Micromineral Toxicity

Many of the microminerals are toxic when consumed in large amounts (2). Inadvertent exposure to a variety of minerals, whether via inhalation, absorption through the skin, or ingestion through food or drink, can elicit a toxic response. The gastrointestinal system offers the first line of defense against ingested excess mineral: vomiting and diarrhea. Through vomiting, contaminated food is expelled. Through diarrhea, excretion of excess consumed mineral is facilitated. This reduces the time that the intestinal tract is exposed to the mineral and thus reduces its subsequent uptake. The defense against excess exposure also involves the kidneys and the bone as well as the bilary tract. The kidney tubules will attempt to reduce the body load by increasing urinary excretion. Some minerals, however, namely, copper, iron, zinc, and lead, are not as subject to renal filtration as are other minerals, namely, magnesium, selenium, sodium, potassium, iodine, calcium, and molybdenum. Those minerals subject to renal filtration will appear in the urine; those that are not filtered out are excreted via the bile into the intestinal tract. When coupled with diarrhea, this provides a stimulated loss pathway. Last, reduction of the circulating toxic load of a micromineral is accomplished via deposit of the excess mineral in the bones. Bone mineral content has been used to document cases of suspected toxicity. Accidental or intentional poisoning can sometimes be masked by other nonspecific symptoms, but bone analysis can provide the

Table 2. Generally Recognized Safe and Adequate Intakes for Selected Minerals

Mineral

Intake

Copper

1.5-3.0 mg/day

Fluoride

1.4-4.0 mg/day

Manganese

2.0-5.0 mg/day

Chromium

50-200 jüg/day

Molybdenum

75-250 /ig/day

Note: These ranges are not age or gender specific.

Note: These ranges are not age or gender specific.

documentation needed to support or deny a supposition of toxicity.

The adverse effects of excess micromineral exposure are as diverse as the minerals themselves. Table 3 lists the characteristic signs and symptoms of micromineral toxicity as well as deficiency. Each mineral has its preferred target in the body. For some, the target is DNA (3). Certain minerals (copper, arsenic, nickel, chromium) bind to DNA in a cross-link fashion. The binding is covalent and is independent of a DNA binding protein. In this setting the excess mineral produces either a nonfunctional DNA or a DNA that cannot repair itself. Evidence of this cross-linking has been demonstrated in vitro using a variety of cell types. Chinese hamster cells have been used to show copper-induced, chromium-induced, and nickel-induced DNA cross-linking, and human fibroblasts and epithelial cells have been used to show arsenic-induced cross-linking.

The concept of chemically induced cross-linkage of DNA as a factor in carcinogenesis has been proposed to explain the role of asbestos and the development of mesothelioma

(4). Mesothelioma is a malignant growth of the pleural and peritoneal cavities and develops as a response to the inhalation of asbestos fibers (pleural growth) or inadvertent ingestion (peritoneal growth) of the fibers. Asbestosis, another symptom of asbestos inhalation, results in impaired pulmonary function. This is due in part to iron-catalyzed free-radical damage to the lung tissue because asbestos contains iron as a contaminant. However, cytokines, growth factors, and proteases as well as effects of asbestos on gene expression are also involved. Malignant tumors are stimulated to grow by the presence of asbestos fibers that act as artificial linkers of DNA, resulting in mutations within the pleural and peritoneal cells (4). Changes in the CDKN2 gene that encodes protein 16 seem to be involved. This gene is either lost or mutated. Its gene product is a regulator of the phosphorylation of protein 105, a tumor suppressor. Unphosphorylated protein 105 can inhibit passage from the G1 to the S phase of the cell cycle, whereas phosphorylated protein 105 permits this passage. Passage inhibition is a common feature of cancer cell initiation. Any substance that interferes with this passage could be regarded as a carcinogen. Minerals in excess quantities can have this effect, and excess intakes of some have been linked with certain forms of cancer.

Excess exposure to certain minerals can invoke the stimulation of free-radical generation. Free radicals can damage membranes, altering their function, and can target numerous intracellular constituents (DNA, enzymes, transporters, signaling systems). Free-radical generation may be one of the responses to excess iron exposure and this in turn may link this mineral to cancer development

(5). The mechanism whereby excess iron has its effect is far from clear. It may induce DNA cross-linking as described previously, but it may also act to stimulate free-radical formation. Free radicals can damage cell membranes and cell constituents as well as DNA. Free-radical attack of DNA could cause mutations and could explain an association between excess iron intake and cancer (6). At this time, more data are needed to support or deny such associations. Excess mineral intake either as a single mineral or as a mixture can have effects on metabolism as well

Table 3. Characteristic Signs of Micromineral Deficiency and Toxicity

Mineral

Deficiency

Toxicity

Iron

Zinc

Fluoride Copper

Iodine Manganese

Molybdenum Selenium

Anemia, i amounts of hemoglobin, ferritin

Poor growth and sexual maturation, anemia, enlarged liver and spleen, rough skin, lethargy

Excess tooth decay

Rare; anemia, poor wound healing, muscle weakness; lethargy, depressed collagen synthesis

Goiter (underproduction of thyroxine)

Abnormal bone and connective tissue growth, decreased Mn superoxide dismutase

No clear-cut symptoms

Decreased glutathione peroxidase activity, fragile red cells; enlarged heart, skeletal muscle degeneration

Bloody diarrhea, vomiting occasionally, liver failure, hemorrhage, metabolic acidosis, shock Nausea, vomiting, epigastric pain, abdominal cramps, diarrhea; central nervous system deficits, copper deficiency Fluorosis; mottling of teeth Rare

None Rare

Rare; interferes with copper use

Neuromuscular defects, trace mineral imbalance, liver and muscle damage as on cellular respiration. Where the mineral is divalent (2+), it can interfere with the actions of other similarly charged ions. Within the normal range of intakes, mineral-mineral interactions are common. However, when these ranges are exceeded, specific metabolic processes will be inhibited.

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