Cadmium liver damage

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. 

Some substances are particularly liable to damage certain organs e.g. hydrocarbon solvents may affect the liver, cadmium may damage the lungs or kidneys. 

Sublethal effects in birds are similar to those in other species and include growth retardation, anemia, renal effects, and testicular damage (Hammons et al. 1978 Di Giulio et al. 1984 Blus et al. 1993). However, harmful damage effects were observed at higher concentrations when compared to aquatic biota. For example, Japanese quail (Coturnix japonica) fed 75 mg Cd/kg diet developed bone marrow hypoplasia, anemia, and hypertrophy of both heart ventricles at 6 weeks (Richardson et al. 1974). In zinc-deficient diets, effects were especially pronounced and included all of the signs mentioned plus testicular hypoplasia. A similar pattern was evident in cadmium-stressed quail on an iron-deficient diet. In all tests, 1% ascorbic acid in the diet prevented cadmium-induced effects in Japanese quail (Richardson et al. 1974). In studies with Japanese quail at environmentally relevant concentrations of 10 pg Cd/kg B W daily (for 4 days, administered per os), absorbed cadmium was transported in blood in a form that enhanced deposition in the kidney less than 0.7% of the total administered dose was recovered from liver plus kidneys plus duodenum (Scheuhammer 1988). 

Cadmium is bound to proteins and red blood cells in blood and transported in this form, but 50% to 75% of the body burden is located in the liver and kidneys. The half-life of cadmium in the body is between 7 and 30 years, and it is excreted through the kidneys, particularly after they become damaged. 

Chemicals which can damage (a) the liver include carbon tetrachloride, paracetamol, bromobenzene, isoniazid, vinyl chloride, ethionine, galactosamine, halothane, dimethyl-nitrosamine (b) the kidney include hexachlorobutadiene, cadmium and mercuric salts, chloroform, ethylene glycol, aminoglycosides, phenacetin (c) the lung include paraquat, ipomeanol, asbestos, monocrotaline, sulfur dioxide, ozone, naphthalene (d) the nervous system include MPTP, hexane, organophosphoms compounds, 6-hydroxydopamine, isoniazid (e) the testes include cadmium, cyclophosphamide, phthalates, ethanemethane sulfonate, 1,3-dinitrobenzene (f) the heart include allylamine, adriamycin, cobalt, hydralazine, carbon disulfide (g) the blood include nitrobenzene, aniline, phenyl-hydrazine, dapsone. 

Numerous substances detected in drinking waters are known to induce toxicity but usually at dose levels much higher than those found in water. Nitrates or nitrites can cause infant methemoglobinemia, lead can affect the hematopoetic or nervous system, cadmium can cause renal damage, and some organohalogens may cause liver toxicity (12). 

Several metal ions are essential or beneficial to life while others, such as lead, cadmium or mercury, are highly detrimental. Many diseases have been associated in a way or another to altered metal ion concentrations in the body. Deficiencies can be as damaging as overloads. Copper deficiency has been associated to anemia while excess copper can lead to Wilson s disease (liver cirrhosis). Anemia may also be caused by a lack of iron and overload of this same metal ion is connected to thalassemia and siderosis [122]. In vivo determination of metal ion distribution is thus highly desirable and progresses have been made towards the design of MRI contrast agents sensitive to the concentration of metal ions. 

Cadmium (Cd) is a non-essensial metal used in industry as an anti-corrosive agent, and is found as a contaminant in food and also in cigarette smoke. The most serious consequence of chronic Cd poisoning is lung- and prostate cancer but the first effect during chronic intake is kidney damage, manifested by marked proteinuria [164]. Under chronic exposure, cadmium is primarily taken up by the liver, where it induces synthesis of metallothionein (MT) and induces formation of cadmium-metallothionein complexes. 

Paints often contain solvents such as toluene, xylene, halogenated aromatic hydrocarbons, and methylene chloride, as well as heavy metals in their pigments including chromium yellow, lemon yellow (barium chromate), vermilion red (cadmium and mercuric sulfides), and flake white (lead). Both acute and chronic exposures to toluene and xylene are associated with neurotoxicity and can also damage the liver and kidneys. 

Outside the hepatic system, MTs facilitate absorption of metals such as cadmium into the kidneys and liver. Also, the induction of MTs via reactive metals protects hepatic enzymes against cellular damage. Without this intervention, zinc may stimulate... 

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