Proteins complexes induced

While many hormones bind to surface receptors the steroid hormones, which are lipid in nature, pass through the cell membrane and bind to receptor proteins in the nucleus. The resulting hormone-protein complexes induce changes in gene expression through regulation of transcription (Fig. 11-1, top). These receptors are considered in Chapter 22 and hormones are considered further in Chapter 30. 

Exposure to chromium(VI) can result in DNA-protein complexes, the identification of which may be useful as biomarkers of exposure to chromates (Costa 1991). Gel electrophoresis and immunochemical techniques were used to identify actin as the protein in a DNA-protein complex induced by potassium chromate in cultured Chinese hamster ovary cells. While the DNA-protein complexes induced by formaldehyde and ultraviolet light were different from those induced by chromate, actin was also identified as the protein in the complex induced by cis-platinum, indicating that the DNA-actin complex is not specific for chromium. However, an experiment in a group of four volunteers did not demonstrate an increase in DNA-protein crosslinks in leukocytes over a 240 minute period following the ingestion of 5 mg chromium(VI) as potassium dichromate in a 10 mg chromium/L solution or the same amount added to 300 mL of orange juice (presumably reducing chromium(VI) to chromium(III)) and diluted to 500 mL with deionized water (Kuykendall et al. 1996). Chromium levels in red cells, plasma and urine were increased. In a separate experiment in this study, a threshold dose of 52 pg chromium(VI)/L was determined for crosslink formation in cultured lymphoma cells. 

CostaM. 1991. DNA-protein complexes induced by chromate and other carcinogens. Environ Health Perspect 92 45-52. 

The most significant change in Chl-protein complexes induced by chilling pretreatment was that CPI.decreased whereas CPI increased. As shown in table 2, CPI.was 10.2% for the control and 5.1% for the chilling pretreated ones. It is known that, CPI.is the reaction center complex of PSI associated with LHC—I, whereas CPI is the reaction center complex of PSI. The decreasing of CPI.while increasing of CPI implied that some LHC-I may be seperated from PSI reaction center and some of them may move to PSII. 

As described above, the formation of xanthan-protein complexes induced by salts such as calcium or magnesium chloride depends strongly on the quality of the solution. It was previously reported that when xanthan solutions contained less impurities, interactions between macromolecules and calcium ions were less important, and that the pH limit corresponding to precipitation was shifted to basic pH (75). Here, when xanthan C broth was centrifuged, thixotropic phenomena were less apparent. So, for this xanthan solution, it is clearly shown that the presence of cellular components was essential to induce interactions between xanthan chains and cations. It can also be noted that the xanthan broth was frozen before all the experiments and thus, that the cells may have been lysed thereby releasing all their constituents inside the medium. Because of the diversity and complexity of the cellular components, it is difficult to predict which kind of interactions can be involved in the aggregation. 

Miller CA III, Costa M (1989) Immunological detection of DNA-protein complexes induced by chromate. Carcinogenesis 10 667-672 Miller CA, Cohen MD, Costa M (1991) Complexing of actin and other nuclear proteins to DNA by cis-diamminodichloroplatinum (II) and chromium compounds. Carcinogenesis 12 269-276... 

Kolubayev T, Geacintov N E, Paillotin G and Breton J 1985 Domain sizes in chloroplasts and chlorophyll-protein complexes probed by fluorescence yield quenching induced by singlet-triplet exciton annihilation Biochimica Biophys. Acta 808 66-76... 

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). 

FIGURE 3.13 Major components of the cubic ternary complex model [25-27]. The major difference between this model and the extended ternary complex model is the potential for formation of the [ARjG] complex and the [RiG] complex, both receptor/ G-protein complexes that do not induce dissociation of G-protein subunits and subsequent response. Efficacy terms in this model are a, y, and 5. 

L The answer is a. (Hardman, pp 1460, 14642) Cosyntropin is related to adrenocorticotropin. It corresponds to the first 24 amino acids of adreno-corticotropin. Cosyntropin complexes with a plasma membrane receptor that brings about the activation of adenylyl cyclase. Adenylyl cyclase catalyzes the formation of cAMP from ATP In the cytoplasm, cAMP activates cAMP-dependent protein kinase, which participates in the phosphorylation of specific substrate proteins (e.g., enzymes). The phosphorylated protein eventually induces the particular response on the target cell. 

Copper is part of several essential enzymes including tyrosinase (melanin production), dopamine beta-hydroxylase (catecholamine production), copper-zinc superoxide dismutase (free radical detoxification), and cytochrome oxidase and ceruloplasmin (iron conversion) (Aaseth and Norseth 1986). All terrestrial animals contain copper as a constituent of cytochrome c oxidase, monophenol oxidase, plasma monoamine oxidase, and copper protein complexes (Schroeder et al. 1966). Excess copper causes a variety of toxic effects, including altered permeability of cellular membranes. The primary target for free cupric ions in the cellular membranes are thiol groups that reduce cupric (Cu+2) to cuprous (Cu+1) upon simultaneous oxidation to disulfides in the membrane. Cuprous ions are reoxidized to Cu+2 in the presence of molecular oxygen molecular oxygen is thereby converted to the toxic superoxide radical O2, which induces lipoperoxidation (Aaseth and Norseth 1986). 

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