Nickel mineral allergy, toxicity, side effects
January 15 2016 by Ray Sahelian, M.D.
Nickel is an important mineral constituent of stainless steel. Nickel also plays key role in the chemical and aerospace industries. Leading producers include Australia, Canada, Norway and Russia. Large reserves of nickel are found in Australia, Cuba, New Caledonia, Canada, Indonesia, the Philippines, and Russia.
Nickel is one of the most common causes of a skin rash that occurs due to contact with an allergen. This type of rash, allergic contact dermatitis, can be caused by nickel in jewelry, a patient's diet, nickel in a medical implant or nickel in a medication that's applied to the skin. Typically, an allergic reaction to this metal occurs in an area of skin that comes into contact with an item such as a necklace, belt buckle, zipper, eyeglass frames or cellphone.
Topical Tacrolimus for Nickel Allergy
Protopic, also known as tacrolimus 0.1 percent ointment, suppresses the signs and symptoms of skin allergy resulting in contact dermatitis among individuals who are sensitive to nickel and who continue to be exposed to this metal. Allergic contact dermatitis -- characterized by inflammation, rash, itching and blistering -- is one of the most common occupationally related conditions in the United States, costing an estimated $1 billion annually due to lost work, reduced productivity, medical care and disability payments. Nickel induces allergic reactions in roughly 5.8 percent of the U.S. population, making it an appropriate model for studying allergic contact dermatitis.
Dalton Trans. 2013. Quinolones and non-steroidal anti-inflammatory drugs interacting with copper, nickel, cobalt and zinc: structural features, biological evaluation and perspectives. The structural features of copper(II), nickel(II), cobalt (II) and zinc (II) complexes with the antimicrobial drugs quinolones and non-steroidal anti-inflammatory drugs (NSAIDs) as ligands are discussed. The binding properties of these complexes to biomolecules (calf-thymus DNA, bovine or human serum albumin) are presented and evaluated. The biological activity (antimicrobial, antioxidant and antiproliferative) of selected complexes is investigated. Further perspectives concerning the synthesis and the biological activity of novel complexes with quinolones or NSAIDs attractive to synthetic chemists, biochemists and/or biologists are presented.
Biochem Biophys Res Commun. 2015. Nickel inhibits mitochondrial fatty acid oxidation. Nickel exposure is associated with changes in cellular energy metabolism which may contribute to its carcinogenic properties. Here, we demonstrate that nickel strongly represses mitochondrial fatty acid oxidation-the pathway by which fatty acids are catabolized for energy-in both primary human lung fibroblasts and mouse embryonic fibroblasts. At the concentrations used, nickel suppresses fatty acid oxidation without globally suppressing mitochondrial function as evidenced by increased glucose oxidation to CO2. Pre-treatment with l-carnitine, previously shown to prevent nickel-induced mitochondrial dysfunction in neuroblastoma cells, did not prevent the inhibition of fatty acid oxidation.