Toxicology and metabolism of nickel compounds. Progress report, December 1, 1974--November 30, 1975. [97433ONE]

• Main Author: Sunderman, F.W. Jr.
• Language: unknown
• Published: 2014
• Subjects: 59 BASIC BIOLOGICAL SCIENCES; AMIDES; BIOLOGICAL EFFECTS; CARBAMATES; ERYTHROCYTES; ABUNDANCE; KIDNEYS; PATHOLOGY; MANGANESE; NICKEL COMPOUNDS; METABOLISM; TOXICITY; PENICILLAMINE; TETA; THIOCTIC ACID; CARCINOGENESIS; EXCRETION; HAMSTERS; HYPERGLYCEMIA; RATS; AMINES; AMINO ACIDS; ANIMALS; BIOLOGICAL MATERIALS; BLOOD; BLOOD CELLS; BODY; BODY FLUIDS; CARBONIC ACID DERIVATIVES; CARBOXYLIC ACID SALTS; CARBOXYLIC ACIDS; CHELATING AGENTS; CLEARANCE; DISULFIDES; DRUGS; ELEMENTS; HETEROCYCLIC ACIDS; HETEROCYCLIC COMPOUNDS; LIPOTROPIC FACTORS; MAMMALS; METALS; ORGANIC ACIDS; ORGANIC COMPOUNDS; ORGANIC NITROGEN COMPOUNDS; ORGANIC SULFUR COMPOUNDS; ORGANS; PATHOGENESIS; RADIOPROTECTIVE SUBSTANCES; RESPONSE MODIFYING FACTORS; RODENTS; Carbonic acid
• Online Access: http://www.osti.gov/servlets/purl/7299576; https://www.osti.gov/biblio/7299576; https://doi.org/10.2172/7299576

The toxicology and metabolism of nickel compounds (NiCl/sub 2/, Ni/sub 3/S/sub 2/, NiS, and Ni powder) were investigated in rats and hamsters. The new knowledge has included: demonstration that hyperglucagonemia is primarily responsible for the acute hyperglycemic effect of parenteral Ni(II) in rats; demonstration that parenteral injection of Ni(II) in rats produces acute nephropathy with proteinuria and amino aciduria, and with ultrastructural lesions of renal glomeruli and tubules; confirmation of the inhibitory effect of manganese upon the carcinogenicity of Ni/sub 3/S/sub 2/ after intramuscular injection in rats, and elucidation of the effects of manganese upon the rates of excretion of nickel, and upon the acute histological reactions produced by Ni/sub 3/S/sub 2/; discovery that the antidotal efficacy of triethylenetetramine (TETA) in acute Ni(II) poisoning in rats is substantially greater than that of other chelating agents, including .cap alpha.-lipoic acid, diethyldithiocarbamate, d-penicillamine, and glycylglycyl-L-histidine-N-methylamide; observation that the acute renal toxicity of Ni(II) is suppressed by administration of TETA, but that the hyperglycemic and hyperglucagonemic responses to Ni(II) are not prevented by TETA; confirmation that marked erythrocytosis is induced in rats by a single intrarenal injection of Ni/sub 3/S/sub 2/, and elucidation of the time-response and dose-response relationships for the Ni-induced erythrocytosis. (auth)