Calcium liver damage

Soriano, M.E., Nicolosi, L., and Bernardi, P., 2004, Desensitization of the permeability transition pore by cyclosporin A prevents activation of the mitochondrial apoptotic pathway and liver damage by tumor necrosis factor-alpha, J. Biol. Chem. 279, pp. 36803-36808 Sparagna, G.C., Gunter, K. K., Sheu, S. S., and Gunter, T. E., 1995, Mitochondrial calcium uptake from physiological-type pulses of calcium. A description of the rapid uptake mode, J. Biol. Chem. 270, pp. 27510-27515... 

Although cell injury results in increased calcium, which causes a variety of damaging effects, the cause and effect relationship of calcium in cell damage is not known. The chemicals that cause liver damage by this mechanism include quinines, peroxides, acetaminophen, iron, and cadmium. 

Shifting of the calcium gradient between the intracellular and extracellular space (normally 1 10,000) results in significant metabolic dysfunctions as well as cholestasis, especially in alcohol-induced liver damage. 

Calcium carbimide has been linked to liver damage (3) (SED-12,1244), but caution is needed in attributing liver damage in alcoholic patients to drugs. 

Ethylene glycol poisoning can canse acidosis, central nervous system depression, pulmonary edema, acute oliguric renal failure with crystalluria, liver damage due to calcium oxalate deposition, nausea, abdominal pain, and cramping, acute colonic ischemia (29), and papilledema and abducens nerve palsy (30). 

The combination present in the laxative Doxidan of dioctyl calcium sulphosuccinate with danthron (1,8-hydroxyanthraquinone) has again been shown to be associated with liver injury almost certainly due to facilitated absorption of the anthraqui-none(24 ). Chronic active hepatitis associated with the use of oxyphenisatin also often occurs in patients whose laxative is combined with dioctyl sulphosuccinates (DSS) (25, 26 ), usuaJly the sodium salt. DSS is excreted in the bile and is toxic in vitro to cultured liver tumour cells (27 -). Oxyphenisatin-induced liver damage may well be promoted by concurrent administration of DSS but chronic active hepatitis can develop during use of oxyphenisatin alone, and challenge with oxyphenisatin alone has induced hepatitis (31). 

In addition to the well-known iron effects on peroxidative processes, there are also other mechanisms of iron-initiated free radical damage, one of them, the effect of iron ions on calcium metabolism. It has been shown that an increase in free cytosolic calcium may affect cellular redox balance. Stoyanovsky and Cederbaum [174] showed that in the presence of NADPH or ascorbic acid iron ions induced calcium release from liver microsomes. Calcium release occurred only under aerobic conditions and was inhibited by antioxidants Trolox C, glutathione, and ascorbate. It was suggested that the activation of calcium releasing channels by the redox cycling of iron ions may be an important factor in the stimulation of various hepatic disorders in humans with iron overload. 

Adults require 1-2 mg of copper per day, and eliminate excess copper in bile and feces. Most plasma copper is present in ceruloplasmin. In Wilson s disease, the diminished availability of ceruloplasmin interferes with the function of enzymes that rely on ceruloplasmin as a copper donor (e.g. cytochrome oxidase, tyrosinase and superoxide dismutase). In addition, loss of copper-binding capacity in the serum leads to copper deposition in liver, brain and other organs, resulting in tissue damage. The mechanisms of toxicity are not fully understood, but may involve the formation of hydroxyl radicals via the Fenton reaction, which, in turn initiates a cascade of cellular cytotoxic events, including mitochondrial dysfunction, lipid peroxidation, disruption of calcium ion homeostasis, and cell death. 

Displaces calcium in bone matter Impacts production of new blood cells Damages liver and kidneys Shock... 

Monitoring Observe for blood dyscrasias, liver or kidney damage, or idiosyncratic reactions. Perform frequent serum electrolyte, calcium, glucose, uric acid, CO2,... 

The common target structures for the various causes of acute liver failure are usually the cellular and subcellular biomembranes of the hepatocytes. Among other things, any damage to these biomembranes causes a massive inflow of calcium into the liver cells, which results in a severe disorder of the cell milieu and ultimately in cell death. 

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