Metals can cause oxidative stress by increasing the formation of reactive oxygen species (ROS), which render antioxidants incapable of defence against growing amounts of free radicals. Metal toxicity is related to their oxidative state and reactivity with other compounds. Our aim is to review the mechanisms on how metals cause oxidative stress and what is known about metal-induced oxidative stress in wildlife. Taking birds as model organisms, we summarize the mechanisms responsible for antioxidant depletion and give a view of how to detect metal-induced oxidative stress in birds by using different biomarkers. The mechanisms producing the harmful effects of oxidative stress are complex with different biomolecular mechanisms associated with ecotoxicological and ecological aspects. The majority of the studies concerning metals and ROS related to oxidative stress have focused on the biomolecular level, but little is known about the effects at the cellular level or at the level of individuals or populations.

This experiment examined the effects of sulfate (S) and reduced glutathione (GSH) on arsenic uptake by arsenic hyperaccumulator Pteris vittata after exposing to arsenate (0, 15 or 30 mg As L-1) with sulfate (6.4, 12.8 or 25.6 mg S L=1) or GSH (0, 0.4 or 0.8 mM) for 2-wk. Total arsenic, S and GSH concentrations in plant biomass and arsenic speciation in the growth media and plant biomass were determined. While both S (18–85%) and GSH (77-89%) significantly increased arsenic uptake in P. vittata, GSH also increased arsenic translocation by 61-85% at 0.4 mM (p < 0.05). Sulfate and GSH did not impact plant biomass or arsenic speciation in the media and biomass. The S-induced arsenic accumulation by P. vittata was partially attributed to increased plant GSH (21-31%), an important non-enzymatic antioxidant countering oxidative stress. This experiment demonstrated that S and GSH can effectively enhance arsenic uptake and translocation by P. vittata.

International audience | The aim of this study was to compare the capacity of two morphologically different moss species to accumulate elements when exposed to three different types of air pollution (rural, urban and industrial). Transplants of Pseudoscleropodium purum and Ceratodon purpureus were exposed for 6 months, and the concentrations of 18 elements (Al, Ti, V, Cr, Mn, Fe, Co, Cu, Zn, As, Mo, Cd, Sn, Sb, Ba, La, Pb and Bi) in the mosses samples were analysed by inductively coupled plasma-mass spectrometry. On the whole, the metals were accumulated by mosses, and this accumulation was correlated with concentrations in the atmospheric particles. Whereas P. purum is to be preferred for Al, Cu, Zn and Fe monitoring, C. purpureus was most efficient at accumulating Mo, Ti, V, As, Sn, La and Pb. In both species, a phenomenon of saturation was observed during the exposure at the most contaminated site (industrial).

Applying an integrated approach using the Comet, micronucleus (MN), and random amplified polymorphic DNA (RAPD) assays, occurrence of erythrocytic nuclear abnormalities (ENAs) and the liver activity of antioxidants enzymes (catalase and glutathione-S-transferase (GST)) was carried out to evaluate the effects of acute (6, 24, and 96 h) and subchronic (15 days) exposures to aluminum on fish Prochilodus lineatus. The Comet assay showed that fish erythrocytes exhibited significantly higher DNA damage after 6 and 96 h of Al exposure. MN frequencies were very low and did not increase significantly after Al exposures, while ENAs frequency increased significantly after all exposure periods. RAPD profiles obtained with DNA from fish fins collected before the toxicity tests were compared to the profiles with DNA from gills and liver of the same fish sampled after Al exposures. Alterations in RAPD profiles, including appearance and disappearance of bands, after 6 h, 24 h, and 15 days of Al exposure were detected. Fish exposed to Al for 6 and 24 h also showed significant increases in GST and catalase activities. These results indicated that Al exposure was genotoxic to P. lineatus, inducing DNA damage in peripheral erythrocytes. The induction of antioxidant enzymes might be an indication that Al causes oxidative damage to DNA, while the very low frequency of MN suggests that Al does not produce clastogenic or aneugenic effects. Genotoxic effects after 15 days of Al exposure was revealed only by RAPD, showing that this assay represents a sensitive method to detect genotoxic damage, occasionally not detected by other genotoxic tests used in toxicological genetics studies.

Purpose Besides classical organic pollutants and pesticides, pharmaceuticals and their residues have nowadays become recognized as relevant environmental contaminants. The risks of these chemicals for aquatic ecosystems are well known, but information about the pharmaca-plant interactions and metabolic pathways is scarce. Therefore, we investigate the process of uptake of acetaminophen (N-Acetyl-4-aminophenol) by Brassica juncea, drug-induced defense responses and detoxification mechanisms in different plant parts. Material and methods Hydroponically grown Indian mustard (Brassica juncea L. Czern.) plants were treated with acetaminophen and root and leaf samples were collected after 24, 72, and 168 h of treatment. The uptake of acetaminophen and the formation of its metabolites were analyzed using LC-MS/MS technique and enzyme activities including glutathione S-transferases (GSTs) as well as several plant defense enzymes like catalase, ascorbat peroxidase, peroxidase, and glutathione reductase were assayed spectrophotometrically. Results We determined the uptake and the translocation of acetaminophen, and we tried to identify the steps of the detoxification process by assaying typical enzymes, supposing the involvement of the same- or similar enzymes and reactions as in the mammalian detoxification process. After 24-h exposure, effective uptake and translocation were observed to the upper part of plants followed by two independent conjugative detoxification pathways. Changes in antioxidant defense enzyme activities connected to the defense pathway towards reactive oxygen species indicate an additional oxidative stress response in the plants. Conclusions The major metabolic pathways in mammals are conjugation with activated sulfate and glucuronic acid, while a small amount of acetaminophen forms a chemically reactive and highly toxic, hydroxylated metabolite. We identified a glutathionyl and a glycoside conjugate, which refer to the similarities to mammalian detoxification. Increased GST activities in leaf tissues were observed correlated with the appearance of the acetaminophen-glutathione conjugate which shows the involvement of this enzyme group in the metabolism of acetaminophen in plants to organic pollutants and xenobiotics. High acetaminophen concentrations lead to oxidative stress and irreversible damages in the plants, which necessitates further investigations using lower drug concentrations for the deeper understanding of the induced detoxification—and defense processes.

Background, aim, and scope Atmospheric pollution is a worldwide problem. Exposure to atmospheric pollutants causes toxic cellular effects. One of the mechanisms of toxicity by these pollutants is the promotion of oxidative stress. Several signaling pathways control cellular redox homeostasis. In this respect, nuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial transcription factor in the cell's response to oxidative stress. Main features In cellular animal models, exposure to atmospheric pollutants activates Nrf2, attenuating its toxic and even its carcinogenic effects. Therefore, we have reviewed the scientific literature in order to indicate that air pollutants, such as particulate matter, polycyclic aromatic hydrocarbons, and gaseous matter, are Nrf2 pathway inductors, triggering self-defense through the establishment of proinflammatory and antioxidant responses. Results and discussion Exposure to reactive molecules as atmospheric pollutants causes the activation of Nrf2 and the subsequent regulation of the expression of cytoprotective and detoxifying enzymes, as well as antioxidants. Moreover, induction of Nrf2 prior to exposure reduces the harmful effects of pollutants. The present article discusses the protective role of the Nrf2 pathway against different atmospheric pollutant insults. Conclusions Nrf2 regulates the expression of numerous cytoprotective genes that function to detoxify reactive species produced during atmospheric pollutant metabolic reactions. From the papers highlighted in this review, we conclude that Nrf2 has an important role in the defense against atmospheric pollutant-induced toxicity. Perspectives Further studies are needed to understand the signaling events that turn on the system in response to atmospheric pollutant stress. This could allow for the possibility of targeting the pathway for prevention benefits in the near future.