Toxic and nutrient elements in yerba mate (Ilex paraguariensis).

Toxic and nutrient elements were investigated in yerba mate (Ilex paraguariensis) from South America. Fifty-four brands of commercialised yerba mate from Argentina, Brazil, Paraguay and Uruguay were analysed for Al, Ba, Ca, Cu, Fe, K, Mg, Mn, P, Sr, and Zn, using inductively coupled plasma optical emission spectrometry (ICP-OES), and Li, Be, Ti, V, Cr, Ni, Co, As, Se, Rb, Mo, Ag, Cd, Sb, La, Ce, Pb, Bi and U using inductively coupled plasma mass spectrometry (ICP-MS). Antimony, Se, Ag and Bi were not detected in any sample whereas the limits of detection (LODs) of these elements were 0.19, 0.40, 0.003 and 0.001 µg g(-1), respectively. Analysis of variance (ANOVA) revealed that the concentrations of Cd, Ti, Ni, As, Mo, U, Li and Be in yerba mate were not statistically different with regard to the country of origin, while those of the other investigated elements differed.

Behavioral, clinical, and pathological characterization of acid metalliferous water toxicity in mallards.

From September to November 2000, United States Fish and Wildlife Service biologists investigated incidents involving 221 bird deaths at 3 mine sites located in New Mexico and Arizona. These bird deaths primarily involved passerine and waterfowl species and were assumed to be linked to consumption of acid metalliferous water (AMW). Because all of the carcasses were found in or near pregnant leach solution ponds, tailings ponds, and associated lakes or storm water retention basins, an acute-toxicity study was undertaken using a synthetic AMW (SAMW) formulation based on the contaminant profile of a representative pond believed to be responsible for avian mortalities. An acute oral-toxicity trial was performed with a mixed-sex group of mallards (Anas platyrhynchos). After a 24-h pretreatment food and water fast, gorge drinking was evident in both SAMW treatment and control groups, with water consumption rates greatest during the initial drinking periods. Seven of nine treated mallards were killed in extremis within 12 h after the initiation of dose. Total lethal doses of SAMW ranged from 69.8 to 270.1 mL/kg (mean ± SE 127.9 ± 27.1). Lethal doses of SAMW were consumed in as few as 20 to 40 min after first exposure. Clinical signs of SAMW toxicity included increased serum uric acid, aspartate aminotransferase, creatine kinase, potassium, and P levels. PCV values of SAMW-treated birds were also increased compared with control mallards. Histopathological lesions were observed in the esophagus, proventriculus, ventriculus, and duodenum of SAMW-treated mallards, with the most distinctive being erosion and ulceration of the kaolin of the ventriculus, ventricular hemorrhage and/or congestion, and duodenal hemorrhage. Clinical, pathological, and tissue-residue results from this study are consistent with literature documenting acute metal toxicosis, especially copper (Cu), in avian species and provide useful diagnostic profiles for AMW toxicity or mortality events. Blood and kidney Cu concentrations were 23- and 6-fold greater, respectively, in SAMW mortalities compared with controls, whereas Cu concentrations in liver were not nearly as increased, suggesting that blood and kidney concentrations may be more useful than liver concentrations for diagnosing Cu toxicosis in wild birds. Based on these findings and other reports of AMW toxicity events in wild birds, we conclude that AMW bodies pose a significant hazard to wildlife that come in contact with them.

[Metallic elements in 31st updating of 67/548/EEC directive]. / Gli elementi metallici nel trentunesimo adeguamento della Direttiva 67/548/CEE.

In this paper the update of directive 67/548/EEC published in Official Journal of the European Union on 16 January 2009 proposes about carcinogenicity of metallic elements is reported and discussed. The main change is represented by the classification R49 and R40 of many species of nickel, organic and inorganic, respectively for their water solubility and particles size. Titanium oxide and 3 tin species are in addition classified as R40. Sodium dichromate moved from R49 (in the 22nd update) to R45 (classified as carcinogen, without restriction on the route of exposure). The list of the 31st updates, if combined with previous list, provides detailed and more precise information on the carcinogenicity of metallic elements in relation to different species, suggesting once again the importance of metallic element speciation.

Carcinogenic metal compounds: recent insight into molecular and cellular mechanisms.

Mechanisms of carcinogenicity are discussed for metals and their compounds, classified as carcinogenic to humans or considered to be carcinogenic to humans: arsenic, antimony, beryllium, cadmium, chromium, cobalt, lead, nickel and vanadium. Physicochemical properties govern uptake, intracellular distribution and binding of metal compounds. Interactions with proteins (e.g., with zinc finger structures) appear to be more relevant for metal carcinogenicity than binding to DNA. In general, metal genotoxicity is caused by indirect mechanisms. In spite of diverse physicochemical properties of metal compounds, three predominant mechanisms emerge: (1) interference with cellular redox regulation and induction of oxidative stress, which may cause oxidative DNA damage or trigger signaling cascades leading to stimulation of cell growth; (2) inhibition of major DNA repair systems resulting in genomic instability and accumulation of critical mutations; (3) deregulation of cell proliferation by induction of signaling pathways or inactivation of growth controls such as tumor suppressor genes. In addition, specific metal compounds exhibit unique mechanisms such as interruption of cell-cell adhesion by cadmium, direct DNA binding of trivalent chromium, and interaction of vanadate with phosphate binding sites of protein phosphatases.

[Mechanisms of action for metallic elements and their species classified carcinogen R 45 and R 49 by EU]. / Meccanismi di azione per gli elementi metallici e loro specie classificati cancerogeni R45 ed R49 dall'UE--parte 2.

In this paper we will deal with mechanism of carcinogenic action of metallic elements and their species (arsenic, beryllium, cadmium, cobalt, chromium, nickel) identified by EU as carcinogen R 45 or R 49. The carcinogenic effect depended on the ability of to penetrate the cell and interacted with the target sites, therefore the state of oxidation, charging, the solubility, type of binding, stereochemistry and the ability to interact with other xenobiotics were crucial. The carcinogenic metallic elements classified R45 or R49 are essentially weak mutagen and do not form adducts with the DNA as initial step of their carcinogenicity In spite of the wide range of metallic elements physicochemical properties, some common general mechanisms of carcinogenesis emerge:from the induction of oxidative stress, to inhibition of DNA repair, from activation of mitogenic signalling, to epigenetic modification of gene expression. However, each species lead to specific molecular interactions and were subject to different bioavailability. It has been also strongly supported the hypothesis that the metallic elements may act as a co-carcinogen with other organic compounds, for example with PAH.