Nickel

About: Nickel is a research topic. Over the lifetime, 79308 publications have been published within this topic receiving 1210058 citations. The topic is also known as: Ni & element 28.

Bioavailability of Nickel in Single‐Wall Carbon Nanotubes

Abstract: The world-wide nanotechnology movement is devoting a rapidly growing literature on biological interactions of carbon nanotubes (CNTs), however the conflicting data have emerged about the biocompatibility and toxicity of carbon nanotubes, and there is no consensus on the overall risk to human health (Hurt et al., 2006; Smart et al., 2006). To resolve this issue, further study is needed, with particular emphasis on understanding the material features of carbon nanotubes, such as size, shape, surface chemistry, and metals content, and we hypothesize that some of the conflicting toxicity data are due to real sample-to-sample variation in these material properties. It is also unclear whether carbon nanotube catalyst residues can trigger these toxicity mechanisms due to apparent encapsulation of the nickel within carbon shells. Nickel, the majority component in Ni-Y catalysts commonly used in the commercial synthesis of single-wall nanotubes (SWNTs) (Journet et al. 1997), is an established human carcinogen that induces gene silencing and hypoxia signaling through mechanisms involving intracellular nickel cation. The early toxicology literature includes nickle effects in SWNT by Lam et al, nickel nanoparticles and mostly nickel compounds such as nickel subsulfide (Lam et al. 2004; Zhang et al. 1998; Costa et al. 2005). Models of nickel induced respiratory tumors suggests that cellular bioavailability of nickel (the delivery of Ni (II) ions to the nucleus of target epithelial cells) is the major determinant for the carcinogenicity of nickel. A key material science question, therefore, is whether sufficient Ni (II) ion can be released from CNT samples. Moreover, the ability of various nickel compounds to be taken up by cells directly influences intracellular nickel levels, and their carcinogenic activity is proportional to cellular uptake(Oller et al., 1997; Costa et al., 1980). Soluble nickel ions can be transported directly, and insoluble or relatively insoluble nickel compounds can be taken up as particles by endocytosis or phagocytosis. Phagocytosis/endocytosis of poorly soluble nickel compounds such as Ni

Occurrence, physiological responses and toxicity of nickel in plants

Abstract: The focus of the review is on the specific aspects of nickel’s effects on growth, morphology, photosynthesis, mineral nutrition and enzyme activity of plants The mobility of nickel in the environment and the consequent contamination in soil and water is of great concern Also, the detrimental effects of excessive nickel on plant growth have been well known for many years Toxic effects of nickel on plants include alterations in the germination process as well as in the growth of roots, stems and leaves Total dry matter production and yield was significantly affected by nickel and also causes deleterious effects on plant physiological processes, such as photosynthesis, water relations and mineral nutrition Nickel strongly influences metabolic reactions in plants and has the ability to generate reactive oxygen species which may cause oxidative stress More recent evidence indicates that nickel is required in small amounts for normal plant growth and development Hence, with the increasing level of nickel pollution in the environment, it is essential to understand the functional roles and toxic effects of nickel in plants

Exploring the molecular mechanisms of nickel-induced genotoxicity and carcinogenicity: a literature review.

Abstract: Nickel, a naturally occurring element that exists in various mineral forms, is mainly found in soil and sediment, and its mobilization is influenced by the physicochemical properties of the soil. Industrial sources of nickel include metallurgical processes such as electroplating, alloy production, stainless steel, and nickel-cadmium batteries. Nickel industries, oil- and coal-burning power plants, and trash incinerators have been implicated in its release into the environment. In humans, nickel toxicity is influenced by the route of exposure, dose, and solubility of the nickel compound. Lung inhalation is the major route of exposure for nickel-induced toxicity. Nickel can also be ingested or absorbed through the skin. The primary target organs are the kidneys and lungs. Other organs such as the liver, spleen, heart, and testes can also be affected to a lesser extent. Although the most common health effect is an allergic reaction, research has also demonstrated that nickel is carcinogenic to humans. The focus of the present review is on recent research concerning the molecular mechanisms of nickel-induced genotoxicity and carcinogenicity. We first present a background on the occurrence of nickel in the environment, human exposure, and human health effects.