Offshore oil and gas activities can result in the discharge of large amounts of drilling muds. While these materials have generally been regarded as non-toxic to marine organisms, recent studies have demonstrated negative impacts to suspension feeding organisms. We exposed the arctic-boreal sponge Geodia barretti to the primary particulate components of two water-based drilling muds; barite and bentonite. Sponges were exposed to barite, bentonite and a natural reference sediment at a range of total suspended solid concentrations (TSS = 0, 10, 50 or 100 mg/L) for 12 h after which we measured a suite of biomarker responses (lysosomal membrane stability, lipid peroxidation and glutathione). In addition, we compared biomarker responses, organic energy content and metal accumulation in sponges, which had been continuously or intermittently exposed to suspended barite and natural sediment for 14 d at relevant concentrations (10 and 30 mg TSS/L). Lysosomal membrane stability was reduced in the sponges exposed to barite at 50 and 100 mg TSS/L after just 12 h and at 30 mg TSS/L for both continuous and intermittent exposures over 14 d. Evidence of compromised cellular viability was accompanied by barite analysis revealing concentrations of Cu and Pb well above reference sediments and Norwegian sediment quality guidelines. Metal bioaccumulation in sponge tissues was low and the total organic energy content (determined by the elemental composition of organic tissue) was not affected. Intermittent exposures to barite resulted in less toxicity than continuous exposure to barite. Short term exposures to bentonite did not alter any biomarker responses. This is the first time that these biomarkers have been used to indicate contaminant exposure in an arctic-boreal sponge. Our results illustrate the potential toxicity of barite and the importance of assessments that reflect the ways in which these contaminants are delivered under environmentally realistic conditions.

Mercury (Hg) is recognized as a dangerous contaminant due to its bioaccumulation and biomagnification within trophic levels, leading to serious health risks to aquatic biota. Therefore, there is an urgent need to unravel the mechanisms underlying the toxicity of Hg. To this aim, a metabolomics approach based on protonic nuclear magnetic resonance (1H NMR), coupled with chemometrics, was performed on the gills of wild golden grey mullets L. aurata living in an Hg-polluted area in Ria de Aveiro (Portugal). Gills were selected as target organ due to their direct and continuous interaction with the surrounding environment. As a consequence of accumulated inorganic Hg and methylmercury, severe changes in the gill metabolome were observed, indicating a compromised health status of mullets. Numerous metabolites, i.e. amino acids, osmolytes, carbohydrates, and nucleotides, were identified as potential biomarkers of Hg toxicity in fish gills. Specifically, decrease of taurine and glycerophosphocholine, along with increased creatine level, suggested Hg interference with the ion-osmoregulatory processes. The rise of lactate indicated anaerobic metabolism enhancement. Moreover, the increased levels of amino acids suggested the occurrence of protein catabolism, further supported by the augmented alanine, involved in nitrogenous waste excretion. Increased level of isobutyrate, a marker of anoxia, was suggestive of onset of hypoxic stress at the Hg contaminated site. Moreover, the concomitant reduction in glycerophosphocholine and phosphocholine reflected the occurrence of membrane repair processes. Finally, perturbation in antioxidant defence system was revealed by the depletion in glutathione and its constituent amino acids. All these data were also compared to the differential Hg-induced metabolic responses previously observed in liver of the same mullets (Brandão et al., 2015). Overall, the environmental metabolomics approach demonstrated its effectiveness in the evaluation of Hg toxicity mechanisms in wild fish under realistic environmental conditions, uncovering tissue-specificities regarding Hg toxic effects namely in gills and liver.

Pb tolerant mechanisms, plant physiological response and Pb sub-cellular localization in the root cells of Iris halophila were studied in sand culture and the Pb mine tailings. Results showed that the activities of superoxide dismutase (SOD) and peroxidase (POD) in the underground parts and the activity of catalase (CAT) in the aboveground and underground parts increased as Pb level was enhanced. Glutathione (GSH) and ascorbic acid (AsA) contents increased by Pb treatments. Pb deposits were found in the middle cell walls or along the inner side of epibiotic protoplasm of some cells which accumulated a large quantity of Pb and died. The dry weights (DWs) of aboveground parts under all Pb tailings treatments decreased insignificantly, while the DW of the underground parts growing in the pure Pb tailings decreased significantly. Pb, Cu, Cd, and Zn contents increased significantly as the levels of Pb tailings were enhanced and Pb contents in the aboveground and underground parts reached 64.75 and 751.75 μg/g DW, respectively, at pure Pb tailings treatment. The results indicated that I. halophila is a promising plant in the phytoremediation of Pb contaminated environment. Some antioxidant enzymes, antioxidants and compartmentalization of Pb were played major roles in Pb tolerance of I. halophila.

Yellow perch (Perca flavescens) collected from 11 lakes in the Canadian mining regions of Sudbury (Ontario) and Rouyn-Noranda (Quebec) display wide ranges in the concentrations of cadmium (Cd), nickel (Ni), selenium (Se), and thallium (Tl) in their livers. To determine if these trace elements, as well as copper (Cu) and zinc (Zn), are causing oxidative stress in these fish, we measured three biochemical indicators (glutathione (GSH), glutathione disulfide (GSSG) and thiobarbituric acid-reactive substances (TBARS)) in their livers. We observed that 44% of the yellow perch that we collected were at risk of cellular oxidative stress and lipid peroxidation. Considering all fish from all lakes, higher liver Se concentrations were coincident with both lower proportions of GSSG compared to GSH and lower concentrations of TBARS, suggesting that the essential trace-element Se acts as an antioxidant. Furthermore, fish suffering oxidative stress had higher proportions of Cd, Cu and Zn in potentially sensitive subcellular fractions (organelles and heat-denatured proteins) than did fish not suffering from stress. This result suggests that reactive oxygen species may oxidize metal-binding proteins and thereby reduce the capacity of fish to safely bind trace metals. High Cd concentrations in metal-sensitive subcellular fractions likely further exacerbate the negative effects of lower Se exposure.

The formaldehyde (FA) is a crosslinking agent that reacts with cellular macromolecules such as proteins, nucleic acids and molecules with low molecular weight such as amino acids, and it has been linked to inflammatory processes and oxidative stress. This study aimed to analyze the oxidative effects on pulmonary inflammatory response in Fischer rats exposed to different concentrations of FA. Twenty-eight Fischer rats were divided into 4 groups (N = 7). The control group (CG) was exposed to ambient air and three groups were exposed to different concentrations of FA: 1% (FA1%), 5% (FA5%) and 10% (FA10%). In the Bronchoalveolar Lavage Fluid (BALF), the exposure to a concentration of 10% promoted the increase of inflammatory cells compared to CG. There was also an increase of macrophages and lymphocytes in FA10% and lymphocytes in FA5% compared to CG. The activity of NADPH oxidase in the blood had been higher in FA5% and FA10% compared to CG. The activity of superoxide dismutase enzyme (SOD) had an increase in FA5% and the activity of the catalase enzyme (CAT) showed an increase in FA1% compared to CG. As for the glutathione system, there was an increase in total glutathione (tGSH), reduced glutathione (GSH) and oxidized glutathione (GSSG) in FA5% compared to CG. The reduced/oxidized glutathione ratio (GSH/GSSG) had a decrease in FA5% compared to CG. There was an increase in lipid peroxidation compared to all groups and the protein carbonyl formation in FA10% compared to CG. We also observed an increase in CCL2 and CCL5 chemokines in the treatment groups compared to CG and in serum there was an increase in CCL2, CCL3 and CCL5 compared to CG. Our results point out to the potential of formaldehyde in promoting airway injury by increasing the inflammatory process as well as by the redox imbalance.

The purpose of this study was to investigate the toxic effects induced by benzo[a]pyrene and phenanthrene. For this purpose, a study was performed on the clam exposed to 0.0, 0.5, 4.5μgL−1 B(a)P and PHE for 15days using parameters of antioxidant defenses and oxidative stress. Antioxidant biomarkers including ethoxyresorufin-O-deethylase, glutathione S-transferase, superoxide dismutase, and glutathione and rylhydrocarbon hydroxylasein gills of Sinonovacula constricta, were analyzed after a 1-, 3-, 9- and 15-day exposure to seawater containing B(a)P and PHE. Integrated biomarker response was calculated by combining multiple biomarkers into a single value. The results showed that the activity of all antioxidant biomarkers was induced throughout the exposure period, and different patterns of variations were detected with exposure time. In addition, the study showed that the two concentrations used caused the activation of different general detoxification mechanisms, and the same concentration at different two PAH compounds induced different toxicity responses.

The effects of gold (ionic form and nanoparticles — AuNPs) and pharmaceuticals (carbamazepine and fluoxetine) on enzymes involved in neurotransmission (acetylcholinesterase — AChE) and biotransformation (glutathione S-transferases — GST) were assessed by their incubation with Mytilus galloprovincialis' hemolymph and subcellular fraction of gills, respectively. AuNPs did not alter enzymatic activities unlike ionic gold that inhibited AChE and GST activities at 2.5 and 0.42mg·L−1, respectively. Carbamazepine inhibited AChE activity at 500mg·L−1 and fluoxetine at 1000mg·L−1. GST was inhibited by carbamazepine at 250mg·L−1 and by fluoxetine at 125mg·L−1. Increased AChE activity was found in simultaneous exposures to fluoxetine and bovine serum albumin coated AuNPs (BSA-AuNPs). Concerning GST, in the simultaneous exposures, AuNPs revealed protective effects against carbamazepine (citrate and polyvinylpyrrolidone coated) and fluoxetine (citrate and BSA coated) induced inhibition. However, BSA-AuNPs increased the inhibition caused by carbamazepine. AuNPs demonstrated ability to interfere with other chemicals toxicity justifying further studies.

The petroleum production has been raised sharply over the past decades, whereas the petroleum exploitation has also caused serious environmental contamination. A pot experiment has been conducted to monitor the dynamic response of antioxidant defense system and the growth reaction of Amorpha fruticosa seedlings to soil petroleum contamination. The results show that (1) in 5 g kg⁻¹ contaminated soil, A. fruticosa removes reactive oxygen species (ROS) by increasing the activities of antioxidant enzymes (glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT)), while in 10–15 g kg⁻¹ long-term contaminated soil, A. fruticosa removes ROS by the cooperation of antioxidant enzymes and antioxidants (SOD, CAT, ascorbate peroxidase (APX), GR, ascorbic acid (AsA), glutathione (GSH), and proline (Pro)). In long-term 20 g kg⁻¹ contaminated soil, the defense ability of APX and AsA decreases sharply, and A. fruticosa removes the ROS by the synergistic effect of antioxidant enzymes (SOD and CAT) and antioxidants (GSH and Pro). Only in 20 g kg⁻¹ long-term petroleum contamination caused significant (P < 0.05) increase in H₂O₂ content in seedlings. (2) SOD, CAT, GR, GSH, and Pro exhibit increases in long-term severely contaminated soil, and these enzymes and antioxidants are the most important defender of A. fruticosa to ROS accumulation caused by petroleum contamination. (3) The growth of A. fruticosa seedlings is less affected in 5 g kg⁻¹ petroleum-contaminated soil, while it significantly decreases in 10, 15, and 20 g kg⁻¹ petroleum-contaminated soils (P < 0.05). (4) Considering comprehensively the response of antioxidant defense system and the growth reaction of seedlings to petroleum contamination, A. fruticosa could be utilized for phytoremediation in ≤15 g kg⁻¹ contaminated soil.

Metals are significant environmental pollutants, and their toxicity is a problem for all living organisms. Indeed, aquatic plants are particularly sensitive to the excess of metal ions. Several researches report that aquatic plants exposed to metal-induced toxicity showed similar responses (e.g. inhibition of growth and induction of oxidative stress). Meanwhile, many studies were involved to counter these toxicities. This paper provides a brief review of the role of the exogenous supply of some compounds in the alleviation or reduction of toxicity in aquatic plants generated by metals. Particular attention is given to the role of polyamine, proline, nitric oxide, glutathione and phytochelatin.

In the presented in vitro experiment, the effect of selenite treatment (0.01, 0.1, 1, 10 and 50 mg L⁻¹ Se(IV)) on Berula erecta was investigated with respect to growth, photochemical efficiency, photosynthetic pigments, anthocyanins and low molecular weight thiols. Lower Se(IV) concentrations (0.01, 0.1 and 1 mg L⁻¹) promoted growth, while higher Se(IV) concentrations (10 and 50 mg L⁻¹) negatively affected it. The photochemical efficiency of photosystem II decreased significantly in plants treated with higher Se(IV) concentrations, compared to that in the control plants. The content of pigments decreased in all the Se(IV) treatments. Both cysteine and glutathione showed alterations in their content and redox state depending on the Se concentration. By evaluating the glutathione/cysteine system and their redox, it was possible to identify a threshold Se content (1-mg Se(IV) L⁻¹ treatment), above which the nature of the effects induced changes from antioxidant to pro-oxidant.