Acute Metal Exposure Research Articles

Association of heavy metals with plastics used in aquaculture

The association of heavy metals with plastics could represent a source of contamination, presenting acute metal exposure to ecosystems. Here, we aimed to evaluate the level of 20 metals on plastics employed in aquaculture areas and their surrounding water. All the selected metals were detected on six different polymers/types of plastics. Despite the difference in sampling sites, there was no significant difference among metal concentrations on plastics. However, some metals showed a significant difference in the surrounding seawater among sites or were not detected. Additionally, the median concentrations of all heavy metals were higher on plastic than in their surrounding water at all sites. Furthermore, multivariate analysis showed that metals accumulate on plastics in a similar pattern among sites but distinct from the surrounding water. This study contributes to understanding the accumulation of metals on plastics used in aquaculture areas.

Repeated pulmonary exposures to zinc ions enhance inflammatory responses to subsequent metal exposures

Aim of Study: Metal contaminants contribute to adverse human health effects via acute and chronic exposures. Acute metal exposures followed by prolonged secondary metal exposures may elicit exaggerated inflammatory responses in certain individuals. The aim of this study is to determine whether repeated pulmonary exposures to zinc chloride (ZnCl2) alter subsequent responses to zinc or cerium exposures. Materials and Methods: Rats were intratracheally (IT) instilled with physiologic saline (n = 24) or 0.05 mg/kg ZnCl2 (n = 16) twice weekly for 4 weeks. Four days after last dosing, the saline group was divided into three subgroups, each IT-instilled with either saline, ZnCl2 or CeCl3 (both at 0.1 mg/kg). The ZnCl2 pre-instilled rats were divided into two subgroups, each instilled with 0.1 mg/kg ZnCl2 or CeCl3. Biomarkers of lung injury/inflammation were assessed in bronchoalveolar lavage (BAL) fluid collected 24 hours later. Oxidative stress was evaluated as total and reduced glutathione in BAL. Results: Increases in inflammatory cells, LDH, albumin, leptin, MCP-1, IP-10, fractalkine, TNFα and RANTES were observed in rats instilled with multiple PBS and then with 0.1 mg/kg ZnCl2 and CeCl3. However, rats pre-exposed repeatedly to 0.05 mg/kg ZnCl2 and then challenged with 0.1 mg/kg ZnCl2 or CeCl3 showed even more eosinophils, lymphocytes, and increased concentrations of hemoglobin and MIP-1α. Significant reduction in GSH/GSSG ratios in BAL in response to all ZnCl2 or CeCl3 exposures indicated oxidative stress. Conclusion: Previous exposure to zinc ions increases responsiveness to subsequent exposures to zinc and cerium ions. These findings suggest enhanced sensitization possibly due to a reduction in antioxidant defenses.

Maladaptation to Acute Metal Exposure in Resurrected Daphnia ambigua Clones after Decades of Increasing Contamination.

Human environmental impacts have driven some of the strongest and fastest phenotypic changes recorded in wild animal populations. Across populations, this variation is often adaptive, because populations evolve fitness advantages in response to human-modified environments. Yet some populations fail to adapt to changing environments. Evidenced by declines in relative fitness, such seemingly maladaptive outcomes are less common but may be more likely in human-modified contexts. Further, our ability to investigate the dynamics of these adaptive and maladaptive responses over time is typically limited in natural systems. I combined resurrection ecology and paleolimnology approaches to examine evolutionary responses of the freshwater zooplankter Daphnia to exposure to heavy metal contamination over the past 50-75 years, using animals hatched from diapausing egg banks. In contrast to the predicted trend of adaptation to metal exposure over time, I observed an increase in sensitivity to both copper and cadmium exposure associated with increasing historic contamination. This potentially maladaptive trend occurred in Daphnia populations in three lakes. Given that the release of toxicants such as heavy metals is widespread and that other researchers have observed local maladaptation to toxicant exposure, it is important to understand the drivers and implications of this pattern.

Characterization and response of antioxidant systems in the tissues of the freshwater pond snail (Lymnaea stagnalis) during acute copper exposure

The response of enzymatic (superoxide dismutase, SOD; catalase, CAT; glutathione peroxidase, GPX and glutathione reductase, GR) and non-enzymatic responses (glutathione, GSH, oxidized glutathione, GSSG and GSH/GSSG) against acute Cu toxicity (2–90μg/mL for 48h) in different tissues of Lymnaea stagnalis were measured. Incubation conditions for enzymatic activity measurements were optimized for L. stagnalis tissues. Three examined tissues, the hepatopancreas, the foot muscle and the mantle, exhibited variable responses in antioxidant parameters as a function of Cu concentrations. The most responsive antioxidant enzymes were GPX and CAT while GR appeared less sensitive. In general antioxidant enzymes at higher Cu concentrations though GSH levels at lower Cu concentrations exhibited the greatest changes in hepatopancreas and foot muscle, respectively. All antioxidant enzymes except GR increased after exposure to the highest Cu concentration in mantle. Total and reduced GSH increased in hepatopancreas but decreased with GSH/GSSG ratios at all Cu concentrations in foot muscle. The present results show that antioxidants respond to acute Cu exposure at concentrations as low as 2μg Cu/L in adult L. stagnalis with variable responses in different tissues. Antioxidants both including enzymatic and non-enzymatic parameters may account, in part, for the high tolerance to acute metal exposure observed in adult L. stagnalis and could form suited biomarkers to evaluate the metal exposure and toxicity in aquatic environment even at relatively low level short term exposure.

Effects of Acute and Chronic Heavy Metal (Cu, Cd, and Zn) Exposure on Sea Cucumbers (Apostichopus japonicus).

Acute and chronic toxicity tests were conducted with sea cucumber (Apostichopus japonicus) exposed to heavy metals. Acute toxicity values (96 h LC50) were 2.697, 0.133, and 1.574 mg L−1 for Zn, Cu, and Cd, respectively, and were ranked in order of toxicity: Cu > Cd > Zn. Under chronic metal exposure the specific growth rates of sea cucumbers decreased with the increase of metal concentration for all the three metals. After acute metal exposure, the oxygen consumption rate (OCR) decreased. The OCRs in all groups were significantly different than control (P < 0.05) except in the group treated with 1.00 mg L−1 Zn (P < 0.05), where the increase of OCR was observed. The OCRs in groups chronically exposed to metals were significantly lower than that in the control group (P < 0.05). The activity of both pyruvate kinase (PK) and hexokinase (HK) in sea cucumbers followed: respiratory tree > muscle > intestine in natural sea water. After chronic Zn, Cu, and Cd exposure, the change pattern of HK and PK in respiratory tree, muscle, and intestine varied slightly. However, the activity of the enzyme showed a general trend of increase and then decrease and the higher the exposure concentration was, the earlier the highest point of enzyme activity was obtained.

Acute Cadmium Exposure Reduces the Local Angiotensin I Converting Enzyme Activity and Increases the Tissue Metal Content.

Cadmium exposure causes health problems that may result from increased oxidative stress and from changes in enzyme metalloproteases activities as angiotensin-converting enzyme (ACE). In fact, cadmium produces inhibition of serum ACE but is not known how cadmium acts on tissue ACE activity and whether following acute exposure tissue cadmium content is increased. In order to elucidate these issues, a cadmium bolus was injected intravenously in Wistar rats, and the cadmium content and the ACE activity were measured in the serum, lungs, aorta and kidneys. Moreover, in order to clarify if the cadmium affects directly tissue ACE activity, acute metal exposure in vitro was performed. Our results demonstrated that 120min following cadmium administration, blood and organ cadmium content were both increased. Serum and lung ACE activity were reduced following acute cadmium exposure, but aortic and kidney ACE activities were not affected. The inhibitory effects induced by cadmium on ACE activity were also observed in the serum, as well as the lungs and the aorta, but not in the kidneys following in vitro exposure. Moreover, the inhibitory effects induced by cadmium on ACE activity were partially restored in vitro by zinc supplementation, suggesting a possible interaction or competition between cadmium and zinc by at the active site of ACE. Summarising, our results suggest that acute cadmium exposure promotes an increase in the tissue metal content that was accompanied by direct inhibition of serum, aorta and lung ACE activity, an effect that is cadmium concentration-dependent and is partially reversed by zinc.

Genome-wide gene expression profiling of acute metal exposures in male zebrafish.

To capture global responses to metal poisoning and mechanistic insights into metal toxicity, gene expression changes were evaluated in whole adult male zebrafish following acute 24 h high dose exposure to three metals with known human health risks. Male adult zebrafish were exposed to nickel chloride, cobalt chloride or sodium dichromate at concentrations corresponding to their respective 96 h LC20, LC40 and LC60 (i.e. 96 h concentrations at which 20%, 40% and 60% lethality is expected, respectively). Histopathology was performed on a subset of metal-exposed zebrafish to phenotypically anchor transcriptional changes associated with each metal exposure. Here we describe in detail the contents and quality controls for the gene expression and other data associated with the study published by Hussainzada and colleagues in BMC Pharmacology and Toxicology (Hussainzada et al., 2014) with the data uploaded to Gene Expression Omnibus (accession number GSE50648).

Whole adult organism transcriptional profiling of acute metal exposures in male Zebrafish

BackgroundA convergence of technological breakthroughs in the past decade has facilitated the development of rapid screening tools for biomarkers of toxicant exposure and effect. Platforms using the whole adult organism to evaluate the genome-wide response to toxicants are especially attractive. Recent work demonstrates the feasibility of this approach in vertebrates using the experimentally robust zebrafish model. In the present study, we evaluated gene expression changes in whole adult male zebrafish following an acute 24 hr high dose exposure to three metals with known human health risks. Male adult zebrafish were exposed to nickel chloride, cobalt chloride or sodium dichromate concentrations corresponding to their respective 96 hr LC20, LC40 and LC60. Histopathology was performed on a subset of metal-exposed zebrafish to phenotypically anchor transcriptional changes associated with each metal.ResultsComparative analysis identified subsets of differentially expressed transcripts both overlapping and unique to each metal. Application of gene ontology (GO) and transcription factor (TF) enrichment algorithms revealed a number of key biological processes perturbed by metal poisonings and the master transcriptional regulators mediating gene expression changes. Metal poisoning differentially activated biological processes associated with ribosome biogenesis, proteosomal degradation, and p53 signaling cascades, while repressing oxygen-generating pathways associated with amino acid and lipid metabolism. Despite appreciable effects on gene regulation, nickel poisoning did not induce any morphological alterations in male zebrafish organs and tissues. Histopathological effects of cobalt remained confined to the olfactory system, while chromium targeted the gills, pharynx, and intestinal mucosa. A number of enriched transcription factors mediated the observed gene response to metal poisoning, including known targets such as p53, HIF1α, and the myc oncogene, and novel regulatory factors such as XBP1, GATA6 and HNF3β.ConclusionsThis work uses an experimentally innovative approach to capture global responses to metal poisoning and provides mechanistic insights into metal toxicity.

Response of Antioxidant System of Tilapia (Oreochromis niloticus) Following Exposure to Chromium and Copper in Differing Hardness

Tilapias (Oreochromis niloticus) were exposed to copper or chromium in soft water (SW) (~80 mg CaCO3/L, conductivity 1.77 mS/cm) or hard water (HW) (~320 mg CaCO3/L, conductivity 5.80 mS/cm) using 2 exposure protocols (20 μM for 48 h and 10 μM for 144 h). Following the exposures, antioxidant enzyme activities [superoxide dismutase (SOD); catalase (CAT); glutathione peroxidase; glutathione reductase; and glutathione S-transferase (GST)] and glutathione (GSH) levels were measured in the liver of fish. SOD and CAT activities of control fish kept in SW were significantly lower than control fish kept in HW. However, the other antioxidant indices (glutathione metabolism) of both control fish were unaffected from water hardness. Acute metal exposures did not alter the glutathione metabolism, whereas SOD activity in SW and CAT activity in both waters changed significantly. In subchronic duration, Cu exposure caused significant decreases in measured parameters, except for GST activity and GSH level. Similarly, GST activity and GSH level were unaffected from Cr exposure. This study showed that SOD and CAT were the most sensitive antioxidant indices, and that glutathione metabolism, in general, was not altered following metal exposures in different waters.

Antioxidant enzyme activities in biofilms as biomarker of Zn pollution in a natural system: An active bio-monitoring study

This study aimed to explore the use of antioxidant enzyme activities (AEA) and biofilm metal accumulation capacity in natural communities as effect-based indicator of metal exposure in fluvial systems. To achieve these objectives, an active biomonitoring using fluvial biofilm communities was performed during 5 weeks. Biofilm was colonized over artificial substrata in a non-polluted site. After 5 weeks, biofilms were translocated to four different sites with different metal pollution in the same stream. The evolution of environmental parameters as well as biofilm responses was analysed over time.Physicochemical parameters were different between sampling times as well as between the most polluted site and the less polluted ones, mainly due to Zn pollution. In contrast, AEA and metal accumulation in biofilms allowed us to discriminate the high and moderate metal pollution sites from the rest. Zn, the metal with the highest contribution to potential toxicity, presented a fast and high accumulation capacity in biofilms. According to the multivariate analysis, AEA showed different responses. While catalase (CAT) and ascorbate peroxidase (APX) variability was mainly attributed to environmental stress (pH, temperature and phosphate concentration), glutathione-S-transferase (GST) changes were related to metal pollution. Glutathione reductase (GR) and superoxide dismutase (SOD) responses were related to both stress factors.AEA and metal accumulation are proposed as sensitive effect-based field methods, to evaluate biofilm responses after acute metal exposure (e.g. an accidental spill) due to their capacity to respond after few hours, but also in routinely monitoring due to their persistent changes after few weeks of exposure. These tools could improve the Common Implementation Strategy (CIS) of the Water Framework Directive (WFD) as expert group request.

Trace metals alter DNA repair and histone modification pathways concurrently in mouse embryonic stem cells

Exposure to metals alters gene expression, changes transcription rates or interferes with DNA repair mechanisms. We tested a hypothesis to determine whether in vitro acute metal exposure, with or without recovery, alters epigenetic pathways in mouse embryonic stem (mES) cells. We measured cell viability, total and histone protein production, changes in gene expression for differentiation and DNA repair, and histone lysine mono-methylation (H3K27me1), in differentiated cells. Confluent differentiated cultures of mES cells were exposed to arsenic (As), cadmium (Cd), copper (Cu), lead (Pb), lithium (Li), mercury (Hg), and nickel (Ni), for 1-h and 24-h, followed by a recovery period. The data demonstrate that maximum cell death occurred during the first few hours of exposure at 24-h IC50 concentrations for all metals. Prolonged in vitro exposure to metals at low concentrations also inhibited protein production and cell proliferation. Subsequently, we determined that metals alter cell differentiation (Oct-4 and egfr) and DNA repair mechanisms (Rad-18, Top-3a and Ogg-1). Interestingly, As, Cd, Hg, and Ni decreased cell proliferation to a greater extent than total histone protein production. Yet, at equivalent concentrations, As and Hg significantly decreased total histone protein production per cell compared to respective controls, suggesting suppression of repair or compensatory mechanisms involving histone pathways. And, acute exposure to As, Cd, Hg and Ni decreased H3K27me1 residue, when compared to control cells. Because activation of cellular differentiation, histone modification, and DNA repair are linked by common transcriptional pathways, and the data propose that metals alter these conduits, then it is reasonable to conclude that trace quantities of metals are capable of suppressing regulation of chromatin structure, cellular differentiation, and controlled cell proliferation in mES cells.

Acute and chronic metal exposure impairs locomotion activity in Drosophila melanogaster: a model to study Parkinsonism

The biometals iron (Fe), manganese (Mn) and copper (Cu) have been associated to Parkinson's disease (PD) and Parkinsonism. In this work, we report for the first time that acute (15mM for up to 5days) or chronic (0.5mM for up to 15days) Fe, Mn and Cu exposure significantly reduced life span and locomotor activity (i.e. climbing capabilities) in Drosophila melanogaster. It is shown that the concentration of those biometals dramatically increase in Drosophila's brain acutely or chronically fed with metal. We demonstrate that the metal accumulation in the fly's head is associated with the neurodegeneration of several dopaminergic neuronal clusters. Interestingly, it is found that the PPL2ab DAergic neuronal cluster was erode by the three metals in acute and chronic metal exposure and the PPL3 DAergic cluster was also erode by the three metals but in acute metal exposure only. Furthermore, we found that the chelator desferoxamine, ethylenediaminetetraacetic acid, and D: -penicillamine were able to protect but not rescue D. melanogaster against metal intoxication. Taken together these data suggest that iron, manganese and copper are capable to destroy DAergic neurons in the fly's brain, thereby impairing their movement capabilities. This work provides for the first time metal-induced Parkinson-like symptoms in D. melanogaster. Understanding therefore the effects of biometals in the Drosophila model may provide insights into the toxic effect of metal ions and more effective therapeutic approaches to Parkinsonism.

Response of Superoxide Dismutase to Pollutant Metal Stress in the Marine Dinoflagellate Gonyaulax polyedra

The response of superoxide dismutase (SOD) activity in the marine dinoflagellate Gonyaulax polyedra to chronic (5.0 ppb Hg, 0.5 ppm Cd, 2.0 ppm Pb and 0.1 ppm Cu, during 30 days) and acute (10.0 ppb Hg, 1.0 ppm Cd, 5.0 ppm Pb and 0.25 ppm Cu, during 48 hours) exposure to metals was investigated. Under chronic exposure to Hg, Cd, Pb, and Cu, total SOD activity of metal-treated cells increased during the first day of exposure to plateau levels of 134, 148, 127, and 139% of control values respectively. Under acute metal exposure, SOD activity increases were of similar magnitude but much more rapid (within several hours) and of shorter duration. In addition, assays for oxidative damage to lipids revealed high levels of lipid peroxidation in cells kept in either chronic or acute exposure to metals reaching values 2-fold greater than the control group. Changes in SOD activity were dependent on the metal, its concentration, and the time of exposure. Non-denaturing polyacrylamide gels revealed induction of Fe-SOD and Mn-SOD but not Cu-Zn-SOD isoforms in cells kept under acute exposure to metals. These results suggest that oxidative stress may be an important mediator of metal toxicity in algal systems, with SOD providing antioxidant protection.