Doses Of Mercury Research Articles

Gold nanoparticles decorated magnetic nanozyme for colorimetric detection of mercury (II) ions via enhanced peroxidase-like activity

Mercury is one of the heavy metal ions that are released to the environment through various means including anthropogenic pollution. A very low dose of mercury in environmental systems such as water can lead to debilitating effects on the health of humans and animals, if consumed untreated. To reduce this effect, it is critical to develop a simple, non-expensive, and non-sophisticated detection and monitoring system of mercury. Here, we report a simple colorimetric method based on the peroxidase-like activity of AuNPs/ZnO/Fe3O4. Different characterization techniques such as scanning electron microscopy (SEM), transmission electron microscopy (TEM), X-ray diffraction (XRD), and surface-enhanced Raman spectroscopy (SERS) were used to investigate the successful formation of these composites. The formation of AuNPs was assisted by ZnO. The low Km value (0.7368 mM) obtained from the kinetic study of the catalytic oxidation of 3, 3′, 5, 5′ − Tetramethylbenzidine (TMB) showed strong affinity of TMB to AgNPs/ZnO/Fe3O4. The peroxidase-like activity of AgNPs/ZnO/Fe3O4, was further enhanced in the presence of mercury (II). The absorption intensities of the resulting oxidized TMB (oxTMB) increased linearly in a concentration range of 0.05 – 20 µM. The method also exhibited high selectivity to mercury (II) ions. The limit of detection (LOD) in this linear range was found to be 28.1 nM. The feasibility of the method in determination of mercury (II) ions from real samples was confirmed from high recovery rates in tap water samples. The method shows a great potential for determination of mercury (II) ions in environmental samples.

Integrative investigation of hematotoxic effects induced by low doses of lead, cadmium, mercury and arsenic mixture: In vivo and in silico approach

The effect of the lead (Pb), cadmium (Cd), mercury (Hg) and arsenic (As) mixture (MIX) on hematotoxicity development was investigated trough combined approach. In vivo subacute study (28 days) was performed on rats (5 per group): a control group and five groups orally exposed to increasing metal(loid) mixture doses, MIX 1- MIX 5 (mg/kg bw./day) (Pb: 0.003, 0.01, 0.1, 0.3, 1; Cd: 0.01, 0.03, 0.3, 0.9, 3; Hg: 0.0002, 0.0006, 0.006, 0.018, 0.06; As: 0.002, 0.006, 0.06, 0.18, 0.6). Blood was taken for analysis of hematological parameters and serum iron (Fe) analysis. MIX treatment increased thrombocyte/platelet count and MCHC and decreased Hb, HCT, MCV and MCH values compared to control, indicating the development of anemia and thrombocytosis. BMDIs with the narrowest width were identified for MCH [pg] (6.030E-03 - 1.287E-01 mg Pb/kg bw./day; 2.010E-02 - 4.290E-01 mg Cd/kg bw./day; 4.020E-04 - 8.580E-03 mg Hg/kg bw./day; 4.020E-03 - 8.580E-02 mg As/kg bw./day). In silico analysis showed target genes connected with MIX and the development of: anemia - ACHE, GSR, PARP1, TNF; thrombocytosis – JAK2, CALR, MPL, THPO; hematological diseases - FAS and ALAD. The main extracted pathways for anemia were related to apoptosis and oxidative stress; for thrombocytosis were signaling pathways of Jak-STAT and TPO. Changes in miRNAs and transcription factors enabled the mode of action (MoA) development based on the obtained results, contributing to mechanistic understanding and hematological risk related to MIX exposure.

Mercurial risk from dental amalgam use in a population of Moroccan dentists: A latent class regression approach.

Dentists using dental amalgam are chronically exposed to low doses of elemental mercury. The complex toxico-kinetics of this systemic toxicant results in polymorphic and variable clinical phenotypes. In this context, adapted statistical methods are required to highlight potential adverse effects of occupational mercury exposure on dentists' health. The present study aims to analyze the distribution of self-reported subjective symptoms, commonly associated with chronic mercury poisoning, according to occupational mercury exposure in a population of Moroccan liberal dentists. In order to achieve the defined objectives, a three-step latent class regression was fitted. First a latent class analysis was performed to cluster the studied population according to their declared symptoms. Dentists were then classified in the defined latent classes based on their posterior probabilities. Finally, a logistic regression is fitted to identify predictors associated with latent classes' membership. The final obtained model showed acceptable calibration and discrimination. Its interpretation revealed that the increase of the frequency of amalgam use was associated with significant higher odds of belonging to the high risk latent class. The present study represents an initial step towards the development of diagnosis model that predict clinical profiles according to occupational mercury exposure.

Possible Molecular Mechanisms Underlying the Decrease in the Antibacterial Activity of Protamine-like Proteins after Exposure of Mytilus galloprovincialis to Chromium and Mercury.

Natural bioactive compounds represent a new frontier of antimicrobial molecules, and the marine ecosystem represents a new challenge in this regard. In the present work, we evaluated the possibility of changes in the antibacterial activity of protamine-like (PL) proteins, the major nuclear basic protein components of Mytilus galloprovincialis sperm chromatin, after the exposure of mussels to subtoxic doses of chromium (VI) (1, 10, and 100 nM) and mercury (1, 10, and 100 pM) HgCl2, since these metals affect some properties of PL. After exposure, we analyzed the electrophoretic pattern of PLs by both acetic acid-urea polyacrylamide gel electrophoresis (AU-PAGE) and SDS-PAGE and determined the MIC and MBC of these proteins on different gram+ and gram- bacteria. PLs, particularly after mussels were exposed to the highest doses of chromium and mercury, showed significantly reduced antibacterial activity. Just at the highest doses of exposure to the two metals, changes were found in the electrophoretic pattern of PLs, suggesting that there were conformational changes in these proteins, which were confirmed by the fluorescence measurements of PLs. These results provide the first evidence of a reduction in the antibacterial activity of these proteins following the exposure of mussels to these metals. Based on the results, hypothetical molecular mechanisms that could explain the decrease in the antibacterial activity of PLs are discussed.

Understanding the mechanistic roles of environmental heavy metal stressors in regulating ferroptosis: adding new paradigms to the links with diseases.

Ferroptosis is a new type of iron-dependent cell death induced by a failure of the lipid repair protein GPX4 or the Xc- antiporter, which is essential for glutathione production. Some heavy metals such as arsenic (As), cobalt (Co), cadmium (Cd), iron (Fe), magnesium (Mg), manganese (Mn), nickel (Ni), mercury (Hg) as well as zinc (Zn) are shown to induce ferroptotic cell death involving the generation of oxidative stress, mitochondrial dysfunctioning, lipid peroxidation, and several other cellular etiologies. However, selenium (Se) treatment has been shown to enhance adaptive transcription responses to protect cells from ferroptosis. Heavy metals like Cadmium exposure activated ALK4/5 signaling via Smad3 and Akt signaling which leads to cell death mechanism. Continuous exposure to a small dose of mercury can damage tissues, and methylmercury bind to sulfhydryl proteins and GSH, this elevates oxidative stress, free radical accumulation, glutathione depletion, mitochondrial damage, and inhibited the nuclear factor-κB pathway which leads to ferroptotic cell death. Animals exposed to nickel and cobalt may have increased lipid peroxidation which can induce ferroptosis. Glutathione depletion is caused by Zn intoxication and exposure to manganese. These metals are systemic toxins that have been shown adverse effects on humans. Ferroptosis has recently been related to several pathological disorders, including, Alzheimer's disease, Parkinson's disease, Huntington's disease, as well as cardiovascular disease, and any type of cancer. For these disorders and some heavy metal toxicity, ferroptosis suppression needs to be looked upon as a promising therapeutic choice.

Human exposure to mercury in the atmosphere and soils in Konongo: an age-old mining centre in the Ashanti Region of Ghana.

The dramatic upsurge of artisanal and small-scale gold mining (ASGM) activities in Ghana has resulted in environmental degradation, water pollution and human exposure to mercury-the main hazardous element used in gold extraction. This study evaluated the degree of human exposure to mercury based on the concentrations found in the air and soil samples taken at a resolution of 1 km2 across Konongo, a historic mining town in Ghana's Ashanti Region. The highest atmospheric mercury concentration was 193ng/m3, which is much higher than the levels the European Union and Japan allowed, which are 10ng/m3 and 40ng/m3, respectively. The concentration in the soil was 3.6mg Hg/kg, which is around ten times higher than the background concentration in nature. Additionally, the soil concentrations were higher above the worrisome levels of soil contamination in agricultural land (4mg/kg) and industrial areas (16mg/kg), respectively. Soils are extremely contaminated with mercury at sites artisanal mining activities take place. The concentrations of mercury in the air and soils were significantly higher (p < 0.5) at locations of prominent mining activities compared to areas not close to mining sites. The inhabitants of the Konongo community are therefore exposed to mercury, most likely emitted from artisanal mining activities. A non-carcinogenic risk is posed to the people by inhaling mercury vapour through the air and vapourisation from the soil. Children are exposed to a higher risk than adults as they receive higher daily doses of mercury than adults.

Water pollution and environmental policy in artisanal gold mining frontiers: The case of La Toma, Colombia

Artisanal and small-scale gold mining (ASGM) is the largest anthropogenic source of mercury emissions globally. Concern over mercury pollution increases due to its long-term impacts on human health and aquatic and terrestrial ecosystems. Using a participatory research methodology, we gathered social and behavioral information regarding daily practices and water usage by an ASGM community in Suárez, Colombia. Based on this information, we identified 18 sampling sites of water sources commonly used by the community. The samples were analyzed for total mercury, total coliforms, pH, electrical conductivity, and total dissolved oxygen. Physicochemical and microbiological parameters from the water assessment were compared with the drinking water thresholds set by the Colombian regulatory agencies, the EPA, and the WHO. Our results showed that the majority of the samples do not meet one or more quality and safety standards. On average, the sampling sites showed total mercury levels below the regulatory limits; however, the data had considerable variability, and in many cases, individual observations fell above the maximum concentration limit for drinking water. We discuss these results within the larger framework of the regulatory gaps for human and environmental protection in ASGM contexts. The total lack of water, sanitation, and hygiene infrastructure, combined with the long-term consumption of sublethal doses of mercury and other water contaminants, constitutes a significant threat to the well-being of communities and territories that necessitates further research and intervention by institutional authorities.

Chemical and biochemical responses to sub−lethal doses of mercury and cadmium in gilthead seabream (Sparus aurata)

Specimens of Sparus aurata were exposed to sub−lethal concentrations of Hg and Cd for 25 days and the levels of both metals were investigated in organs and tissues. Bioaccumulation of Hg decreased as follow: gills > kidney > liver > skin > muscle, while the order of Cd bioaccumulation was: liver > kidney > gills > skin > muscle. Immediately after exposure, both metals showed the highest bioaccumulation in gills and skin indicating that these organs are reliable targets for biomonitoring studies after short term exposure. Metals introduction caused a significant time-dependent concentrations increase in kidney and liver, while in the muscle a significant increase of Hg was recorded only at the end of the experimentation.The effects of exposure were also investigated, at biochemical level, in the liver, which represents the main target of xenobiotics biotransformation and metabolism in fish. Exposed fishes exhibited a reduction of total lipid level, a decrease of polyunsaturated fatty acids (PUFA), together with a MDA increase. This suggests a direct effect of contaminants on oxidative stress induction that, through the MDA increase, altered the membrane fatty acids composition decreasing the PUFA content. As it regards molecular markers related to oxidative stress and lipid metanolism, a significant increase of Nrf2, Hif−1α and Ampk and a decrease of Fas were observed after exposure to both metals, while an Nf−kB increase was recorded in specimens exposed to Hg, docuemnting a correlation with oxidative stress and consequent metabolism adaptation. Finally, these results suggest the possibility to adopt these biomarkers to explore fish metabolic responses to environmental pollution.

Evaluation of the acute effect of heavy metals exposure on lipid profile of albino wistar rats

Acute effect of heavy metals exposure on lipid profile of male albino wistar rats was evaluated. Sixteen (16) animals weighing 292-298g were randomly assigned four groups of four rats each. Groups 1 and 2 were orally treated ones with 40 percent below the lethal doses (LD50) of Lead and Mercury respectively. Group 3 was treated with both heavy metals (20 percent below the LD50 each of the metals). Group 4 was not treated with either of the heavy metals and served as control. Each group of animals was allow free access to commercial rat mash and water for one week that the study lasted. After the 7 days experimentation, the results revealed a non-significant increase (P &gt; 0.05) in serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL) cholesterol and very low-density lipoprotein (VLDL) cholesterol in group 1 when compared to the control. A significant decrease in serum low-density lipoprotein (LDL) cholesterol (P &lt; 0.05) in group 1 was recorded when compared to the control. Groups 2 and 3 animals died 24 hours and 48 hours respectively after treatment. The implications of these results are discussed.

Mercury impairs human primary endometrial stromal cell function†.

Heavy metal exposures could compromise endometrial cells. Although studies assessed mercury toxicity in cell lines, limited data are available on the concentration of mercury that damage human endometrial stromal cells (hEnSCs) and alter endometrial function. This research aims to study the effects of mercury exposure on cell viability and functional features of hEnSCs. Primary hEnSCs were isolated from 23 endometrial biopsies obtained from healthy donors. After in vitro mercury exposure cell viability of hEnSCs was evaluated via tetrazolium salt metabolism and oxidative stress was assessed by 2', 7'-dichlorofluorescin diacetate assay. hEnSCs were decidualized in vitro in the presence of mercury (0, 25, 50, 75, 250, and 350 nM). Decidualization was evaluated based on prolactin and insulin-like growth factor-binding protein (IGFBP1) secretion and cytoskeletal rearrangement (F-actin staining). Cell proliferation and apoptosis were evaluated by Ki67 immunostaining and TUNEL assay. Mercury doses of 250 nM (P = 0.028) and 500 nM (P = 0.026) increased reactive oxygen species production in hEnSCs after 24 h. Cell viability significantly decreased after 48 h and 72 h (P < 0.05) of mercury exposure at 500 nM. After in vitro decidualization and mercury treatment, decidual hEnSCs showed a dose-dependent decrease in prolactin and IGFBP1 secretion, particularly at 350 nM (P = 0.016). Cell proliferation was decreased in hEnSCs treated with 350 nM mercury (P < 0.001); an increase in apoptosis followed a dose-dependent trend in non-decidual and decidual hEnSCs. These findings support that mercury-induced damage could be due to an increase in ROS production.

Civa klorür (HgCl2) uygulanan gökkuşağı alabalığı (Oncorhynchus mykiss) karaciğer dokusunda nitrozatif ve oksidatif stresin rolü

The aim of this study was to determine oxidative stress caused by mercury chloride (HgCl2) in rainbow trout (Oncorhynchus mykiss) liver tissue. For this purpose, the LD50 value of HgCl2 on rainbow trout was determined as 551 μg/L. In the study, 40 fish in four groups were exposed to 25% and 50% (138 and 276 µg/L) of the two subletal doses of HgCl2 for 2 and 7 days, with 10 fish (n=10) in each group. To determine oxidative stress; peroxynitrite (ONOO−), total oxidant level (TOS), total antioxidant level (TAS), oxidative stress index (OSI) and malondialdehyde (MDA) were analyzed. In the study, it was observed that the differences between the groups in terms of ONOO−, TOS, TAS and OSI levels in the liver tissues was significant (P&lt;0.05), however, this difference was not significant (P&gt;0.05) in terms of MDA values. As a result, it can be concluded that HgCl2 increases ONOO−, TOS, TAS, OSI and MDA levels in liver tissue and even small doses of mercury are toxic to fish.

Lead and mercury 28 day exposure at small concentrations reduces smooth muscle relaxation by decreasing cGMP

Cardiovascular diseases are among the main causes of mortality in the world. There is evidence of cardiovascular harm after exposure to low lead or mercury concentrations, but the effects of chronic exposure to the association of low doses of these toxic metals are still unknown. This work evaluated after 4 weeks, the association effects of low concentrations of lead and mercury on blood pressure and vascular resistance reactivity. Wistar rats were exposed for 28 days to lead acetate (1st dose of 4 μg/100 g and subsequent doses of 0.05 μg /100 g/day to cover daily losses) and mercury chloride (1st dose of 2.17 μg/kg and subsequent doses of 0.03 μg/kg/ day to cover daily losses) and the control group received saline, i.m. Results showed that treatment increased blood pressure and induced left ventricular hypertrophy. The mesenteric vascular reactivity to phenylephrine and the endothelium-dependent vasodilator response assessed by acetylcholine did not change. Additionally, reduced involvement of vasoconstrictor prostanoids derived from cyclooxygenase was observed in the PbHg group. By other regulatory routes, such as potassium channels, the vessel showed a greater participation of BKCa channels, and a reduction in the participation of Kv channels and SKCa channels. The endothelium-independent smooth muscle relaxation was significantly impaired by reducing cGMP, possibly through the hyperstimulation of Phosphodiesterase-5 (PDE5). Our results suggested that exposure to low doses of lead and mercury triggers this compensatory mechanism, in response to the augment of arterial pressure.

In Search of Sexual Health: Diagnosing and Treating Syphilis in Hot Springs, Arkansas, 1890–1940 by Elliott Bowen

Reviewed by: In Search of Sexual Health: Diagnosing and Treating Syphilis in Hot Springs, Arkansas, 1890–1940 by Elliott Bowen Sean Morey Smith In Search of Sexual Health: Diagnosing and Treating Syphilis in Hot Springs, Arkansas, 1890–1940. By Elliott Bowen. (Baltimore: Johns Hopkins University Press, 2020. Pp. xiv, 217. $49.95, ISBN 978-1-4214-3856-6.) In Search of Sexual Health: Diagnosing and Treating Syphilis in Hot Springs, Arkansas, 1890–1940 intervenes in the historiography of both medical tourism and venereal disease (VD) by examining these subjects in one location: Hot Springs, Arkansas. For half a century, more sufferers of syphilis traveled to Hot Springs than to all other treatment destinations in the United States combined. As Elliott Bowen argues, Hot Springs' unique location "played a key role in determining treatment norms, attitudes, and parameters around syphilis" (p. 2). Using sources written by patients and doctors, especially patient letters and case files, allows Bowen to write a bottom-up history of VD and its connection with health tourism. This perspective, Bowen argues, emphasizes the largely unexamined therapeutic aspects of medical tourism and also decenters government action in the history of VD treatment. Most crucially, this therapeutic perspective enables Bowen to demonstrate that the historiographical view of VD treatment as "'sin vs. science'" has overstated the separation between these positions (p. 15). This perspective also showcases the importance of medicine and therapy as located in a specific place. Bowen shows that, starting in the late nineteenth century, syphilis treatments in Hot Springs did not fit neatly into a medicine or morals binary. Though white men were generally the only people able to participate in such medical tourism, they received therapies alongside faith cures and hygienic behavioral regulations. The unique environment at Hot Springs also allowed for particular variations on the nationally accepted treatment for syphilis: mercury rubs. In Hot Springs, the heat of the spring waters allowed physicians to prescribe greater doses of mercury without them being fatal. Doctors continued to stress the importance of the local waters after the development of the first syphilis drug, Salvarsan. From the 1910s, they stressed both that the water cure was a time-tested tradition and that Hot Springs' waters worked best because they contained radium. Bowen also uses patient narratives from Army and Navy Hospital, which opened in Hot Springs in 1887, to demonstrate that syphilis diagnosis changed [End Page 541] less in the early twentieth century than previously believed. He traces greater patient openness in sharing sexual histories after 1910 to a change in policy, rather than a change in morality, and he rejects the common assumption that a "'laboratory revolution'" altered VD diagnosis (p. 77). Specifically, he shows that the Wassermann blood test, used to detect syphilis, was predominantly ordered only after patient histories pointed to a syphilis diagnosis. How physicians used syphilis to reinforce existing forms of racialization is a major theme running throughout In Search of Sexual Health. Bowen demonstrates that white doctors "carve[d] a color line through VD" in order to separate their mostly white clientele from stereotypes of African Americans as a "'syphilis-soaked race'" (pp. 53, 64). Physicians treated syphilis in African Americans solely as a physical disease and argued that African Americans' natural amorality rendered hygienic treatment inapplicable to them. White doctors, meanwhile, positioned their own work in terms of treating a disease caused by urbanism and over-civilization and thereby preventing the destruction of the white race. Race also affected the Depression-era VD efforts of the U.S. Public Health Service (PHS). For instance, the PHS opened Camp Garraday in 1935 solely for white men, a site where they could receive food, shelter, and medical care in an environment isolated from outside prejudice. While women as well as nonwhite men could receive aid, they were not granted the privacy of an isolated camp. Despite Bowen's emphasis on locality, the book perhaps engages less with the South than readers of this journal might expect. Jim Crow is mentioned, and race is an important theme. However, given that racial segregation existed in many forms throughout the country, Bowen could explicitly consider whether it took an especially southern form in Hot Springs...

Dietary exposure to mercury and its relation to cytogenetic instability in populations from “La Mojana” region, northern Colombia

Fish consumption and chronic exposure to low doses of mercury (Hg) seems to activate several molecular mechanisms leading to carcinogenic and/or teratogenic processes. However, Hg genotoxic effects on humans are not completely described. In the present study, we assessed cytogenetic damage in isolated human peripheral lymphocytes using the cytokinesis-block micronucleus cytome assay (CBMN-Cyt), micronucleus formation with anti-kinetochore antibody (CREST staining), levels of total Hg in hair (T-Hg), fish consumption, and estimated Hg dose. The study comprised 39 non-exposed, and 73 residents from La Mojana region, an area with a well-documented Hg contamination. Data showed a significant increase in micronuclei (MNBN), nucleoplasmic bridges (NPB), and necrotic and apoptotic cell frequencies in residents of “La Mojana.” The overall mean T-Hg level in hair for exposed residents was 1.12 ± 0.94 mg kg−1 and 0.15 ± 0.05 in individuals from the reference area. Approximately 40% of analyzed individuals showed T-Hg levels that exceeded US Environmental Protection Agency (USEPA) reference dose. Increased T-Hg levels in hair were related to increased MNBN frequencies and high fish consumption. Other cellular markers, such as necrotic and apoptotic cell frequencies, were also correlated with high fish intake and T-Hg contents. Results of the CREST staining demonstrated that in vivo exposure to Hg induces genetic instability by chromosome fragment loss (clastogenic). Additionally, a high average intake of some fish species, particularly with carnivorous habits like Caquetaia kraussii, Hoplias malabaricus, and Sorubin cuspicaudus, seems to increase MNBN frequencies significantly.

Simulation of Chronic Intoxication in Rats Exposed to Cadmium and Mercury

Cadmium and mercury are widespread and non-biodegradable pollutants of great concern to human and animal health. In this study, the influence of exposure to low doses of cadmium and mercury on Wistar rats was investigated. The experiments aimed to identify suitable markers of chronic intoxication with heavy metals in rats. The subjects were 48 naive young rats (24 females and 24 males), four weeks old, grouped randomly into three distinct groups—control group, group exposed to cadmium and group exposed to mercury. The control group received sham treatment—clean untreated water. Cd exposed group received water containing cadmium chloride dihydrate and Hg exposed group received water with mercury dichloride. Both cadmium and mercury were administered to experimental rats in drinking water in concentrations exceeding the maximum acceptable concentration of these metals 500 times, i.e., 0.5 mg Hg and 2.5 mg Cd per liter of water. The results were evaluated quarterly during the experiment (52 weeks). Selected physiological parameters (life span, body weight changes and intake of food and water), reproductive parameters (number of births (litters), number of born pups and number of raised pups) and toxicological parameters (average daily dose, total dose received and the amount of toxic metal received) were studied. The results of the experiments indicate differences between both individual groups and between males and females, which confirmed that these parameters are essential in such experiments of chronic exposure to subtoxic doses of heavy metals.

Assessment of the Dependence of Mercury Intake into the Human Body on the Peculiarities of the Human Diet. Estimation of Intake of Small and Ultra-Low Doses of Mercury in the Human Body with Food

Assessment of the Dependence of Mercury Intake into the Human Body on the Peculiarities of the Human Diet. Estimation of Intake of Small and Ultra-Low Doses of Mercury in the Human Body with Food

Environmental Factors and Pollution Stresses Select Bacterial Populations in Association With Protists

Digestion-resistant bacteria (DRB) refer to the ecological bacterial group that can be ingested, but not digested by protistan grazers, thus forming a specific type of bacteria-protist association. To test the hypothesis that the environment affects the assembly of DRB in protists, a mixotrophic ciliate, Paramecium bursaria, and a heterotrophic ciliate, Euplotes vannus, were reared at different temperatures, light conditions, and concentration gradients of antibiotic oxytetracycline and heavy metals. Community profiling indicated that the composition of DRB in both species varied significantly across the manipulated conditions, except for in P. bursaria under light/dark treatments. Clone library analysis of bacterial 16S rRNA genes showed that DRB were diverse. Pseudomonas became more abundant during the warmer treatment of P. bursaria, whereas the dominance of Pseudoalteromonas weakened and Vibrio became more abundant in E. vannus at a higher temperature. During the treatment of diel light:dark cycles, Aestuariibacter and Alteromonas were selected for in E. vannus but not Pseudoalteromonas, which was highly represented in the all-light and alldark treatments. In contrast, P. bursaria consistently hosted Nevskia, Curvibacter, and Asticcacaulis under all light conditions. There were many bacterial species co-resistant to oxytetracycline and to protistan digestion, in which Sphingomonas, Alteromonas, Aestuariibacter, Puniceicoccaceae (Verrucomicrobia), Pseudomonas, and Sulfitobacter were frequently abundant. Flectobacillus and Aestuariibacter were major lead-resistant bacteria associated with the studied protists. Acinetobacter and Hydrogenophaga were abundant in the P. bursaria treated with a high dose of mercury. Aestuariibacter was found as a dominant group of DRB in E. vannus across all cadmium treatments. In summary, this study demonstrates for the first time that environmental stress selects for bacterial populations associated with protists and that there are diverse bacterial species that not only are resistant to pollution stresses but can also survive protistan predation. This work highlights that bacteria-protists associations need to be taken into account in understanding ecological and environmental issues, such as resilience of bacterial community and function, microbial co-occurrence, and quantity and distribution of antibiotic resistant bacteria and genes.

Investigation of the potential human health risk of toxic mercury determined in the grapevine exposed to mine gallery waters

In the present study, mercury was selected because of its toxicity. It was detected in the grapevines exposed to mine gallery waters. The potentialhealth risk of mercury in leaves of grapevine those are consumed by human worldwide was investigated. The grapevines were harvested and separated into organs of roots, stems, and leaves. The concentrations of mercury were determined in roots, stems, and leaves. The translocation and bioconcentration factors were calculated. Maximum concentrations of mercury were stem < root < leaf. The health risk potential of mercury on human health was calculated. The estimated daily exposure doses of mercury followed an order for children and adults: dietary > ingestion > inhalation > dermal. The HQ values calculated for exposure ways of dietary, ingestion and inhalation were male < female < children. As a result, it was determined that grapevine exposed to mine gallery waters that cause environmental contamination may cause non-carcinogenic risks on human health.

Inorganic mercury‑induced MIP‑2 expression is suppressed by N‑acetyl‑L‑cysteine in RAW264.7 macrophages

Macrophages play an important role in neurotoxicity caused by methylmercury exposure through inflammatory responses. Methylmercury is known to demethylate to inorganic mercury in the brain, and macrophages are likely to be involved in this process. However, the inflammatory responses of macrophages against exposure to inorganic mercury are unclear. In the present study, inflammatory cytokine expression profiles were examined in the presence of non-toxic doses of inorganic mercury (Hg2+) using RAW264.7 macrophages, focusing on the expression of C-X-C motif chemokine 2 (MIP-2)/platelet-derived growth factor-inducible protein KC (KC) and C-C motif chemokine 12 (MCP-5). Furthermore, the suppressive effect of N-acetyl-L-cysteine (NAC) on inorganic mercury-induced MIP-2 expression was also examined. Inorganic mercury-induced mRNA expression was measured using reverse transcription-quantitative PCR. The mRNA expression of MIP-2 and MCP-5 was significantly upregulated by exposure to 20 µM Hg2+ (non-toxic levels), but not that of KC. The suppressive effect of NAC on these cytokine expression levels was examined by its addition to the culture medium together with Hg2+ (co-treatment), and pre- and post-treatments in which the cells were treated with NAC before and after Hg2+ exposure, respectively. Hg2+-upregulated MIP-2 expression was suppressed by NAC regardless of the time sequence of the treatment, suggesting that the suppressive role of NAC in Hg2+-induced inflammation manifests as a possible chelator and antioxidant/reactive oxygen species scavenger.

Atomic absorption determination of mercury in urine by cold steam method using mercury- hydride prefix

Mercury is one of the most common in various industries and at the same time dangerous chemicals. It is able to be deposited in the body and have a toxic effect for a long time after the cessation of contact. Under the influence of mercury, workers can develop various intoxications, as a result of which pathological changes in the nervous, cardiovascular, endocrine, immune and reproductive systems are possible.Under production conditions, mercury enters the body, usually in the form of vapors (absorbed about 80%) and suspended particles. Inorganic forms of mercury are excreted mainly in the urine (60%). However, insufficient attention is currently being paid to the problem of determining the mercury content in urine samples. To date, in world practice there is no systematic approach to the determination of small doses of mercury in the body, as a result of which it is difficult to timely identify public health disorders. This is largely due to the lack of highly sensitive and highly effective methods of analysis, allowing routine measurements with minimal cost and high accuracy. The methods currently used are either quite expensive or have low accuracy/sensitivity.The aim of the study was to develop a method of atomic absorption determination of mercury in urine by cold steam, which would allow at minimal cost to increase the accuracy and sensitivity of mercury detection in the body.Materials and methods. Quantitative measurement of mercury in urine samples was carried out on an atomic absorption spectrometer with a mercury-hydride prefix using model solutions of different concentrations.Results. The study determined the optimal conditions for sample preparation of urine samples, set the range of concentrations for the construction of the calibration schedule, studied the effect of the matrix on the accuracy of the analysis by the “introduced-found” method. The lower limit of detection of the developed technique was 0.05 mcg/l, the upper limit–100 mcg/l (if necessary, it can be increased by additional dilution). The relative error of determination depending on the concentration varied from 3 to 15%.Conclusions. A highly sensitive, affordable and relatively inexpensive method for the determination of mercury in urine has been developed, which will allow to diagnose with high accuracy the background contents of mercury in urine, which is especially important when inspecting workers of industries associated with the use of mercury and its compounds, as well as the population living in areas close to these industries.