Heavy metals generate reactive oxygen species in terrestrial and aquatic ciliated protozoa

Author(s):  
Daniel Rico ◽  
Ana Martín-González ◽  
Silvia Díaz ◽  
Pilar de Lucas ◽  
Juan-Carlos Gutiérrez
2021 ◽  
Vol 1 (1) ◽  
Author(s):  
Yoo-Hun Noh ◽  
Byung-Ju Jeon ◽  
Seungah Lee ◽  
Jaeho Myeong ◽  
Ga-Young Kim ◽  
...  

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 102 ◽  
Author(s):  
Ewa Muszyńska ◽  
Mateusz Labudda ◽  
Adam Kral

This research aimed to indicate mechanisms involved in protection against the imbalanced generation of reactive oxygen species (ROS) during heavy metals (HMs) exposition of Silene vulgaris ecotypes with different levels of metal tolerance. Specimens of non-metallicolous (NM), calamine (CAL), and serpentine (SER) ecotypes were treated in vitro with Zn, Pb, and Cd ions applied simultaneously in concentrations that reflected their contents in natural habitats of the CAL ecotype (1× HMs) and 2.5- or 5.0-times higher than the first one. Our findings confirmed the sensitivity of the NM ecotype and revealed that the SER ecotype was not fully adapted to the HM mixture, since intensified lipid peroxidation, ultrastructural alternations, and decline in photosynthetic pigments’ content were ascertained under HM treatment. These changes resulted from insufficient antioxidant defense mechanisms based only on ascorbate peroxidase (APX) activity assisted (depending on HMs concentration) by glutathione-S-transferase (GST) and peroxidase activity at pH 6.8 in the NM ecotype or by GST and guaiacol-type peroxidase in the SER one. In turn, CAL specimens showed a hormetic reaction to 1× HMs, which manifested by both increased accumulation of pigments and most non-enzymatic antioxidants and enhanced activity of catalase and enzymes from the peroxidase family (with the exception of APX). Interestingly, no changes in superoxide dismutase activity were noticed in metallicolous ecotypes. To sum up, the ROS scavenging pathways in S. vulgaris relied on antioxidants specific to the respective ecotypes, however the synthesis of polyphenols was proved to be a universal reaction to HMs.


2008 ◽  
Vol 1 ◽  
pp. BCI.S1007 ◽  
Author(s):  
F. Gagné ◽  
C. André ◽  
C. Blaise

The purpose of this study was to examine the function of metallothioneins (MT) in respect to the mobilization of heavy metals and superoxide anion (O2–) scavenging in aquatic organisms. Using an O2– generating system, liberation of free zinc from native and zinc MT (Zn-MT) was measured in vitro. Addition of the O2– generating system and H2O2 readily increased the di- and trimeric forms of MT as determined by gel electrophoresis analysis. To determine whether the proportion of oxidized MT could change in contaminated environments, metal-contaminated Mya arenaria clams were collected from a harbour in the St. Lawrence Estuary. The levels of labile zinc, superoxide dismutase (O2– scavenging enzyme), lipid peroxidation (LPO) and the oxidized/metallic form of MT were determined in the digestive gland. The results revealed that the induction of total MT levels was the result of increased oxidized MT at the expense of the reduced or metallic form of MT. Both superoxide dismutase (SOD) and labile zinc (Zn) levels were induced and they were significantly correlated with the oxidized form of MT, but not the metallic form, in feral clam populations. We concluded that the level of total MT was related to Zn mobility and the activation of antioxidant mechanisms such as SOD, and corresponded to the levels of oxidized MT. The metallic form of MT was negatively associated with Zn mobility but positively associated with oxidative damage such as LPO. Overall, the oxidized fraction of MT appeared to be more closely related to detoxification, while the metallic form of MT was associated with metal mobility and toxicity via oxidative damage. The protective effect of MT during heavy-metal contamination depends on the availability of metals and on its capacity to sequester reactive oxygen species.


Author(s):  
Sandip V. Mulay ◽  
Youngsam Kim ◽  
Woo Hyun Lee ◽  
Shubhangi Singh ◽  
David G. Churchill

Environments ◽  
2019 ◽  
Vol 6 (4) ◽  
pp. 42 ◽  
Author(s):  
Kai Zhang ◽  
Dongyang Nie ◽  
Mindong Chen ◽  
Yun Wu ◽  
Xinlei Ge ◽  
...  

PM2.5 pollution is of great concern in China due to its adverse health effects. Many diseases have been proven to be associated with PM2.5 components, but the effects of chemical characteristics of PM2.5 on toxicological properties, especially in different human organs, are poorly understood. In this study, two seasonal PM2.5 samples (summer and winter) were collected in Nanjing, and their chemical compositions (heavy metals, water-soluble ions, organic carbon (OC), and elemental carbon (EC)) were analyzed. Human lung epithelial carcinoma cells (A549), human hepatocellular liver carcinoma cells (HepG2), and human neuroblastoma cells (Sh-Sy5y) were employed to evaluate the toxicological properties of the collected PM2.5. The results showed that the average mass concentrations of PM2.5 were lower in summer (51.3 ± 21.4 μg/m3) than those in winter (62.1 ± 21.5 μg/m3). However, the mass fractions of heavy metals, OC, and EC exhibited an opposite seasonal difference. Among all tested fractions, water-soluble ions were the major compositions of particles in both summer and winter, especially the secondary ions (SO42−, NO3− and NH4+). Besides, the ratio of OC/EC in PM2.5 was greater than two, indicating serious secondary pollution in this area. The NO3–/SO42− ratio (< 1) suggested that fixed sources made important contributions. The toxicological results showed that PM2.5 in the summer and winter significantly inhibited cell viability (p < 0.01) and induced intracellular reactive oxygen species (ROS) production (p < 0.01). Moreover, the viability inhibition in A549, Sh-Sy5y, and HepG2 cells was more prominent in summer, especially at high PM2.5 (400 μg/mL) (p < 0.05), and the induction of reactive oxygen species (ROS) in A549 and Sh-Sy5y cells was also more evident in summer. Such seasonal differences might be related to the variations of PM2.5 components.


2021 ◽  
Vol 12 ◽  
Author(s):  
Indrani Manna ◽  
Saikat Sahoo ◽  
Maumita Bandyopadhyay

Scientists anxiously follow instances of heavy metals augmenting in the environment and undergoing bioaccumulation and trace their biomagnification across food webs, wary of their potent toxicity on biological entities. Engineered nanoparticles supplement natural pools of respective heavy metals and can mimic their effects, exerting toxicity at higher concentrations. Thus, a thorough understanding of the underlying mechanism of this precarious interaction is mandatory. Most urban and industrial environments contain considerable quantities of nickel oxide nanoparticles. These in excess can cause considerable damage to plant metabolism through a significant increase in cellular reactive oxygen species and perturbation of its cross-talk with the reactive nitrogen species. In the present work, the authors have demonstrated how the intrusion of nickel oxide nanoparticles (NiO-NP) affected the exposed roots of Allium cepa: starting with disruption of cell membranes, before being interiorized within cell organelles, effectively disrupting cellular homeostasis and survival. A major shift in the reactive oxygen species (ROS) and nitric oxide (NO) equanimity was also observed, unleashing major altercations in several crucial biochemical profiles. Altered antioxidant contents and upregulation of stress-responsive genes, namely, Catalase, Ascorbate peroxidase, Superoxide dismutase, and Rubisco activase, showing on average 50–250% rise across NiO-NP concentrations tested, also entailed increased cellular hydrogen peroxide contents, with tandem rise in cellular NO. Increased NO content was evinced from altered concentrations of nitric oxide synthase and nitrate reductase, along with NADPH oxidase, when compared with the negative control. Though initially showing a dose-dependent concomitant rise, a significant decrease of NO was observed at higher concentrations of NiO-NP, while cellular ROS continued to increase. Modified K/Na ratios, with increased proline concentrations and GABA contents, all hallmarks of cellular stress, correlated with ROS–NO perturbations. Detailed studies showed that NiO-NP concentration had a significant role in inducing toxicity, perturbing the fine balance of ROS–NO, which turned lethal for the cell at higher dosages of the ENP precipitating in the accumulation of stress markers and an inevitable shutdown of cellular mechanisms.


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