY-9 and LJ-7, were screened as sensitive and tolerant varieties according to changes of morphological and physiological indicators. Metabolic research was then conducted using gas chromatography−mass spectrometry combined with diverse analyses. Results showed that LJ-7 was more active in metabolite profiles and adopted more effective antioxidant defense machinery to protect itself against oxidative damages induced by BDE-47 than YY-9. For LJ-7, the contents of 13 amino acids and 24 organic acids, especially l-glutamic acid, beta-alanine, glycolic acid and glyceric acid were up-regulated significantly which contributed to scavenging reactive oxygen species. In the treatment of 500 μg/L BDE-47, the contents of these four metabolites increased by 33.6-, 19.3-, 10.6- and 10.2-fold, respectively. The levels of most saccharides (such as d-glucose, lactulose, maltose, sucrose and d-cellobiose) also increased by 1.7–12.4 fold which promoted saccharide-related biosynthesis metabolism. Elevation of tricarboxylic acid cycle and glyoxylate and dicarboxylate metabolism enhanced energy-producing processes. Besides, the contents of secondary metabolites, chiefly polyols and glycosides increased significantly to act on defending oxidative stress induced by BDE-47. In contrast, the levels of most metabolites decreased significantly for YY-9, especially those of 13 amino acids (by 0.9%–67.1%) and 19 organic acids (by 7.8%–70.0%). The positive metabolic responses implied LJ-7 was tolerant to BDE-47, while the down-regulation of most metabolites indicated the susceptible nature of YY-9. Since metabolic change might affect the yield and quality of rice, this study can provide useful reference for rice cultivation in PBDEs-polluted areas.

The mechanisms contributing to toxic effects of airborne lower-chlorinated PCB congeners (LC-PCBs) remain poorly characterized. We evaluated in vitro toxicities of environmental LC-PCBs found in both indoor and outdoor air (PCB 4, 8, 11, 18, 28 and 31), and selected hydroxylated metabolites of PCB 8, 11 and 18, using reporter gene assays, as well as other functional cellular bioassays. We focused on processes linked with endocrine disruption, tumor promotion and/or regulation of transcription factors controlling metabolism of both endogenous compounds and xenobiotics. The tested LC-PCBs were found to be mostly efficient anti-androgenic (within nanomolar – micromolar range) and estrogenic (at micromolar concentrations) compounds, as well as inhibitors of gap junctional intercellular communication (GJIC) at micromolar concentrations. PCB 8, 28 and 31 were found to partially inhibit the aryl hydrocarbon receptor (AhR)-mediated activity. The tested LC-PCBs were also partial constitutive androstane receptor (CAR) and pregnane X receptor (PXR) agonists, with PCB 4, 8 and 18 being the most active compounds. They were inactive towards other nuclear receptors, such as vitamin D receptor, thyroid receptor α, glucocorticoid receptor or peroxisome proliferator-activated receptor γ. We found that only PCB 8 contributed to generation of oxidative stress, while all tested LC-PCBs induced arachidonic acid release (albeit without further modulations of arachidonic acid metabolism) in human lung epithelial cells. Importantly, estrogenic effects of hydroxylated (OH-PCB) metabolites of LC-PCBs (4-OH-PCB 8, 4-OH-PCB 11 and 4′-OH-PCB 18) were higher than those of the parent PCBs, while their other toxic effects were only slightly altered or suppressed. This suggested that metabolism may alter toxicity profiles of LC-PCBs in a receptor-specific manner. In summary, anti-androgenic and estrogenic activities, acute inhibition of GJIC and suppression of the AhR-mediated activity were found to be the most relevant modes of action of airborne LC-PCBs, although they partially affected also additional cellular targets.

Our previous study showed that the tea extract, epigallocatechin-3-gallate (EGCG), protects against microcystin-LR (MC-LR) -mediated apoptosis of human umbilical vein endothelial cells (HUVECs); however, the mechanism underlying MC-LR-induced HUVEC apoptosis remains incompletely understood. In this study, we investigated whether the nuclear factor erythroid-like 2 (NRF2)/heme oxygenase-1 (HO-1) pathway, which regulates antioxidant transcriptional regulation of oxidative stress and apoptosis, is involved in this process. Mitochondrial membrane potential (MMP) and caspase-3/-9 activities were evaluated in HUVECs by JC-1 staining and colorimetric activity assay, and a DCFH-DA fluorescent probe assay was used to quantitate reactive oxygen species (ROS) generation. The effects of MC-LR, EGCG, NF2, and HO-1 on HUVEC apoptosis were explored by western blotting and small interfering RNA (siRNA) analyses. MC-LR treatment downregulated HUVEC mitochondrial membrane potential, and decreased levels of cytochrome c release and activated caspase-3/-9, ROS generation, consequently inducing HUVEC apoptosis. EGCG treatment attenuated MC-LR-mediated HUVEC oxidative stress and mitochondria-related apoptosis. EGCG induced NRF2/HO-1 expression and activation in MC-LR treated HUVECs, while downregulation of NRF2/HO-1 by specific siRNAs revealed that NRF2/HO-1 signaling was involved in EGCG attenuation of MC-LR-induced HUVEC apoptosis. Our findings indicate that EGCG treatment protects against MC-LR-mediated HUVEC apoptosis via activation of NRF2/HO-1 signaling.

The widely used Di-(2-ethylhexyl) phthalate (DEHP) has been reported to exhibit ubiquitous environmental and global health hazards. The bioaccumulation and environmental persistence of DEHP can cause serious health hazards in wildlife animals and human. However, DEHP-induced nephrotoxicity in bird is remained unknown. Thus, this study explored the related mechanism of DEHP nephrotoxicity in quail. For this purpose, quail were exposed with DEHP at doses of 0, 250, 500, and 1000 mg/kg body weight daily by gavage administration for 45 days. The results showed that DEHP exposure induced renal injury, oxidative stress, and endoplasmic reticulum (ER) degeneration. Low level DEHP (250 mg/kg) exposure inhibited Nrf2 signaling pathway and induced renal injury via oxidative stress and suppressed the unfolded protein response (UPR) signaling pathway and induced ER stress in the kidney. But surprisingly, high level DEHP (500 mg/kg and 1000 mg/kg) exposure activated Nrf2 and UPR signaling pathways and protected kidney, but they still couldn't resist the toxicity of DEHP. Our study demonstrated that DEHP-induced nephrotoxicity in quail was associated with activating Nrf2-mediated antioxidant defense response and UPR signaling pathway.

Plants have the ability to adapt themselves under stressed conditions through reprogramming their growth and development. Understanding the mechanisms regulating overall growth of stressed plant is an important issue for plant and environmental biology research. Although the role of NO in modulating arsenic (As) toxicity is known, nitric oxide (NO) induced alteration in auxin and nutrient related transporters during As stress in rice is poorly understood. Experimental results showed that As exposure decreased gene expression level of polar auxin transporter (PIN proteins), and nutrient transporter related genes (AMT, NRT, NiR, PHT, KTP). The improved tolerance induced by As + NO combination is attributed to reduced As accumulation in rice seedlings, improved root architectural changes, overall growth of plant, chlorophyll, protein content, and accumulation of mineral nutrients by reducing the ROS generation. Further, enhanced transcript levels of PIN proteins and mineral nutrition related genes were also observed under As + NO treatment. Additional biochemical data revealed enhanced oxidative stress by increasing the level of antioxidant enzymes, and stress-related parameters. Overall, the study provides an integrated view of plant response during As + NO interaction to change the plant metabolism through different cellular processes.

Ground-level ozone (O3) concentrations have been elevating in the last century. While there has been a notable progress in understanding O3 effects on vegetation, O3 effects on ecological stoichiometry remain unclear, especially early in the oxidative stress. Ethyelenediurea (EDU) is a chemical compound widely applied in research projects as protectant of plants against O3 injury, however its mode of action remains unclear. To investigate O3 and EDU effects early in the stress, we sprayed willow (Salix sachalinensis) plants with 0, 200 or 400 mg EDU L−1, and exposed them to either low ambient O3 (AOZ) or elevated O3 (EOZ) levels during the daytime, for about one month, in a free air O3 controlled exposure (FACE); EDU treatment was repeated every nine days. We collected samples for analyses from basal, top, and shed leaves, before leaves develop visible O3 symptoms. We found that O3 altered the ecological stoichiometry, including impacts in nutrient resorption efficiency, early in the stress. The relation between P content and Fe content seemed to have a critical role in maintaining homeostasis in an effort to prevent O3-induced damage. Photosynthetic pigments and P content appeared to play an important role in EDU mode of action. This study provides novel insights on the stress biology which are of ecological and toxicological importance.

Aluminum (Al) phytotoxicity is a major limitation in the production of crops in the soils with pH ≤ 5. Boron (B) is indispensable nutrient for the development of higher plants and B role has been reported in the alleviation Al toxicity. Trifoliate orange rootstock was grown in two B and two Al concentrations. The results of the present study showed that Al toxicity adversely inhibited root elongation and exhibited higher oxidative stress in terms of H2O2 and O2− under B-deficiency. Additionally, the X-ray diffraction (XRD) analysis confirmed the increase of the cellulose crystallinity in the cell wall (CW). Al-induced remarkable variations in the CW components were prominent in terms of alkali-soluble pectin, 2-keto-3-deoxyoctonic acid (KDO) and the degree of methyl-esterification (DME) of pectin. Interesting, B supply reduced the pectin (alkali-soluble) under Al toxicity. Moreover, the results of FTIR (Fourier transform infrared spectroscopy) and 13C-NMR (13C nuclear magnetic resonance) spectra revealed the decrease of carboxyl groups and cellulose by B application during Al exposure. Furthermore, B supply tended to decrease the Al uptake, CW thickness and callose formation. The study concluded that B could mitigate Al phytotoxicity by shielding potential Al binding sites and by reducing Al induced alterations in the CW cellulose and pectin components.