Team of researchers from the University of Cincinnati (UC) has identified the gene responsible for spreading the poisonous (toxic) effects of cadmium--a finding, say the researchers, that may one day lead to the prevention of cadmium toxicity in humans.
Cadmium--a heavy metal suspected of causing human birth defects, lung cancer and testicular cancer--is found in cigarette smoke, some shellfish and seafood, soil and some plants.
It is known to damage the human central nervous system, the kidneys, lungs and developing embryos.
The UC researchers, studying low doses of cadmium in mice, found that the gene Slc39a8 works to transport cadmium to the testes, causing tissue to die.
"We suspect that cadmium at higher doses could be transported to other regions of the body via the Slc39a8 gene or another gene in this family," says Dr. Nebert.
"We know that humans carry the same gene and gene family.
When populations are malnourished or have iron-deficient anemia, the damaging effects of cadmium increase dramatically.
Industrialization, however, has introduced many nonessential heavy metals, such as cadmium, lead, silver, mercury, nickel, arsenic and chromium into the environment.
In the 1920s, UC researchers determined that exposure to lead (a nonessential heavy metal) in gasoline resulted in birth defects, mental retardation, loss of balance and other brain, kidney, liver or lung damage.
Since then, there have been many studies on heavy metal toxicity, but until now no study has determined how nonessential heavy metals cause toxicity in humans or other vertebrates.
"We believe that the Slc39a8 gene could be responsible for the transportation not only of cadmium, but also of other nonessential heavy metals such as lead, nickel and mercury," says Dr. Nebert.
"Identification and characterization of this gene in mice is a significant breakthrough that will improve our understanding of how heavy metals actually cause toxicity and cancer in humans."