Highly efficient removal of metal ion pollutants, such as toxic and nuclear waste-related metal ions, remains a serious task from the biological and environmental standpoint because of their harmful effects on human health and the environment. Recently, highly porous metal–organic frameworks (MOFs), with excellent chemical stability and abundant functional groups, have represented a new addition to the area of capturing various types of hazardous metal ion pollutants. This review focuses on recent progress in reported MOFs and MOF-based composites as superior adsorbents for the efficient removal of toxic and nuclear waste-related metal ions. Aspects related to the interaction mechanisms between metal ions and MOF-based materials are systematically summarized, including macroscopic batch experiments, microscopic spectroscopy analysis, and theoretical calculations. The adsorption properties of various MOF-based materials are assessed and compared with those of other widely used adsorbents. Finally, we propose our personal insights into future research opportunities and challenges in the hope of stimulating more researchers to engage in this new field of MOF-based materials for environmental pollution management.

Metal–organic framework-based materials: superior adsorbents for the capture of toxic and radioactive metal ions

Arsenic, cadmium, lead, and mercury are toxic elements that are almost ubiquitously present at low levels in the environment because of anthropogenic influences. Dietary intake of plant-derived food represents a major fraction of potentially health-threatening human exposure, especially to arsenic and cadmium. In the interest of better food safety, it is important to reduce toxic element accumulation in crops. A molecular understanding of the pathways responsible for this accumulation can enable the development of crop varieties with strongly reduced concentrations of toxic elements in their edible parts. Such understanding is rapidly progressing for arsenic and cadmium but is in its infancy for lead and mercury. Basic discoveries have been made in Arabidopsis, rice, and other models, and most advances in crops have been made in rice. Proteins mediating the uptake of arsenic and cadmium have been identified, and the speciation and biotransformations of arsenic are now understood. Factors controlling the efficiency of root-to-shoot translocation and the partitioning of toxic elements through the rice node have also been identified.

Toxic Heavy Metal and Metalloid Accumulation in Crop Plants and Foods

Multiple functions of p21 in cell cycle, apoptosis and transcriptional regulation after DNA damage.

Arsenic-induced oxidative stress and its reversibility

Transition metal ions are key elements of various biological processes ranging from oxygen formation to hypoxia sensing, and therefore, their homeostasis is maintained within strict limits through tightly regulated mechanisms of uptake, storage and secretion. The breakdown of metal ion homeostasis can lead to an uncontrolled formation of reactive oxygen species, ROS (via the Fenton reaction, which produces hydroxyl radicals), and reactive nitrogen species, RNS, which may cause oxidative damage to biological macromolecules such as DNA, proteins and lipids. An imbalance between the formation of free radicals and their elimination by antioxidant defense systems is termed oxidative stress. Most vulnerable to free radical attack is the cell membrane which may undergo enhanced lipid peroxidation, finally producing mutagenic and carcinogenic malondialdehyde and 4-hydroxynonenal and other exocyclic DNA adducts. While redox-active iron (Fe) and copper (Cu) undergo redox-cycling reactions, for a second group of redox-inactive metals such as arsenic (As) and cadmium (Cd), the primary route for their toxicity is depletion of glutathione and bonding to sulfhydryl groups of proteins. While arsenic is known to bind directly to critical thiols, other mechanisms, involving formation of hydrogen peroxide under physiological conditions, have been proposed. Redox-inert zinc (Zn) is the most abundant metal in the brain and an essential component of numerous proteins involved in biological defense mechanisms against oxidative stress. The depletion of zinc may enhance DNA damage by impairing DNA repair mechanisms. Intoxication of an organism by arsenic and cadmium may lead to metabolic disturbances of redox-active copper and iron, with the occurrence of oxidative stress induced by the enhanced formation of ROS/RNS. Oxidative stress occurs when excessive formation of ROS overwhelms the antioxidant defense system, as is maintained by antioxidants such as ascorbic acid, alpha-tocopherol, glutathione (GSH), carotenoids, flavonoids and antioxidant enzymes which include SOD, catalase and glutathione peroxidase. This review summarizes current views regarding the role of redox-active/inactive metal-induced formation of ROS, and modifications to biomolecules in human disease such as cancer, cardiovascular disease, metabolic disease, Alzheimer's disease, Parkinson's disease, renal disease, blood disorders and other disease. The involvement of metals in DNA repair mechanisms, tumor suppressor functions and interference with signal transduction pathways are also discussed.

Redox- and non-redox-metal-induced formation of free radicals and their role in human disease.

Arsenic (As) is a toxic metalloid element that is present in air, water and soil. Inorganic arsenic tends to be more toxic than organic arsenic. Examples of methylated organic arsenicals include monomethylarsonic acid [MMA(V)] and dimethylarsinic acid [DMA(V)]. Reactive oxygen species (ROS)-mediated oxidative damage is a common denominator in arsenic pathogenesis. In addition, arsenic induces morphological changes in the integrity of mitochondria. Cascade mechanisms of free radical formation derived from the superoxide radical, combined with glutathione-depleting agents, increase the sensitivity of cells to arsenic toxicity. When both humans and animals are exposed to arsenic, they experience an increased formation of ROS/RNS, including peroxyl radicals (ROO•), the superoxide radical, singlet oxygen, hydroxyl radical (OH•) via the Fenton reaction, hydrogen peroxide, the dimethylarsenic radical, the dimethylarsenic peroxyl radical and/or oxidant-induced DNA damage. Arsenic induces the formation of oxidized lipids which in turn generate several bioactive molecules (ROS, peroxides and isoprostanes), of which aldehydes [malondialdehyde (MDA) and 4-hydroxy-nonenal (HNE)] are the major end products. This review discusses aspects of chronic and acute exposures of arsenic in the etiology of cancer, cardiovascular disease (hypertension and atherosclerosis), neurological disorders, gastrointestinal disturbances, liver disease and renal disease, reproductive health effects, dermal changes and other health disorders. The role of antioxidant defence systems against arsenic toxicity is also discussed. Consideration is given to the role of vitamin C (ascorbic acid), vitamin E (α-tocopherol), curcumin, glutathione and antioxidant enzymes such as superoxide dismutase, catalase and glutathione peroxidase in their protective roles against arsenic-induced oxidative stress.

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Arsenic: toxicity, oxidative stress and human disease.

OBJECTIVE To induce, evaluate and classify advanced stages of mammary gland tumours induced by MNU. METHODS Female Sprague-Dawley rats were injected intraperitoneally with 1-methyl-1-nitrosourea (MNU; 50 mg.kg-1) on the day 33, 40, 47, 54 and 61 of age in the first experiment and on 50th and 113th day in the second experiment. On the 117th day (first experiment) and on the 153rd day of age (second experiment) the rats were sacrificed by decapitation and their mammary glands were evaluated both macroscopically and microscopically for the presence of grossly detectable mammary tumours. Mammary tumours were classified according to Russo et al. (1990). RESULTS AND CONCLUSIONS The final incidence of palpable carcinomas was ranging from 60 % to 76 %. All microscopically evaluated tumours were malignant. Among the total number of lesions classified the percentage of invasive tumours ranged from 35 % to 44 %. No metastases were observed in other organs in MNU treated animals.

Histopathology of mammary tumours in female rats treated with 1-methyl-1-nitrosourea.

Classification of thyroid tumours and their variants is described with special respect to some recent findings on somatic mutations characteristics which are associated with individual types of malignity. Special attention is paid to the interrelations between thyroid nodules and malignity and predictive risk factors are listed. For details see .

Thyroid tumors: histological classification and genetic factors involved in the development of thyroid cancer.

A 26-week oral toxicity and micronucleus assays of the new cardioprotective drug stobadine (CAS 95751-51-2), in the form of dipalmitate salt (DP 1031) were performed in Wistar rats of both sexes. DP 1031 was administered daily orally in doses of 7.07, 23.60 and 70.07 mg/kg. Physical appearance and general behaviour of the treated animals were normal, with a small deviation (hypoactivity in the highest dose group at the start of experiment). Food and water consumption as well as body weight gain exhibited similar values in the control and experimental groups of animals. No drug-related changes were noted in the haematological, biochemical, histopathological and genotoxicological examinations. Neither sex differences nor dose-related changes were noted under these conditions.

Chronic toxicity and micronucleus assay of the new cardioprotective agent stobadine in rats

Expression of nuclear hormone receptors, their coregulators and type I iodothyronine 5'-deiodinase gene in mammary tissue of nonlactating and postlactating rats.

Líska J

Papers

Arsenic: toxicity, oxidative stress and human disease.

Histopathology of mammary tumours in female rats treated with 1-methyl-1-nitrosourea.

Thyroid tumors: histological classification and genetic factors involved in the development of thyroid cancer.

Chronic toxicity and micronucleus assay of the new cardioprotective agent stobadine in rats

Expression of nuclear hormone receptors, their coregulators and type I iodothyronine 5'-deiodinase gene in mammary tissue of nonlactating and postlactating rats.