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cadmium-metallothionein complex

metallothionein which serves in a metal-sequestering mechanism
Also Known As:
CdMT complex
Networked: 4 relevant articles (1 outcomes, 3 trials/studies)

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Bio-Agent Context: Research Results

Related Diseases

1. Acute Kidney Injury (Acute Renal Failure)
07/01/1998 - "We have shown that: (1) MT-transgenic and -null mice have altered tissue MT protein levels; (2) MT-transgenic and -null mice appear to be normal in other detoxifying systems examined, except for slight alterations in tissue Zn concentration; (3) MT does not appear to inhibit Cd absorption from the gastrointestinal tract, nor affect Cd tissue distribution; (4) MT reduces the elimination of Cd from liver; (5) MT protects against acute inorganic Cd-induced lethality and hepatotoxicity, and the mechanism of the protection appears to be due to its ability to sequester Cd in the cytosol, thus reducing the amount of Cd in critical organelles; (6) MT modulates Cd-induced expression of protooncogene(c-jin) and tumor suppress genes (p53) in mouse liver; (7) MT does not protect against CdMT-induced acute renal injury, and Zn-induced protection against CdMT-induced acute nephrotoxicity does not appear to be mediated through MT; (8) Chronic Cd administration produces renal injury inb MT-null mice, indicating that Cd-induced nephrotoxicity is not necessarily mediated through the CdMT complex; (9) MT protects against chronic CdC12 nephropathy, suggesting that intracellular MT is an important adaptive mechanism decreasing CdC12 nephrotoxicity, and that a single injection of CdMT may not be a good model to study chronic Cd nephropathy; (10) genetic background of mouse strains, rather than constitutive MT levels, is a more important determinant for Cd-induced acute testicular injury. "
2. Neoplasms (Cancer)
07/01/1998 - "We have shown that: (1) MT-transgenic and -null mice have altered tissue MT protein levels; (2) MT-transgenic and -null mice appear to be normal in other detoxifying systems examined, except for slight alterations in tissue Zn concentration; (3) MT does not appear to inhibit Cd absorption from the gastrointestinal tract, nor affect Cd tissue distribution; (4) MT reduces the elimination of Cd from liver; (5) MT protects against acute inorganic Cd-induced lethality and hepatotoxicity, and the mechanism of the protection appears to be due to its ability to sequester Cd in the cytosol, thus reducing the amount of Cd in critical organelles; (6) MT modulates Cd-induced expression of protooncogene(c-jin) and tumor suppress genes (p53) in mouse liver; (7) MT does not protect against CdMT-induced acute renal injury, and Zn-induced protection against CdMT-induced acute nephrotoxicity does not appear to be mediated through MT; (8) Chronic Cd administration produces renal injury inb MT-null mice, indicating that Cd-induced nephrotoxicity is not necessarily mediated through the CdMT complex; (9) MT protects against chronic CdC12 nephropathy, suggesting that intracellular MT is an important adaptive mechanism decreasing CdC12 nephrotoxicity, and that a single injection of CdMT may not be a good model to study chronic Cd nephropathy; (10) genetic background of mouse strains, rather than constitutive MT levels, is a more important determinant for Cd-induced acute testicular injury. "
3. Proteinuria
4. Necrosis

Related Drugs and Biologics

1. D-4-chloro-17 beta-hydroxy-3-oxo-17 alpha-methylandrosta-1,4-diene
2. cadmium-binding protein
3. Cadmium Chloride (Cadmium Dichloride)
4. Metallothionein
5. Cadmium