Two luminescent Cd(II)-organic frameworks Cd
(L1)(tdc)
(H
O)
(1) and Cd(L2)
(tdc)
(2) (L1 = 1,5-bis(1-(pyridine-4-ylmethyl)-1
-benzo
imidazol-2-yl)pentane, L2 = 1,6-bis(1-(pyridine-4-ylmethyl)-1
...-benzo
imidazol-2-yl)hexane, and H
tdc = 2,5-thiophenedicarboxylic acid) were hydrothermally synthesized and characterized. 1 displays a rare binodal (3,4)-connected 2D cem-d network, while 2 exhibits a 3D mog (moganite) framework. The two MOFs are highly thermally durable and water-stable in a wide pH range from 3 to 12. Interestingly, 1 and 2 represent the first reported examples of multi-responsive probes based on MOFs for selectively detecting levofloxacin, benzaldehyde, and Fe
ions with reusability. The luminescence sensing mechanisms of the two CPs were explored in detail.
La población en general y en particular las mujeres embarazadas están expuestas a diferentes metales, entre los que se encuentra el talio (Tl), además se reportó que existe relación causal entre la ...concentración de talio en muestras de orina y sangre de mujeres embarazadas con parto prematuro y bajo peso al nacer. En modelos in vivo se demostró que el talio atraviesa la placenta y produce anormalidades externas y óseas en fetos de hembras tratadas con acetato de talio (CH3COOTl). En linfocitos cultivados in vitro se encontró que compuestos de este metal producen efectos genotóxicos y citotóxicos. Por lo que el objetivo de este trabajo fue evaluar el posible efecto genotóxico y citotóxico en los fetos y en las hembras tratadas durante la organogénesis con CH3COOTl. Se emplearon tres grupos de cuatro ratonas CD-1 preñadas: grupo I testigo (0.1 mL H2O/10 g de peso corporal), grupos II y III tratados con CH3COOTl (5.28 y 6.16 mg/Kg respectivamente), los tratamientos se administraron ip los días 6, 8, 10, 12, 14 y 16 de gestación. El efecto citotóxico se evaluó con la relación de eritrocitos policromáticos (EPC) presentes en 2000 eritrocitos totales y viabilidad celular; el efecto genotóxico se evaluó contando eritrocitos policromáticos micronucleados (EPC-MN) obtenidos de sangre periférica de las hembras y los fetos. El manejo de los organismos se realizó de acuerdo con la NOM-062ZOO-1999. El proyecto fue aprobado por el Comité de Ética de la FESZaragoza. Los resultados mostraron que las hembras tratadas con la dosis de 5.28 mg/Kg presentaron aumento del número de EPCMN en todas las horas de muestreo, el número de EPC no mostró diferencias significativas. En los fetos aumentó el número de EPC-MN en ambas dosis. La viabilidad celular fue superior al 97% en las hembras y los fetos. El CH3COOTl fue genotóxico para las hembras y los fetos sin ocasionar citotoxicidad. Proyecto financiado PAPIIT/UNAM No. IN229220.
The first health effects of cadmium (Cd) were reported already in 1858. Respiratory and gastrointestinal symptoms occurred among persons using Cd-containing polishing agent. The first experimental ...toxicological studies are from 1919. Bone effects and proteinuria in humans were reported in the 1940's. After World War II, a bone disease with fractures and severe pain, the itai-itai disease, a form of Cd-induced renal osteomalacia, was identified in Japan. Subsequently, the toxicokinetics and toxicodynamics of Cd were described including its binding to the protein metallothionein. International warnings of health risks from Cd-pollution were issued in the 1970's. Reproductive and carcinogenic effects were studied at an early stage, but a quantitative assessment of these effects in humans is still subject to considerable uncertainty. The World Health Organization in its International Program on Chemical Safety, WHO/IPCS (1992) (Cadmium. Environmental Health Criteria Document 134, IPCS. WHO, Geneva, 1–280.) identified renal dysfunction as the critical effect and a crude quantitative evaluation was presented. In the 1990's and 2000 several epidemiological studies have reported adverse health effects, sometimes at low environmental exposures to Cd, in population groups in Japan, China, Europe and USA (reviewed in other contributions to the present volume). The early identification of an important role of metallothionein in cadmium toxicology formed the basis for recent studies using biomarkers of susceptibility to development of Cd-related renal dysfunction such as gene expression of metallothionein in peripheral lymphocytes and autoantibodies against metallothionein in blood plasma. Findings in these studies indicate that very low exposure levels to cadmium may give rise to renal dysfunction among sensitive subgroups of human populations such as persons with diabetes.
Practically all human populations are environmentally exposed to cadmium (Cd), mostly through plant-derived food. A growing body of epidemiological evidence suggests that there is no margin of safety ...between current Cd exposure levels and the threshold for adverse health effects and, hence, there is an urgent need to lower human Cd intake. Here we review recent studies on rice (Oryza sativa) and Cd-hyperaccumulating plants that have led to important insights into the processes controlling the passage of Cd from the soil to edible plant organs. The emerging molecular understanding of Cd uptake, root retention, root-to-shoot translocation and grain loading will enable the development of low Cd-accumulating crops.
More than one and a half centuries ago, adverse human health effects were reported after use of a cadmium-containing silver polishing agent. Long-term cadmium exposure gives rise to kidney or bone ...disease, reproductive toxicity and cancer in animals and humans. At present, high human exposures to cadmium occur in small-scale mining, underlining the need for preventive measures. This is particularly urgent in view of the growing demand for minerals and metals in global climate change mitigation. This review deals with a specific part of cadmium toxicology that is important for understanding when toxic effects appear and, thus, is crucial for risk assessment. The discovery of the low-molecular-weight protein metallothionein (MT) in 1957 was an important milestone because, when this protein binds cadmium, it modifies cellular cadmium toxicity. The present authors contributed evidence in the 1970s concerning cadmium binding to MT and synthesis of the protein in tissues. We showed that binding of cadmium to metallothionein in tissues prevented some toxic effects, but that metallothionein can increase the transport of cadmium to the kidneys. Special studies showed the importance of the Cd/Zn ratio in MT for expression of toxicity in the kidneys. We also developed models of cadmium toxicokinetics based on our MT-related findings. This model combined with estimates of tissue levels giving rise to toxicity, made it possible to calculate expected risks in relation to exposure. Other scientists developed these models further and international organizations have successfully used these amended models in recent publications. Our contributions in recent decades included studies in humans of MT-related biomarkers showing the importance of MT gene expression in lymphocytes and MT autoantibodies for risks of Cd-related adverse effects in cadmium-exposed population groups. In a study of the impact of zinc status on the risk of kidney dysfunction in a cadmium-exposed group, the risks were low when zinc status was good and high when zinc status was poor. The present review summarizes this evidence in a risk assessment context and calls for its application in order to improve preventive measures against adverse effects of cadmium exposures in humans and animals.
•We model chronic ingestion of environmental lead and cadmium in axenic mice.•We addressed the role of the microbiota in heavy-metal dissemination in organs.•We delineate the direct impact of the ...non-absorbed heavy metals on gut homeostasis.•We measure transport- and oxidative-gene expression in intestine.•It enlightens risk assessment of heavy metals in intestinal disease's susceptibility.
Environmental exposure to pollutants such as heavy metal(s) is responsible for various altered physiological functions which are detrimental for health. The gut microbiota is critical for intestinal homeostasis but its role on xenobiotic handling is not fully understood, especially when continuous sub-chronic exposure is addressed. We first confirmed the essential role of the intestinal microbiome to limit heavy metal body burden by using germ-free mice following 6-weeks oral exposure. Significant increases of cadmium and lead absorption and dissemination in blood and target organs were measured in germ-free mice when compared with conventional specific pathogen free (SPF) mice. Besides the “barrier” function of the luminal microbiota, this may involve specific host-genes such as metallothioneins, which are differentially expressed in the gastrointestinal tract of each group of mice. Considering genes relevant for divalent metal transporters and oxidative pathways, significant differences in basal gene expression were measured between control and germ-free mice. Moreover, the magnitude of induction of these genes upon stimulation by heavy metals varied greatly depending on the dose and type of metal as well as the microbial status of the animal. Collectively, these data illustrate the complex host-microbes interplay occurring with environmental pollutants inside the gut.
Cadmium is a widespread toxic pollutant of occupational and environmental concern because of its diverse toxic effects: extremely protracted biological half-life (approximately 20-30 years in ...humans), low rate of excretion from the body and storage predominantly in soft tissues (primarily, liver and kidneys). It is an extremely toxic element of continuing concern because environmental levels have risen steadily due to continued worldwide anthropogenic mobilization. Cadmium is absorbed in significant quantities from cigarette smoke, food, water and air contamination and is known to have numerous undesirable effects in both humans and animals. Cadmium has a diversity of toxic effects including nephrotoxicity, carcinogenicity, teratogenicity and endocrine and reproductive toxicities. At the cellular level, cadmium affects cell proliferation, differentiation, apoptosis and other cellular activities. Current evidence suggests that exposure to cadmium induces genomic instability through complex and multifactorial mechanisms. Most important seems to be cadmium interaction with DNA repair mechanism, generation of reactive oxygen species and induction of apoptosis. In this article, we have reviewed recent developments and findings on cadmium toxicology.
•Cadmium toxicity arises from the bioavailability and bioaccumulation of Cd2+ ions.•Different cadmium compounds show different levels of bioavailability.•Ion availability for absorption is determined ...by its release in biological fluids.•This release (bioaccessibility) can be measured and used to inform in vivo studies.•In vitro analysis of bioaccessibility supports the estimation of bioavailability and potential for target tissue toxicity.
Cadmium toxicity occurs where there is absorption and accumulation of cadmium ions (Cd2+) in tissues beyond tolerable levels. Significant differences in the release of Cd2+ from cadmium compounds in biological fluids, like gastric fluid, may indicate differences in bioavailability and absorption. This means that direct read-across from high solubility cadmium compounds to lower solubility compounds may not accurately reflect potential hazards. Here, the relative bioaccessibility in gastric fluid of cadmium telluride and cadmium chloride was evaluated using in vitro bioelution tests whilst the toxicokinetic behavior of these two compounds were compared after dietary administration for 90 days in male and female Wistar Han rats following OECD TG 408. Cadmium chloride was highly bioaccessible, whilst cadmium telluride showed low solubility in simulated gastric fluid (90 % and 1.5 % bioaccessibility, respectively). This difference in bioaccessibility was also reflected by a difference in bioavailability as shown by the difference in the liver and kidney concentrations of cadmium after repeat oral exposure. Feeding at doses of 750 and 1500 ppm of cadmium telluride did not result in tissue cadmium levels above the lower limit of quantification (LLOQ). In contrast, feeding with a lower test substance concentration yet higher concentration of bioaccessible cadmium (30 ppm cadmium chloride) resulted in tissue accumulation of cadmium. Only slight, non-adverse changes in hematology and clinical chemistry parameters were seen at these doses, indicating an absence of significant cadmium mediated toxicity towards target organs (kidney and liver), reflected in minimal cadmium accumulation in these organs.
This study demonstrates that bioelution tests can help determine the bioaccessibility of cadmium, which can be used to estimate the potential for target tissue toxicity based on known toxicokinetic profiles and threshold levels for cadmium toxicity, while reducing and refining animal testing.
Cadmium (Cd) is a highly hepatotoxic heavy metal, which is widely dispersed in the environment. Acute Cd hepatotoxicity has been well studied in experimental animals; however, effects of prolonged ...exposure to Cd doses on the liver remain unclear. In the present study, to evaluate chronic Cd hepatotoxicity, we examined specimens from cases of itai-itai disease, the most severe form of chronic Cd poisoning. We compared 89 cases of itai-itai disease with 27 control cases to assess Cd concentration in organs. We also examined 80 cases of itai-itai disease and 70 control cases for histopathological evaluation. In addition, we performed immunohistochemistry for metallothionein, which binds and detoxifies Cd. Hepatic Cd concentration was higher than Cd concentration in all other organs measured in the itai-itai disease group, whereas it was second highest following renal concentration in the control group. In the liver in the itai-itai disease group, fibrosis was observed at a significantly higher rate than that in the control group. Metallothionein expression was significantly higher in the itai-itai disease group than that in the control group. Prolonged exposure to low doses of Cd leads to high hepatic accumulation, which can then cause fibrosis; however, it also causes high expression of metallothionein, which is thought to reduce Cd hepatotoxicity.
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