Iron liver damage

Overproduction of free radicals by erythrocytes and leukocytes and iron overload result in a sharp increase in free radical damage in T1 patients. Thus, Livrea et al. [385] found a twofold increase in the levels of conjugated dienes, MDA, and protein carbonyls with respect to control in serum from 42 (3-thalassemic patients. Simultaneously, there was a decrease in the content of antioxidant vitamins C (44%) and E (42%). It was suggested that the iron-induced liver damage in thalassemia may play a major role in the depletion of antioxidant vitamins. Plasma thiobarbituric acid-reactive substances (TBARS) and conjugated dienes were elevated in (3-thalassemic children compared to controls together with compensatory increase in SOD activity [386]. The development of lipid peroxidation in thalassemic erythrocytes probably depends on a decrease in reduced glutathione level and decreased catalase activity [387]. 

Iron dust from most iron compounds is harmful if inhaled and toxic if ingested. Iron dust and powder (even filings) are flammable and can explode if exposed to an open flame. As mentioned, excessive iron in the diet may cause liver damage. 

Iron (Fe) Hemoglobin Food supply Intestinal tract, liver damage 10 to 15 mg... 

Most iron salts and compounds may be safely handled following common safe laboratory practices. Some compounds are irritants. A more serious threat is ingestion of massive quantities of iron salts which results in diarrhea, hemorrhage, liver damage, heart damage, and shock. A lethal dose is 200 250 mg/kg of body weight. The majority of the victims of iron poisoning are children under five years of age. 

Without a mechanism for its excretion, iron accumulates in vital organs (Pietrangelo, 2002). Because the liver binds both circulating nontransferrin and transferrin-bound iron, the liver is at particular risk for iron overload. Excess iron causes damage to hepatocytes primarily through induction of oxidative stress (Parkilla et al., 2001). 

A biopsy is often required to make a diagnosis of most types of liver disease. A specimen of liver can be used to identify fibrosis, cirrhosis, cholestasis and hepatitis, both acute and chronic, and tumours. Biochemical measurements can also be taken from a biopsy specimen to determine iron and copper content, virology, microbiology and haematology (e.g. increased numbers of eosinophils in a drug-induced cause). The biopsy can give an indication of the extent of the liver damage. See Chapter 3 for slides of liver biopsies. 

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. 

Structural hepatocellular damage causes iron to leave the cell and subsequently results in an increase in serum iron. After diffuse liver damage has worn off, the elevated serum iron level takes a relatively long time to return to normal. This leads to the conclusion that hepatocellular damage is terminated (detectable in the return of enzymatic activities to normal) before the hepatocyte regains the ability to store iron. 

Accidental ingestion of iron tablets by children is common and may be life threatening. Symptoms include nausea and vomiting, abdominal pain, diarrhoea and haematemesis. In severe cases, hypotension, liver damage and coma can result. Serum iron is increased and transferrin is saturated (>70%). 

Up to 30% of ingested zinc is absorbed from the small intestine, although absorption is controlled by a homeostatic mechanism. Despite its essentiality, too much zinc interferes with iron and copper metabolism which may result in copper deficiency. Excessive absorption can result in symptoms such as nausea, cramps and vomiting. Inhalation of zinc, zinc oxide and zinc chloride fumes by occupationally exposed workers causes pulmonary oedema and metal fume fever, with symptoms such as fever, chills, sweating and weakness occurring within 4-6 hours of exposure. Chronic inhalation of zinc compounds can result in liver damage. 

There is a downside to this abundance of iron in the general food supply. Well over a million Americans suffer from an inherited genetic disorder called hemochromatosis, or iron overload disease. Such individuals accumulate excess iron in their bodies. The excess iron causes damage to major organs such as the liver, pancreas, and heart. The disease most often affects men between the ages of 30 and 50. Women with the disorder are often protected from developing all the complications of the disease because of their natural loss of iron through menstruation. However, they do develop some of the complications. 

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