Biological monitoring of environmental pollution and human exposure to some trace elements

The extent of environmental pollution and resulting human exposure to hazardous toxic chemicals in the environment is often difficult to assess. One of the possible alternative approaches to this problem is the use of the biological indicators to demonstrate environmental pollution. This approach appears to be particularly suitable for demonstrating exposure to potentially toxic trace elements. In addition to analyses of plant and animal specimens the element content of human hair as an indicator of exposures to arsenic, mercury, cadmium, lead, antimony, manganese, nickel and cobalt has been repeatedly confirmed as reliable, provided the analyses were carried out and evaluated on group diagnostic basis and were done in groups of individuals occupationally not exposed to these metals. Preferably groups of 10-year-old children are to be used when only environmental pollution is to be taken into account. Hair samples are incomparably easier to collect, transport and store than the alternative biological material such as blood and urine used commonly to demonstrate exposure to various toxic agents. Biological monitoring of environmental pollution cannot replace the standard procedures of measuring air, water and soil pollution; however, the technique appears to have the potential of being an effective tool search for the extent of environmental pollution and for delimitation of territorial boundaries of areas affected most by hazardous emissions containing potentially toxic trace elements.     

Cadmium and copper inhibit both DNA repair activities of polynucleotide kinase

Human exposure to heavy metals is of increasing concern due to their well-documented toxicological and carcinogenic effects and rising environmental levels through industrial processes and pollution. It has been widely reported that such metals can be genotoxic by several modes of action including generation of reactive oxygen species and inhibition of DNA repair. However, although it has been observed that certain heavy metals can inhibit single strand break (SSB) rejoining, the effects of these metals on SSB end-processing enzymes has not previously been investigated. Accordingly, we have investigated the potential inhibition of polynucleotide kinase (PNK)-dependent single strand break repair by six metals: cadmium, cobalt, copper, nickel, lead and zinc. It was found that micromolar concentrations of cadmium and copper are able to inhibit the phosphatase and kinase activities of PNK in both human cell extracts and purified recombinant protein, while the other metals had no effect at the concentrations tested. The inhibition of PNK by environmentally and physiologically relevant concentrations of cadmium and copper suggests a novel means by which these toxic heavy metals may exert their carcinogenic and neurotoxic effects.     

New aspects on the distribution and metabolism of essential trace elements after dietary exposure to toxic metals

Under present environmental conditions, an increase in pollution owing to metals such as cadmium (Cd), lead (Pb), and methylmercury (MeHg) must be expected. The resulting effects would be seen particularly in the food chain. The daily intake of toxic metals in various parts of the world is different and depends on both the dietary habits and the concentration in foodstuffs. Oral ingestion of these toxic metals perturbs the metabolism of essential elements, especially zinc (Zn), copper (Cu), iron (Fe), and selenium (Se). The elemental composition of body tissues and fluids is an indicator of the nutritional and pathological status of humans. This review will describe the dietary intake and gut absorption of essential and toxic elements. Furthermore, it will discuss threshold values, toxic effects in relation to body burden of toxic metals, the biological indices of exposure, and the interaction between toxic and essential elements. The overall ratio of Cu, Zn, Fe, and Se concentration to Cd in the human kidney is the lowest in comparison to Hg and Pb. Increased kidney copper and urinary losses may be common denominators in the manifestation of renal toxicity induced by heavy metals. Factors affecting availability and loss of copper should be identified and measured. The critical kidney concentration for Cd, Pb, and MeHg should be revised in relation to essential elements.     

A Review on Heavy Metals Contamination in Soil: Effects,Sources, and Remediation Techniques

Soil heavy metal pollution has become a worldwide environmental issue that has attracted considerable public attention, largely from the increasing concern for the security of agricultural products. Heavy metals refer to some metals and metalloids possessing biological toxicity, such as cadmium, mercury, arsenic, lead, and chromium. These elements enter the soil agro-ecosystem through natural processes derived from parent materials, and through anthropogenic activities. Heavy metal pollution poses a great threat to the health and well-being of organisms and human beings due to potential accumulation risk through the food chain. Remediation using chemical, physical, and biological methods has been adopted to solve the problem. Phytoremediation has proven to be a promising alternative to conventional approaches as it is cost effective, environmentally friendly, and aesthetically pleasing. To date, based on the natural ability of extraction, approximately 500 taxa have been identified as hyperaccumulators of one or more metals. In addition, further research integrating biotechnological approaches with comprehensive multidisciplinary research is needed to improve plant tolerance and reduce the accumulation of toxic metals in soils. This review discusses harmful effects, sources of heavy metals, and the remediation technologies for soil contaminated by heavy metals.     

Levels of Arsenic, Cadmium, Lead, Manganese and Zinc in Biological Samples of Paralysed Steel Mill Workers with Related to Controls

The determination of essential trace and toxic elements in the biological samples of human beings is an important clinical screening procedure. This study aimed to assess the possible effects of environmental exposure on paralysed male workers (n?=?75) belonging to the production and quality control departments of a steel mill. In this investigation, the concentrations of arsenic, cadmium, lead, manganese and zinc were determined in biological samples (blood, urine and scalp hair samples) of exposed paralysis and non-paralysed steel mill workers. For comparative purposes, unexposed healthy subjects of same age group were selected as referents. The elements in the biological samples were measured by atomic absorption spectrophotometry prior to microwave-assisted acid digestion. The validity of the methodology was checked by the biological certified reference materials. The results indicate that the level understudy elements in all three biological samples were significantly higher in paralysed workers of both groups (quality control and production) as compared to referents (p?相似文献   

Metal Toxicity Links to Alzheimer's Disease and Neuroinflammation

As the median age of the population increases, the number of individuals with Alzheimer's disease (AD) and the associated socio-economic burden are predicted to worsen. While aging and inherent genetic predisposition play major roles in the onset of AD, lifestyle, physical fitness, medical condition, and social environment have emerged as relevant disease modifiers. These environmental risk factors can play a key role in accelerating or decelerating disease onset and progression. Among known environmental risk factors, chronic exposure to various metals has become more common among the public as the aggressive pace of anthropogenic activities releases excess amount of metals into the environment. As a result, we are exposed not only to essential metals, such as iron, copper, zinc and manganese, but also to toxic metals including lead, aluminum, and cadmium, which perturb metal homeostasis at the cellular and organismal levels. Herein, we review how these metals affect brain physiology and immunity, as well as their roles in the accumulation of toxic AD proteinaceous species (i.e., β-amyloid and tau). We also discuss studies that validate the disruption of immune-related pathways as an important mechanism of toxicity by which metals can contribute to AD. Our goal is to increase the awareness of metals as players in the onset and progression of AD.     

Metallothionein induction in human peripheral blood lymphocytes by heavy metals

Human peripheral blood lymphocytes have the capacity to produce metallothioneins (MTs) as a protective response to cadmium exposure. To define the range of metal species inducing lymphocyte MTs, cellular proteins synthesized after exposure to each of 11 heavy metals were analyzed by gel electrophoresis. Toxic metals such as cadmium, mercury and silver were found to induce thioneins (apoproteins of MTs) at relatively low concentrations (maximum at approximately 10 microM), whereas less toxic metals such as zinc, copper and nickel were inductive at relatively high concentrations (maximum at approximately 200 microM). Tin, lead, iron, cobalt, and manganese did not induce thioneins. The heavy metal specificity of MT induction in the lymphocyte resembles that in the liver, and the regulatory mechanism of MT production seems to be similar in both of these tissues. In the cells exposed to highly toxic metals such as cadmium and mercury, expression of cytotoxicity (represented by decline of cysteine uptake) was remarkable at the metal concentrations higher than those saturating thionein induction, supporting the protective role of MTs against heavy metals.     

The effects of 17beta-estradiol and ethanol on zinc- or manganese-induced toxicity in SK-N-SH cells

Serious neurodegenerative disorders are increasingly prevalent in our society and excessive oxidative stress may be a key mediator of neuronal cell death in many of these conditions. A variety of metals, such as manganese and zinc, are essential trace elements but can reach localized toxic concentrations through various disease processes or environmental exposures and have been implicated as having a role in neurodegeneration. Both manganese and zinc exist as bivalent cations and are essential cofactors/activators for numerous enzymes. Evidence suggests one action of these metals, when concentrated beyond physiological levels, may be to inhibit cellular energy production, ultimately leading to increased radical formation. Our studies were undertaken to directly investigate the toxic effects of manganese and zinc in an immortalized neuronal-like cell line (SK-N-SH) by testing interactions with the antioxidant, 17beta-estradiol, and the neurotoxin, ethanol. Employing undifferentiated SK-N-SH cells, we found that these metals caused biphasic effects, enhancing cell proliferation at low doses and inducing cell death at higher doses. Zinc was both more efficacious and more potent than manganese in enhancing growth and in causing cell death. 17beta-Estradiol and ethanol enhanced the proliferative actions of zinc and manganese across a wide concentration range. Furthermore, co-treatment with either 17beta-estradiol or ethanol afforded protection against manganese-, but not zinc-induced toxicity. Finally, combined administration of 17beta-estradiol and ethanol to SK-N-SH cells resulted in both a loss of growth enhancement and protective properties that were observed when these substances were administered individually. We also noted that the toxic effects occurred more rapidly from zinc than manganese exposure. Taken together, these data suggest that oxidative stress likely has a role in cell death resulting from toxic exposure to either zinc or manganese, but there is a difference in the precise mechanism of their effects.     

Exposure to nickel, chromium, or cadmium causes distinct changes in the gene expression patterns of a rat liver derived cell line

Many heavy metals, including nickel (Ni), cadmium (Cd), and chromium (Cr) are toxic industrial chemicals with an exposure risk in both occupational and environmental settings that may cause harmful outcomes. While these substances are known to produce adverse health effects leading to disease or health problems, the detailed mechanisms remain unclear. To elucidate the processes involved in the toxicity of nickel, cadmium, and chromium at the molecular level and to perform a comparative analysis, H4-II-E-C3 rat liver-derived cell lines were treated with soluble salts of each metal using concentrations derived from viability assays, and gene expression patterns were determined with DNA microarrays. We identified both common and unique biological responses to exposure to the three metals. Nickel, cadmium, chromium all induced oxidative stress with both similar and unique genes and pathways responding to this stress. Although all three metals are known to be genotoxic, evidence for DNA damage in our study only exists in response to chromium. Nickel induced a hypoxic response as well as inducing genes involved in chromatin structure, perhaps by replacing iron in key proteins. Cadmium distinctly perturbed genes related to endoplasmic reticulum stress and invoked the unfolded protein response leading to apoptosis. With these studies, we have completed the first gene expression comparative analysis of nickel, cadmium, and chromium in H4-II-E-C3 cells.     

Transition metal homeostasis: from yeast to human disease

Transition metal ions are essential nutrients to all forms of life. Iron, copper, zinc, manganese, cobalt and nickel all have unique chemical and physical properties that make them attractive molecules for use in biological systems. Many of these same properties that allow these metals to provide essential biochemical activities and structural motifs to a multitude of proteins including enzymes and other cellular constituents also lead to a potential for cytotoxicity. Organisms have been required to evolve a number of systems for the efficient uptake, intracellular transport, protein loading and storage of metal ions to ensure that the needs of the cells can be met while minimizing the associated toxic effects. Disruptions in the cellular systems for handling transition metals are observed as a number of diseases ranging from hemochromatosis and anemias to neurodegenerative disorders including Alzheimer??s and Parkinson??s disease. The yeast Saccharomyces cerevisiae has proved useful as a model organism for the investigation of these processes and many of the genes and biological systems that function in yeast metal homeostasis are conserved throughout eukaryotes to humans. This review focuses on the biological roles of iron, copper, zinc, manganese, nickel and cobalt, the homeostatic mechanisms that function in S. cerevisiae and the human diseases in which these metals have been implicated.     

Heavy metals in some Chinese herbal plants

The concentrations of nine heavy metals, cadmium, cobalt, copper, iron, manganese, nickel, lead, zinc and mercury in 42 Chinese herbal medicinal plants were determined. Generally, all the samples studied had, relative to the other trace metals, higher concentrations of iron, manganese, and zinc. The concentration range of the metals determined was comparable to that in many of the East Asian vegetables and fruits. A few samples were found to contain relatively higher concentrations of the toxic metals such as cadmium, lead, and mercury. This was probably caused by contamination during air-drying and preservation.     

Cadmium toxicity: Effects on cytoskeleton,vesicular trafficking and cell wall construction

Cadmium is a well-known environmental pollutant with distinctly toxic effects on plants. It can displace certain essential metals from a wealth of metalloproteins, and thus disturb many normal physiological processes and cause severe developmental aberrant. The harmful effects of cadmium stress include, but are not limited to: reactive oxygen species overproduction, higher lipid hydroperoxide contents, and chloroplast structure change, which may lead to cell death. Plants have developed diverse mechanisms to alleviate environmental cadmium stress, e.g., cadmium pump and transporting cadmium into the leaf vacuoles. This mini-review focuses on the current research into understanding the cellular mechanisms of cadmium toxicity on cytoskeleton, vesicular trafficking and cell wall formation in plants.     

The Effects of Chronic Lifelong Activation of the AHR Pathway by Industrial Chemical Pollutants on Female Human Reproduction

Environmental chemicals, such as heavy metals, affect female reproductive function. A biological sensor of the signals of many toxic chemical compounds seems to be the aryl hydrocarbon receptor (AHR). Previous studies demonstrated the environmental of heavy metals in Taranto city (Italy), an area that has been influenced by anthropogenic factors such as industrial activities and waste treatments since 1986. However, the impact of these elements on female fertility in this geographic area has never been analyzed. Thus, in the present study, we evaluated the AHR pathway, sex steroid receptor pattern and apoptotic process in granulosa cells (GCs) retrieved from 30 women, born and living in Taranto, and 30 women who are living in non-contaminated areas (control group), who were undergoing in vitro fertilization (IVF) protocol. In follicular fluids (FFs) of both groups the toxic and essential heavy metals, such as chromiun (Cr), Manganese (Mn), iron (Fe), cobalt (Co), nickel (Ni), copper (Cu), zinc (Zn), cadmium (Cd) and lead (Pb), were also analyzed. Higher levels of Cr, Fe, Zn and Pb were found in the FFs of the women from Taranto as compared to the control group, as were the levels of AHR and AHR-dependent cytochrome P450 1A1 and 1B1; while CYP19A1 expression was decreased. The anti-apoptotic process found in the GCs of women fromTaranto was associated with the highest levels of progesterone receptor membrane component 1 (PGRMC1), a novel progesterone receptor, the expression of which is subjected to AHR activated by its highest affinity ligands (e.g., dioxins) or indirectly by other environmental pollutants, such as heavy metals. In conclusion, decreased production of estradiol and decreased number of retrieved mature oocytes found in women from Taranto could be due to chronic exposure to heavy metals, in particular to Cr and Pb.     

Adverse health effects in Canada geese (Branta canadensis) associated with waste from zinc and lead mines in the Tri-State Mining District (Kansas, Oklahoma, and Missouri, USA)

Lead and zinc poisoning have been recorded in a variety of bird species, including migrating waterfowl such as Canada Geese (Branta canadensis), at sites contaminated with mine waste from lead and zinc mines in the Tri-State Mining District, Kansas, Oklahoma, and Missouri, USA. The adverse health impacts from mine waste on these birds may, however, be more extensive than is apparent from incidental reports of clinical disease. To characterize health impacts from mine waste on Canada Geese that do not have observable signs of poisoning, four to eight apparently healthy birds per site were collected from four contaminated sites and an uncontaminated reference site, and examined for physical and physiologic evidence of metals poisoning. Tissue concentrations of silver, aluminum, arsenic, barium, cadmium, cobalt, chromium, copper, iron, magnesium, manganese, molybdenum, nickel, lead, selenium, thallium, vanadium, and zinc were determined by inductively coupled plasma mass spectroscopy. Adverse health effects due to lead were characterized by assessing blood δ-aminolevulinic acid dehydratase (ALAD) enzyme activity. Adverse effects associated with zinc poisoning were determined from histologic examination of pancreas tissues. Elevated tissue lead concentrations and inhibited blood ALAD enzyme activities were consistently found in birds at all contaminated sites. Histopathologic signs of zinc poisoning, including fibrosis and vacuolization, were associated with elevated pancreatic zinc concentrations at one of the study sites. Adverse health effects associated with other analyzed elements, or tissue concentrations indicating potentially toxic exposure levels to these elements, were not observed.     

Effect of DMT1 knockdown on iron,cadmium, and lead uptake in Caco-2 cells

DMT1 (divalent metal transporter 1) is ahydrogen-coupled divalent metal transporter with a substrate preferencefor iron, although the protein when expressed in frog oocytestransports a broad range of metals, including the toxic metals cadmiumand lead. Wild-type Caco-2 cells displayed saturable transport of leadand iron that was stimulated by acid. Cadmium and manganese inhibitedtransport of iron, but zinc and lead did not. The involvement of DMT1in the transport of toxic metals was examined by establishing clonalDMT1 knockdown and control Caco-2 cell lines. Knockdown cell linesdisplayed much lower levels of DMT1 mRNA and a smaller V_max for iron uptake compared with control celllines. One clone was further characterized and found to display an~50% reduction in uptake of iron across a pH range from 5.5 to 7.4. Uptake for cadmium also decreased 50% across the same pH range, butuptake for lead did not. These results show that DMT1 is important in iron and cadmium transport in Caco-2 cells but that lead enters thesecells through an independent hydrogen-driven mechanism.

     

Modulations in antioxidant enzymes in different tissues of marine bivalvePerna viridis during heavy metal exposure

Lipid peroxidation induced by metals at sub-lethal levels, alter physiological and biochemical characteristics of biological systems. To counter the detrimental effects of the prooxidant activity of metals, a group of antioxidant enzyme systems function in the organisms. The present study was performed to investigate into the lipid peroxidation product formation due to the exposure to effects of the metals namely aluminium, lead and cadmium at sub-lethal concentrations and the biological response through protective antioxidant enzyme activity in the marine mussels,Perna viridis Lin. This organism is a known bioindicator and bioconcentrator of metals in the environment.The results of the present study were: (a) accumulation of lead showed a definite linear increase during the period of exposure whereas aluminium and cadmium showed fluctuations. Mantle and gill tissues showed greater accumulation of metals when compared to digestive gland; (b) lead and aluminium induced lipid peroxidation was greater in tissues than the peroxidation induced by cadmium. Cadmium induced peroxidation was observed only after the day 7 of the exposure; (c) anti-oxidant enzymes activity levels were significantly higher in digestive gland and mantle than gills; (d) mantle was observed to significantly contribute to the organismal response to lipid peroxidation as indicated by high activity levels of anti-oxidant enzymes.     

Comparative and interactive effects of mercury, cadmium and lead on tissue GSH levels in Oreochromis aureus (Steindachner): implications for monitoring heavy metal pollution

The effects of 45 days exposure to mercury, cadmium and lead on tissue GSH levels were studied in Oreochromis aureus (Steindachner). Liver, brain, gill filaments, intestine and caudal muscle were assayed after exposure to these heavy metals singly, or in combination. Significant increases in intestinal GSH concentrations consistently occurred after exposure to mixtures of heavy metals. Exposure to cadmium or lead did not change hepatic GSH levels, while exposure to two different concentrations of mercury caused significant increases in hepatic GSH.     

Disease-toxicant screen reveals a neuroprotective interaction between Huntington's disease and manganese exposure

Recognizing the similarities between Huntington's disease (HD) pathophysiology and the neurotoxicology of various metals, we hypothesized that they may exhibit disease-toxicant interactions revealing cellular pathways underlying neurodegeneration. Here, we utilize metals and the ST Hdh mouse striatal cell line model of HD to perform a gene–environment interaction screen. We report that striatal cells expressing mutant Huntingtin exhibit elevated sensitivity to cadmium toxicity and resistance to manganese toxicity. This neuroprotective gene–environment interaction with manganese is highly specific, as it does not occur with iron, copper, zinc, cobalt, cadmium, lead, or nickel ions. Analysis of the Akt cell stress signaling pathway showed diminished activation with manganese exposure and elevated activation after cadmium exposure in the mutant cells. Direct examination of intracellular manganese levels found that mutant cells have a significant impairment in manganese accumulation. Furthermore, YAC128Q mice, a HD model, showed decreased total striatal manganese levels following manganese exposure relative to wild-type mice. Thus, this disease-toxicant interaction screen has revealed that expression of mutant Huntingtin results in heightened sensitivity to cadmium neurotoxicity and a selective impairment of manganese accumulation.