Kidney copper excess

Vitamin C [ascorbic acid) Men 90 mg/d Women 75 mg/d Cofactor for reactions requiring reduced copper or iron met-alloenzyme and as a protective antioxidant prevents scurvy Gastrointestinal disturbances, kidney stones, excess iron absorption... 

Excess copper is the result of either excessive copper absorption or ineffective copper excretion. The most common diseases associated with copper excess are (1) Wilson s disease, a genetic disease resulting in mutations in the Wilson s disease P-type ATPase and excessive hepatocyte copper accumulation (2) renal disease, in patients on hemodialysis due to kidney failure when dialysate solutions become contaminated with excess copper and (3) biliary obstruction. Excessive use of copper supplements may also contribute to copper toxicity and is clinically manifested by severe anemia, nausea and vomiting, abdominal pain, and diarrhea. 

Copper is an essential trace element. It is required in the diet because it is the metal cofactor for a variety of enzymes (see Table 50—5). Copper accepts and donates electrons and is involved in reactions involving dismu-tation, hydroxylation, and oxygenation. However, excess copper can cause problems because it can oxidize proteins and hpids, bind to nucleic acids, and enhance the production of free radicals. It is thus important to have mechanisms that will maintain the amount of copper in the body within normal hmits. The body of the normal adult contains about 100 mg of copper, located mostly in bone, liver, kidney, and muscle. The daily intake of copper is about 2—A mg, with about 50% being absorbed in the stomach and upper small intestine and the remainder excreted in the feces. Copper is carried to the liver bound to albumin, taken up by liver cells, and part of it is excreted in the bile. Copper also leaves the liver attached to ceruloplasmin, which is synthesized in that organ. 

An excess of zinc will cause problems in humans. Excessive doses can lead to biochemical control system damage, while doses slightly higher than optimal can cause disorders in iron and copper metabolism, resulting in incurable anemia, decrease in activity of zinc protein enzymes, and pancreas and kidney damage (Boularbah et ah, 1999 Seiler et ah, 1994). Increased levels of zinc have been observed in nuclei of neoplastic cells and in cases of acute dental caries, however its role in these diseases has not been explained. 

Copper (Cu) Synthesis of hemoglobin Food supply Toxicity is very rare, deficiency - anemia excess - liver and kidney 1.5 to 3.0 mg... 

For almost 50 years following the description of Wilson disease, there was no effective treatment for this progressive fatal disorder. The damage to vital organs (liver, brain, kidney) in Wilson disease is caused by the toxic action exerted by excessive amounts of copper deposited primarily in these organs. There are several pharmacologic regimens and therapeutic modalities available for the treatment of Wilson disease (Table 2). 

Excess— results in liver disease, various neurologic disturbances, dementia, copper cataracts. These occur in Wilson s Disease, where there is excess coj r deposition in the brain, liver, cornea, lens, and kidney. 

It is believed that as the disease progresses, binding aflBnity of copper protein is diminished, thus resulting in the release of large amounts of copper into plasma, causing severe hemolysis. Some of the excess copper finds its way into the vascular system where it is deposited in such vital organs as kidney, brain, corneas, and liver. 

Copper helps form red blood cells and connective tissues. Copper is a cofactor enzyme that initiates metabolic reactions in the body. Copper is necessary to produce norepinephrine and dopamine (neurotransmitters). Copper is absorbed in the intestine. Foods rich in copper are shellfish (crabs and oysters), liver, nuts, seeds (sunflower, sesame), legumes, and cocoa. Copper deficiency results in anemia, causes decreased hair and skin pigmentation, decreased white blood count, intolerance to glucose, and mental retardation in young patients. Excess serum levels of copper indicate Wilson s disease, which results in the accumulation of copper in the liver, brain, cornea, and kidney. 

The deficit of this element leads to delay in crop maceration, as well as to different anemia, disease of bone systems and endemic ataxia of animal organisms. However, the excessive uptake and accumulation of copper in animals is accompanied by hemolytic jaundice, kidney disease, and by plant chlorosis. 

Two studies discuss the acute absorption of radiolabeled maneb in rodents. The first study (Brocker and Schlatter 1979) used unfasted adult female rats dosed with [ " Mnjmaneb at a dose of 4-10 mg/kg. The rats were kept in metabolism cages which allowed the collection of respired air, urine, and feces for several hours post-dosing. The maneb was given alone or in conjunction with different metal compounds. Radioanalysis of excreta and selected tissues revealed that at 72 hours post-dosing, only 4-6% of the radioactivity was retained in the body with the majority of the label located within the liver and kidney. For 2 different chemical preparations of maneb, the recovery of label in feces was 94-96%, with the remainder in the urine. The respired air of two rats contained only 0.24 and 0.60% of the label, respectively. When molar excesses of the chloride salts of zinc, copper, iron, and mercury were added with the maneb. 

Copper is present in all metabolicaily active tissues. The highest concentrations are found in liver and in kidney, with significant amounts in cardiac and skeletal musele and in bone. The liver contains 10% of the total body content of I2(X) (.unol (80 mg). Excess copper is excreted in bile into the gut. and the faecal copper output (12.5 imol/24 h) is the sum of unabsorbed dietary copper and that re-excreted into the gut. 

---