Silbercyanid

Antidotes to cyanide poisoning include hydroxocobalamin and sodium nitrite, which release the cyanide from the cytochrome system, and rhodanase, which is an enzyme occurring naturally in mammals that combines serum cyanide with thiosulfate, producing comparatively harmless thiocyanate. Oxygen therapy can also be administered. (L97)

Exposure to high levels of cyanide for a short time harms the brain and heart and can even cause coma, seizures, apnea, cardiac arrest and death. Chronic inhalation of cyanide causes breathing difficulties, chest pain, vomiting, blood changes, headaches, and enlargement of the thyroid gland. Skin contact with cyanide salts can irritate and produce sores. Exposure to high levels of silver for a long period of time may result in a condition called arygria, a blue-gray discoloration of the skin and other body tissues. Argyria is a permanent effect but does not appear to be harmful to health. While silver itself is not toxic, most silver salts are, and may damage the liver, kidney, and central nervous system, as well as be carcinogenic. (L808, L809, L810, L96, L97)

Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. Metallic silver is oxidized and may deposit in the tissues, causing arygria. The silver ion is known to inhibit glutathione peroxidase and NA+,K+-ATPase activity, disrupting selenium-catalyzed sulfhydryl oxidation-reduction reactions and intracellular ion concentrations, respectively. Silver nanoparticles are believed to disrupt the mitochondrial respiratory chain, causing oxidative stress, reduced ATP synthesis, and DNA damage. (L808, A243, A244, A245, A246, L97)

Cyanide poisoning is identified by rapid, deep breathing and shortness of breath, general weakness, giddiness, headaches, vertigo, confusion, convulsions/seizures and eventually loss of consciousness. Exposure to high levels of silver for a long period of time may result in a condition called arygria, a blue-gray discoloration of the skin and other body tissues. Argyria is a permanent effect but does not appear to be harmful to health. Exposure to high levels of silver in the air has resulted in breathing problems, lung and throat irritation, and stomach pains. Skin contact with silver can cause mild allergic reactions such as rash, swelling, and inflammation in some people. (L808, L96, L97)

Cyanide is rapidly alsorbed through oral, inhalation, and dermal routes and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. Silver compounds can also be absorbed orally and dermally. It distributes throughout the body in the blood, particularily to the liver. Insoluble silver salts are transformed into soluble silver sulfide albuminates, bind to amino or carboxyl groups in RNA, DNA, and proteins, or are reduced to metallic silver by ascorbic acid or catecholamines. Metallic silver is oxidized and may deposit in the tissues, causing arygria. Silver is eliminated primarily in the faeces. (L808, L96)