International audience | The production and use of pharmaceutical products have increased over the past decades, and several are considered potential or proved hazardous wastes. When contaminating the environment, they can severely impact biodiversity. The catecholamine epinephrine (adrenaline) is no exception. Epinephrine can be administered as growth promoter in cattle, and is used for anaphylaxis treatment in human. While a range of studies has examined the effects of this catecholamine on vertebrate tissues, and evidenced that it can disrupt the oxidative stress status, the effects epinephrine could have on insects have remained poorly considered. Here, we examined the physiological effects of different concentrations (0, 25, 50, and 100 mu g/mL) of epinephrine on larvae of the flesh fly Sarcophaga dux. Following experimental treatments, levels of H2O2, GSH, CAT, GPx, and CEH were measured from the fat body, cuticle, gut, and hemolymph of 3rd instars. Significant differences are reported for these physiological endpoints among the considered body compartments, and epinephrine concentrations. Epinephrine treatments did not increase reactive oxygen species production (H2O2 amounts), except for gut tissues. Increased levels of GSH suggest that epinephrine may have enhanced glucose metabolism and flux towards the pentose phosphate pathway, while reducing glutamine oxidation. CAT activity was slightly increased when the concentration of epinephrine was higher. The decreased GPx activity in the fat body was consistent with GSH variations. In sum, the injection of epinephrine seemed to elicit the antioxidant response in S. dux larvae, in turn attenuating ROS production.

Arsenic (As) toxicity is a problem that needs to be solved in terms of both human health and agricultural production in the vast majority of the world. The presence of As causes biomass loss by disrupting the balance of biochemical processes in plants and preventing growth/water absorption in the roots and accumulating in the edible parts of the plant and entering the food chain. A critical method of combating As toxicity is the use of biosafe, natural, bioactive compounds such as hesperidin (HP) or chlorogenic acid (CA). To this end, in this study, the physiological and biochemical effects of HP (100 μM) and CA (50 μM) were investigated in Zea mays under arsenate stress (100 μM). Relative water content, osmotic potential, photosynthesis-related parameters were suppressed under stress. It was determined that stress decreased the activities of the antioxidant system and increased the level of saturated fatty acids and, gene expression of PHT transporters involved in the uptake and translocation of arsenate. After being exposed to stress, HP and CA improved the capacity of superoxide dismutase (SOD), catalase (CAT), peroxidase (POX), glutathione S-transferase (GST) and glutathione peroxidase (GPX) and then ROS accumulation (H₂O₂) and lipid peroxidation (TBARS) were effectively removed. These phenolic compounds contributed to maintaining the cellular redox status by regulating enzyme/non-enzyme activity/contents involved in the AsA-GSH cycle. HP and CA reversed the adverse effects of excessive metal ion accumulation by re-regulated expression of the PHT1.1 and PHT1.3 genes in response to stress. Exogenously applied HP and CA effectively maintained membrane integrity by regulating saturated/unsaturated fatty acid content. However, the combined application of HP and CA did not show a synergistic protective activity against As stress and had a negative effect on the antioxidant capacity of maize leaves. As a result, HP and CA have great potentials to provide tolerance to maize under As stress by reducing oxidative injury and preserving the biochemical reactions of photosynthesis.

Metalaxyl is a broad-spectrum chiral fungicide that used for the protection of plants, however extensive use of metalaxyl resulted in serious environmental problems. Thus, a study on the detoxification mechanism in algae/cyanobacteria and their ability for phycoremediation is highly recommended. Here, we investigated the physiological and biochemical responses of two cyanobacterial species; Anabaena laxa and Nostoc muscorum to R-metalaxyl toxicity as well as their ability as phycoremediators. Two different levels of R-metalaxyl, at mild (10 mg/L) and high dose (25 mg/L), were applied for one-week. We found that A. laxa absorbed and accumulated more intracellular R-metalaxyl compared to N. muscorum. R-metalaxyl, which triggered a dose-based reduction in cell growth, photosynthetic pigment content, and photosynthetic key enzymes’ activities i.e., phosphoenolpyruvate carboxylase (PEPC) and ribulose‒1,5‒bisphosphate carboxylase/oxygenase (RuBisCo). These decreases were significantly less pronounced in A. laxa. On the other hand, R-metalaxyl significantly induced oxidative damage markers, e.g., H₂O₂ levels, lipid peroxidation (MDA), protein oxidation and NADPH oxidase activity. However, these increases were also lower in A. laxa compared to N. muscorum. To alleviate R-metalaxyl toxicity, A. laxa induced the polyphenols, flavonoids, tocopherols and glutathione (GSH) levels as well as peroxidase (POX), glutathione peroxidase (GPX), glutathione reductase (GR) and glutathione-s-transferase (GST) enzyme activities. On the contrary, the significant induction of antioxidants in N. muscorum was restricted to ascorbate, catalase (CAT) and ascorbate peroxidase (APX), dehydroascorbate reductase (DHAR) enzyme activities. Although A. laxa accumulated more R-metalaxyl, it experienced less stress due to subsequent induction of antioxidants. Therefore, A. laxa may be a promising R-metalaxyl phycoremediator. Our results provided basic data for understanding the ecotoxicology of R-metalaxyl contamination in aquatic habitats and the toxicity indices among cyanobacteria.

In the marine environment, microplastic contamination and acidification may occur simultaneously, this study evaluated the effects of ocean acidification and microplastics on oxidative stress responses and digestive enzymes in mussels. The thick shell mussels Mytilus coruscus were exposed to four concentrations of polystyrene microspheres (diameter 2 μm, 0, 10, 10⁴ and 10⁶ particles/L) under two pH levels (7.7 and 8.1) for 14 days followed by a 7-day recovery acclimation. Throughout the experiment, we found that microplastics and ocean acidification exerted little oxidative stress to the digestive gland. Only catalase (CAT) and glutathione (GSH) showed a significant increase along with increased microplastics during the experiment, but recovered to the control levels once these stressors were removed. No significant effects of pH and microplastics on glutathione peroxidase (GPx) and superoxide dismutase (SOD) were observed. The responses of digestive enzymes to both stressors were more pronounced than antioxidant enzymes. During the experiment, pepsin (PES), trypsin (TRS), alpha-amylase (AMS) and lipase (LPS) were significantly inhibited under microplastics exposure and this inhibition was aggravated by acidification conditions. Only PES and AMS tended to recover during the recovery period. Lysozyme (LZM) increased significantly under microplastic exposure conditions, but acidification did not exacerbate this effect. Therefore, combined stress of microplastics and ocean acidification slightly impacts oxidative responses but significantly inhibits digestive enzymes in mussels.

Cadmium (Cd), a heavy metal contaminant, exists in humans and animals throughout life and closely associate with severe hepatotoxicity. Selenium (Se) has been recognized as an effective chemo-protectant of Cd, but the underlying mechanisms remain unclear. The objective of the present study is to illustrate the antagonistic effect of Se against Cd-induced hepatotoxicity. Primary hepatocytes were cultured in the presence of 5 μM Cd, 1 μM Se and the mixture of 1 μM Se and 5 μM Cd for 24 h. Cell viability and morphology, antioxidant status, endoplasmic reticulum (ER) stress response and selenotranscriptome were assessed. It was observed that Se treatment dramatically alleviated Cd-induced hepatocytes death and morphological change. Simultaneously, Se mitigated Cd-induced oxidative stress by reducing ROS production, increasing reduced glutathione (GSH) level and increasing selenoenzyme (glutathione peroxidase, GPX) activity. Cd induced hepatotoxicity via disordering ER-resident selenoproteins transcription and triggering ER stress and unfolded protein response. Supplementary Se evidently relieved hepatocytes injury via modulating ER-resident selenoproteins transcription to inhibit ER stress. Collectively, our findings showed a potential protection of Se against Cd-induced hepatotoxicity via suppressing ER stress response.

The Gulf of Mexico (GoM) is exposed to a diversity of contaminants, such as hydrocarbons and heavy metal(oid)s, either from natural sources or as a result of uncontrolled coastal urbanisation and industrialisation. To determine the effect of these contaminants on the marine biota along the Mexican GoM, the biological responses of the shoal flounder Syacium gunteri, naturally exposed, were studied. The study area included all the Mexican GoM, which was divided into three areas: West-southwest (WSW), South-southwest (SSW) and South-southeast (SSE). The biological responses included the global DNA methylation levels, the expression of biomarker genes related to contaminants (cytochrome P450 1A, glutathione S-transferase, glutathione reductase, glutathione peroxidase, catalase, and vitellogenin), histopathological lesions and PAH metabolites in bile (hydroxynaphthalene, hydroxyphenanthrene, hydroxypyrene and Benzo[a]pyrene). The correlation between the biological responses and the concentration of contaminants (hydrocarbons and metal(oid)s), present in both sediments and organisms, were studied. The shoal flounders in WSW and SSW areas presented higher DNA hypomethylation, less antioxidative response and biotransformation gene expression and a higher concentration of PAH metabolites in bile than SSE area; those responses were associated with total hydrocarbons and metals such as chromium (Cr). SSE biological responses were mainly associated with the presence of metals, such as cadmium (Cd) and copper (Cu), in the tissue of shoal flounders. The results obtained on the physiological response of the shoal flounder can be used as part of a permanent active environmental surveillance program to watch the ecosystem health of the Mexican GoM.

Antimonite [Sb(III)] and antimonate [Sb(V)] are known to have different toxicity to plants, but the corresponding mechanisms are not fully understood. This study was conducted to investigate reactive oxygen species (ROS), antioxidant systems, and levels of certain essential elements in response to exposure to Sb(III) and Sb(V). Results showed that exposure to Sb(V) caused oxidative stress in a rice plant (Yangdao No.6). Sb(III) was shown to be more toxic than Sb(V) as judged from a lower shoot biomass, a higher loss of essential elements, and higher production of superoxide anion free radicals (O₂⁻). The toxicity of Sb(III) might partially be due to the disturbance of the O₂ˉ dismutation reaction, which resulted in root cell membrane damage under exposure to 20 mg L⁻¹ Sb(III). Sb(V) stimulated the shoot fresh weight and the shoot uptake of many essential elements. Moreover, Sb(V) and Sb(III) both stimulated the accumulation of calcium in the shoots and roots, and calcium was found to significantly correlate with the concentrations of many essential elements and with some parameters correlated to antioxidant systems, suggesting a Ca-induced regulatory mechanism. The activity of glutathione peroxidase was significantly enhanced by Sb(V) and Sb(III), suggesting a role in scavenging hydrogen peroxide. Catalase was activated by exposure to 20 mg L⁻¹ Sb(III) in the roots and by exposure to 20 mg L⁻¹ Sb(V) both in the shoots and roots. However, peroxidase was activated by exposure to 5 mg L⁻¹ Sb(III) in the shoots and by exposure to 5 mg L⁻¹ Sb(V) in the roots. This study, for the first time, showed the differences between Sb(V) and Sb(III) toxicity when looking at the antioxidant response and essential element uptake.

Oxidative stress is considered a main commonly reported mechanism of nanoparticles toxicity, so this study aimed to evaluate oxidative stress and biochemical alterations in the haemolymph and digestive gland of snail, Monacha cartusiana exposed to sublethal concentrations of zinc oxide nanoparticles (ZnONPs) for 14 days (d). The results indicated that, ZnONPs induced significant increases in lipid peroxidation (LPO) and lactate dehydrogenase (LDH) in treated animals and did not return to normal levels after recover period. A significant decline of glutathione peroxidase (GPx), glutathione-S-transferase (GST) activities, and glutathione (GSH) content in the haemolymph and digestive gland of snails was observed when compared with control. A significant increase was observed in catalase (CAT), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) activities of treated animals. In general, nano-materials are able to induce oxidative stress in exposed animals. The present findings indicate that, alterations of antioxidant enzyme activities, increase of LPO, LDH, and reducing of GSH content and GST, GPx activities are recognized to oxidative stress and cell damage. This species could be considered a good bioindicator to assess nano-materials exposure.

PM2.5 is becoming a worldwide environmental problem, which profoundly endangers public health, thus progressively capturing public attention this decade. As a fragile target of PM2.5, the underlying mechanisms of endothelial cell damage are still obscure. According to the previous microarray data and signaling pathway analysis, a new form of cell death termed ferroptosis in the current study is proposed following PM2.5 exposure. In order to verify the vital role of ferroptosis in PM2.5-induced endothelial lesion and further understand the potential mechanism involved, intracellular iron content, ROS release and lipid peroxidation, as well as biomarkers of ferroptosis were detected, respectively. As a result, uptake of particles increases cellular iron content and ROS production. Meanwhile, GSH depletion, and the decrease of GSH-Px and NADPH play significant roles in PM2.5-induced endothelial cell ferroptosis. Moreover, significantly changed expression of TFRC, FTL and FTH1 hinted that dysfunction of iron uptake and storage is a major inducer of ferroptosis. Importantly, index monitored above can be partially rescued by lipid peroxidation inhibitor ferrostatin-1 and iron chelator deferoxamine mesylate, which mediated antiferroptosis activity mainly depends on the restoration of antioxidant activity and iron metabolism. In conclusion, our data basically show that PM2.5 enhances ferroptosis sensitivity with increased ferroptotic events in endothelial cells, in which iron overload, lipid peroxidation and redox imbalance act pivotal roles.

In the study, the effects of dimethyl phthalate (DMP) on the antioxidant defense capacity and immune functions of human erythrocytes were experimentally explored. DMP affected the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) and the contents of glutathione (GSH) and malondialdehyde (MDA) in erythrocytes, thus impairing the function of antioxidant defense system of erythrocytes. When DMP concentration increased from 0 to 28 μmol L⁻¹, the SOD and GPX activities were increased firstly and then gradually decreased. When DMP concentration was below 20 μmol L⁻¹, the relative activity of SOD was enhanced by DMP and the effect was known as hormesis. The relative activity of GPX was also increased when the concentration of DMP was below 12 μmol L⁻¹. The CAT activity was more significantly inhibited by DMP than the activities of SOD and GPX, whereas the relative GSH content was increased by DMP. MDA levels were significantly changed after the exposure to DMP (0–24 μmol L⁻¹). The experimental results of the activity of SOD and CAT, and the content of MDA also suggested that DMP could inhibit the immune functions of red blood cells (RBCs), which were further proved by the decrease of two indicators (RBC-C₃b and RBC-IC) due to the destruction of C₃b receptor with immune adherence function on erythrocyte membrane. The study provides a deep understanding of the toxicity of DMP on erythrocytes.