Cadmium is a heavy metal which is naturally found in soil and water. It has similar properties to copper, zinc and calcium, and it may disrupt essential metal homeostasis. The toxicity of cadmium is magnified by its extremely long biological half-life in the body, between 10 to 30 years. Although the primary body burden is found in the liver and kidneys, the testis is extremely sensitive to cadmium, and acute exposure results intesticular edema and hemorrhagic necrosis. While most animals with scrotal testes are susceptible to the testicular toxicity of cadmium, strain-related differences to this effect occur in mice. For this dissertation, the mechanism(s) of murine strain differences to cadmium-induced testicular toxicity was studied using sensitive (129/J) and resistant (A/J) mice. We found significantly decreased cadmium concentrations in the testis, epididymis and seminal vesicle 24 hr after subcutaneous cadmium exposure in the resistant A/J mice, as compared to the sensitive 129/J mice. The transport of cadmium across vascular barriers was also markedly different in the two strains. Influx rates of $\sp{109}$Cd into the brain, testis and epididymis were found to be significantly lower in A/J mice. To help identify the natural ligand for the transport system in these tissues, $\sp{65}$Zn influx rates were studied. Zinc is an essential element, and a transport system should exist to facilitate passage into tissues. Since cadmium is a nonessential and toxic metal, specific mechanisms would not be expected to be present to maintain homeostatic concentrations of this cation. Cadmium and zinc share many properties, and the two elements have been shown to compete for transport. Thus, cadmium may use the zinc transporter to enter tissues. The resistant A/J mice demonstrated a significantly reduced zinc entry into the testis and brain when compared to $\sp{129}$/J mice. Cadmium and zinc transport were significantly lower in A/J mice, suggesting that the resistant mice may have a decreased number of zinc transporters, or a mutation in the transporters that makes them less active. Therefore, the nature of murine strain resistance to the testicular effects of cadmium may be related to a relative deficiency or a mutation in the zinc transporter / acase@tulane.edu
| Identifer | oai:union.ndltd.org:TULANE/oai:http://digitallibrary.tulane.edu/:tulane_25964 |
| Date | January 1998 |
| Contributors | King, Laura Marie (Author), George, William J (Thesis advisor) |
| Publisher | Tulane University |
| Source Sets | Tulane University |
| Language | English |
| Detected Language | English |
| Rights | Access requires a license to the Dissertations and Theses (ProQuest) database., Copyright is in accordance with U.S. Copyright law |
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