This study aimed to investigate the role of non-enzymatic antioxidants on adaptive skills over time in the bivalve Scrobicularia plana environmentally exposed to mercury. Inter-age (2⁺, 3⁺, 4⁺, 5⁺ year old) and organ-specific (gills, digestive gland) approaches were applied in bivalves collected from moderately and highly contaminated sites at Ria de Aveiro (Portugal). S. plana's adaptive skills were dependent on the contamination extent; under moderate contamination scenario, the intervention of the different antioxidants took place harmoniously, evidencing an adjustment capacity increasing with the age. Under higher contamination degree, S. plana failed to cope with mercury threat, showing an age-dependent deterioration of the defense abilities. In organ-specific approach, the differences were particularly evident for thiol-compounds, since only gills displayed the potential to respond to moderate levels by increasing non-protein thiols and total glutathione. Under high contamination degree, both organs were unable to increase thiol-compounds, which were compensated by the ascorbic acid elevation.

Environmental contamination by arsenic constitutes a problem in many countries, and its accumulation in food crops may pose health complications for humans. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are involved at various levels in the mechanism of responding to environmental stress in higher plants. Using Arabidopsis seedlings exposed to different arsenate concentrations, physiological and biochemical parameters were analyzed to determine the status of ROS and RNS metabolisms. Arsenate provoked a significant reduction in growth parameters and an increase in lipid oxidation. These changes were accompanied by an alteration in antioxidative enzymes and the nitric oxide (NO) metabolism, with a significant increase in NO content, S-nitrosoglutathione reductase (GSNOR) activity and protein tyrosine nitration as well as a concomitant reduction in glutathione and S-nitrosoglutathione (GSNO) content. Our results indicate that 500 μM arsenate (AsV) causes nitro-oxidative stress in Arabidopsis, being the glutathione reductase and the GSNOR activities clearly affected.

Differences in the toxicological and metabolic pathway of inorganic arsenic compounds are largely unknown for aquatic species. In the present study the effects of short-time and acute exposure to AsIII and AsV were investigated in gills and liver of the common carp, Cyprinus carpio (Cyprinidae), measuring accumulation and chemical speciation of arsenic, and the activity of glutathione-S-transferase omega (GST Ω), the rate limiting enzyme in biotransformation of inorganic arsenic. Oxidative biomarkers included antioxidant defenses (total glutathione-S-transferases, glutathione reductase, glutathione, and glucose-6-phosphate dehydrogenase), total scavenging capacity toward peroxyl radicals, reactive oxygen species (ROS) measurement and lipid peroxidation products. A marked accumulation of arsenic was observed only in gills of carps exposed to 1000 ppb AsV. Also in gills, antioxidant responses were mostly modulated through a significant induction of glucose-6-phosphate dehydrogenase activity which probably contributed to reduce ROS formation; however this increase was not sufficient to prevent lipid peroxidation. No changes in metal content were measured in liver of exposed carps, characterized by lower activity of GST Ω compared to gills. On the other hand, glutathione metabolism was more sensitive in liver tissue, where a significant inhibition of glutathione reductase was concomitant with increased levels of glutathione and higher total antioxidant capacity toward peroxyl radicals, thus preventing lipid peroxidation and ROS production. The overall results of this study indicated that exposure of C. carpio to AsIII and AsV can induce different responses in gills and liver of this aquatic organism. Common carp (Cyprinus carpio) presented marked differences between gills and liver after arsenic exposure in terms of antioxidant responses and also in biotransformation.

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.

Environmental pollutants exert immunotoxical effects on aquatic organisms. The aim was to determine the antioxidant response, markers of oxidative damage and reactive oxygen species production in hemocytes of Pinna nobilis, the largest endemic bivalve in the Mediterranean Sea, under anthropogenic pressure. P. nobilis individuals were collected from two locations along Mallorca Island waters attending to different degree of human impact and the hemocytes were obtained. Specimens from the impacted area showed increased activities of the antioxidant enzymes – catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase –, myeloperoxidase activity and reduced glutathione levels. No differences in oxidative damage markers – malondiahdehyde and carbonyl index – were evidenced between the pristine and polluted areas. Hemocytes from the polluted area presented increased capability to generate reactive oxygen species and nitrite/nitrate when activated. In conclusion, the human activities primed hemocytes for oxidative burst and increased the antioxidant mechanism without evidence of oxidative damage.

This study intended to determine whether the redox state in plants of Nicotiana tabacum ‘Bel-W3’ fluctuates in response to the environmental factors in a sub-tropical area contaminated by ozone (São Paulo, SE – Brazil) and which environmental factors are related to this fluctuation, discussing their biomonitoring efficiency. We comparatively evaluated the indicators of redox state (ascorbic acid, glutathione, superoxide dismutase, ascorbate peroxidase, and glutathione reductase) and leaf injury in 17 field experiments performed in 2008. The redox state was explained by the combined effects of chronic levels of O₃ and meteorological variables 4–6 days prior to the plant sampling. Moderate leaf injury was observed in most cases. The redox state of tobacco decreases few days after their placement in the sub-tropical environment, causing them to become susceptible to oxidative stress imposed by chronic doses of O₃. Its bioindicator efficiency would not be diminished in such levels of atmospheric contamination.

Biomarkers comprising activities of biotransformation enzymes (ethoxyresorufin-O-deethylase –EROD–, dibenzylfluorescein dealkylase –DBF–, glutathione S-transferase –GST), antioxidant enzymes (glutathione reductase –GR– and glutathione peroxidase –GPX), lipid peroxidation –LPO– and DNA strand breaks were analyzed in the clam Ruditapes philippinarum caged at Cádiz Bay, Santander Bay and Las Palmas de Gran Canaria (LPGC) Port (Spain). Sediments were characterized. Digestive gland was the most sensitive tissue to sediment contamination. In Cádiz Bay, changes in LPO regarding day 0 were related with metals. In LPGC Port, DBF, EROD, and GST activity responses suggested the presence of undetermined contaminants which might have led to DNA damage. In Santander Bay, PAHs were related with EROD activity, organic and metal contamination was found to be associated with GR and GST activities and DNA damage presented significant (p < 0.05) induction. R. philippinarum was sensitive to sediment contamination at biochemical level. Biomarkers allowed chemical exposure and sediment quality assessment.

This study assessed the oxidative stress status, antioxidant metabolism and polypeptide patterns in salt marsh macrophyte Juncus maritimus shoots exhibiting differential mercury burdens in Ria de Aveiro coastal lagoon at reference and the sites with highest, moderate and the lowest mercury contamination. In order to achieve these goals, shoot-mercury burden and the responses of representative oxidative stress indices, and the components of both non-glutathione- and glutathione-based H₂O₂-metabolizing systems were analyzed and cross-talked with shoot-polypeptide patterns. Compared to the reference site, significant elevations in J. maritimus shoot mercury and the oxidative stress indices such as H₂O₂, lipid peroxidation, electrolyte leakage and reactive carbonyls were maximum at the site with highest followed by moderate and the lowest mercury contamination. Significantly elevated activity of non-glutathione-based H₂O₂-metabolizing enzymes such as ascorbate peroxidase and catalase accompanied the studied damage-endpoint responses, whereas the activity of glutathione-based H₂O₂-scavenging enzymes glutathione peroxidase and glutathione sulfo-transferase was inhibited. Concomitantly, significantly enhanced glutathione reductase activity and the contents of both reduced and oxidized glutathione were perceptible in high mercury-exhibiting shoots. It is inferred that high mercury-accrued elevations in oxidative stress indices were obvious, where non-glutathione-based H₂O₂-decomposing enzyme system was dominant over the glutathione-based H₂O₂-scavenging enzyme system. In particular, the glutathione-based H₂O₂-scavenging system failed to coordinate with elevated glutathione reductase which in turn resulted into increased pool of oxidized glutathione and the ratio of oxidized glutathione-to-reduced glutathione. The substantiation of the studied oxidative stress indices and antioxidant metabolism with approximately 53-kDa polypeptide warrants further studies.

Arsenic (As) contamination in the environment has attracted considerable attention worldwide. The objective of the present study was to see the comparative effect of As species As(III) and As(V) on accumulation, biochemical responses, and gene expression analysis in Brassica juncea var. Pusa Jaganath (PJn). Hydroponically grown 14-day-old seedlings of B. juncea were treated with different concentrations of As(III) and As(V). Accumulation of total As increased with increasing concentration of both As species and exposure time, mainly in roots. Reduction in seed germination, root–shoot length, chlorophyll, and protein content were observed with increasing concentration and exposure time of both As species, being more in As(III)-treated leaves. PJn variety showed that antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX)) and stress-related parameters (cysteine, proline, and malondialdehyde (MDA)) were stimulated and allows plant to tolerate both As species. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis in leaves showed significant changes in protein profile with more stringent effect with As(III) stress. Semiquantitative RT-PCR analysis showed regulation in expression of phytochelatin synthase (PCS), metallothionine-2 (MT-2), glutathione reductase (GR), and glutathione synthetase (GS) genes under both As(III) and As(V) stresses. Results suggested that accumulation and inhibition on physiological parameters differ according to the As species, while molecular and biochemical parameters showed a combinatorial type of tolerance mechanism against As(III) and As(V) stresses.

This in vitro study investigates the impact of silica-coated magnetite particles (Fe₃O₄@SiO₂/SiDTC, hereafter called IONP; 2.5 mg L⁻¹) and its interference with co-exposure to persistent contaminant (mercury, Hg; 50 μg L⁻¹) during 0, 2, 4, 8, 16, 24, 48, and 72 h on European eel (Anguilla anguilla) brain and evaluates the significance of the glutathione (GSH) redox system in this context. The extent of damage (membrane lipid peroxidation, measured as thiobarbituric acid reactive substances, TBARS; protein oxidation, measured as reactive carbonyls, RCs) decreased with increasing period of exposure to IONP or IONP + Hg which was accompanied with differential responses of glutathione redox system major components (glutathione reductase, GR; glutathione peroxidase, GPX; total GSH, TGSH). The occurrence of antagonism between IONP and Hg impacts was evident at late hour (72 h), where significantly decreased TBARS and RC levels and GR and glutathione sulfo-transferase (GST) activity imply the positive effect of IONP + Hg concomitant exposure against Hg-accrued negative impacts [vs. early (2 h) hour of exposure]. A period of exposure-dependent IONP alone and IONP + Hg joint exposure-accrued impact was perceptible. Additionally, increased susceptibility of the GSH redox system to increased period of exposure to Hg was depicted, where insufficiency of elevated GR for the maintenance of TGSH required for membrane lipid and cellular protein protection was displayed. Overall, a fine-tuning among brain glutathione redox system components was revealed controlling IONP + Hg interactive impacts successfully.