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At least 217 records · Page 12Linked to original sources
PubMed1977

The effect of cadmium on soluble proteins, enzymes, and essential metals of the duodenal mucosa.

In this study, it was observed that Cd administration had effects on metal distribution and enzyme activities and induced metallothionein in the soluble fraction of the duodenal mucosa. Wistar rats were given water containing 100 ppm of Cd ad libitum for 30 days. Cd treatment caused a significant increase in the mucosal weight and in the soluble protein. The existence of metallothionein was apparent and 40% of the soluble Cd was bound to the thionein. Most of the remaining Cd was bound to the larger proteins. The activities of isocitrate dehydrogenase (ICDH) and glucose-6-phosphate dehydrogenase (G6PDH) enzymes, localized in the soluble fraction, were significantly increased by Cd ingestion. The increase of Zn and the decrease of Mn and Mg were also observed in the soluble fraction of the duodenal mucosa.

Adenosine Triphosphatases↗
PubMed1988

Mucin abnormality of colonic mucosa in ulcerative colitis associated with carcinoma and/or dysplasia.

Twenty cases of resected specimens of carcinoma and/or dysplasia complicating ulcerative colitis were histochemically investigated by the periodic acid-thionein Schiff/potassium hydroxide/periodic acid-Schiff (PAT/KOH/PAS) staining method to see mucin characteristics of carcinoma, dysplasia, and the background mucosa of these lesions. As a control, 11 resected specimens of ulcerative colitis without dysplastic changes and 26 specimens of colonic carcinoma were examined also. All dysplasia and carcinoma in ulcerative colitis stained blue, whereas normal colonic mucin stained red in 65 percent. In 14 of 20 specimens with carcinoma and/or dysplasia, the background mucosa appeared normal with hematoxylin and eosin staining, but showed a mosaic staining pattern with PAT/KOH/PAS. However, only two of 11 specimens of ulcerative colitis without dysplasia and none of 26 specimens of flat mucosa with colorectal carcinoma showed a mosaic staining pattern. From these observations it was concluded that the PAT/KOH/PAS staining method could be useful as a histochemical marker of premalignant change in longstanding ulcerative colitis.

Colitis, Ulcerative↗
PubMed1993

Interactions of mercury in rat brain.

In order to study the metabolism of mercury (Hg), its affinity to metallothionein (MT), and its influence on levels of the essential metals copper and zinc in the brain tissue of rats exposed to elemental mercury (HgO) vapor was investigated. The major findings were: 1. After long-term exposure, about 40% of mercury was found in the brain water-soluble phase (supernatant); 2. In brain supernatant, about 80% of Hg was found in the range of low-molecular-weight proteins; the MT-like protein Hg-Cu-Zn-thionein was isolated and partially characterized; 3. HgO vapor exposure resulted in increased tissue levels of essential Cu and Zn in addition to exogenous Hg; and 4. Experiments showed that HgO vapor exposure can induce the stimulation of rat brain MT synthesis.

Animals↗
PubMed2005

Analysis of cytotoxicities of platinum compounds.

Extent of DNA platination, loss of cell viability, DNA fragmentation, and impairment of cellular mitochondrial oxygen consumption are measures of drug cytotoxicity. We measured and compared these effects for cisplatin, oxaliplatin and carboplatin. Because reaction with intracellular thiols may be responsible for drug resistance, we also determined the rates of Pt drug reactions with metallothionein. Jurkat cells were exposed at 37 degrees C to 25 microM Pt drugs for 3 h. Pt-DNA adducts were determined at the end of the incubation period by atomic absorption spectroscopy. Viability, DNA fragmentation, and cellular respiration (microM O2/min/10(6) cells) were determined 24 h post drug exposure. The average amount of Pt-DNA adducts (Pt atoms/10(6) nucleotides) produced by cisplatin was 43.4, by oxaliplatin 4.8 and by carboplatin 1.5. Cisplatin decreased the rate of respiration by approximately 63% and oxaliplatin by approximately 37%. DNA fragmentation by cisplatin and oxaliplatin was very similar. Carboplatin produced an unnoticeable effect on cellular respiration, and only approximately 10% of the DNA fragmentation was produced by cisplatin or oxaliplatin. Although, for a given drug, all four measures of cytotoxicity were proportional, this did not hold for comparisons between the drugs. The rate constants (M-1 s-1) for reaction of cisplatin, oxaliplatin and carboplatin with Cd/Zn thionein were 0.75, 0.44 and 0.012, respectively. For comparison, the rate constants (M-1 s-1) for reaction of cisplatin, oxaliplatin and carboplatin with glutathione were 0.027, 0.038 and 0.0012, respectively. The low reactivity of carboplatin with metallothionein and glutathione suggests that its low cytotoxic activities are not due to reaction of Pt2+ with cellular thiols. Despite a tenfold difference in Pt-DNA adducts between cisplatin and oxaliplatin, the cytotoxicities of these compounds are very similar, suggesting that oxaliplatin lesions are more potent than cisplatin lesions. The results demonstrate a large influence of the ligands occupying Pt coordination spheres on the chemical and biologic activities of Pt drugs.

Antineoplastic Agents↗
PubMed1990

Quantitation of Cu-containing metallothionein by a Cd-saturation method.

A rapid and sensitive method for determining Cu-containing metallothionein (MT) is described. The main features of this Cd-saturation assay are: high-molecular-weight Cd-binding compounds are denatured with acetonitrile (50% final concentration), Cu bound to MT is removed with ammonium tetrathiomolybdate, excessive tetrathiomolybdate and its Cu complexes are removed with DEAE-Sephacel, apothionein is saturated with Cd, and excessive Cd is bound to Chelex 100. The thiomolybdate assay is capable of reliably detecting 14 ng MT and thus is particularly suitable for measuring MT in small tissue samples (e.g., biopsies), in extrahepatic tissues, and in cultured cells. Moreover, the combination of the thiomolybdate assay with the recently developed Cd-Chelex assay also makes it possible to determine the portion of MT which binds Cu (Cu load of MT), provided that the amount of non-Cu-thionein exceeds 100 ng, the detection limit of the Cd-Chelex assay.

Animals↗
PubMed1982

Metabolism of cadmium in the neonate: effect of hepatic zinc, copper and metallothionein concentrations on the uptake of cadmium in the rat liver.

The accumulation and subcellular distribution of Cd2+ (1 mg/kg body wt, i.p.) in the liver of the neonatal rat is age-dependent. At 4 hr after treatment the liver Cd2+ contents in the 12-day-old, 20-day-old and adult rat are similar and greater than in the 2-day-old animal. The differences in hepatic Cd2+ concentration in the older age groups are consistent with the nonlinear weight gain of the liver in the developing animal. In the hepatic cytosol Cd2+ is incorporated into a high molecular weight and metallothionein fractions and transferred from the former to the latter. This process occurs less rapidly with increasing age. The uptake of Cd2+ by the whole liver and th hepatic metallothionein is not related to the total liver concentration of Zn2+ or copper and is not significantly influenced by the concentration of pre-existing metallothionein or the concentration of thionein-bound Zn2+ or copper. The results are discussed in relation to the possible effects of Cd2+ on the liver metabolism and tissue distribution of Zn2+ and copper in the developing animal.

Animals↗
PubMed1985

Effect of various amounts of selenium on the metabolism of mercuric chloride in mice.

Male ddY mice were given one injection of (1) mercury (mercuric chloride) simultaneously with various doses of selenium (sodium selenite), (2) mercury alone, or (3) various doses of selenium alone. The interaction between mercury and selenium in the liver and kidneys at 1, 5, 24, 120, and 240 hr after administration was investigated. The concentrations of mercury in the liver of mice receiving mercury and selenium simultaneously were higher than those after administration of mercury alone, while the concentrations of mercury in the kidney decreased markedly over a 1-120 hr period after administration, depending on the dose of selenium administered simultaneously with mercury. Clearly, selenium had a different effect on the accumulation of mercury in the liver and kidneys. Subcellular distribution studies revealed that mercury and selenium which were administered simultaneously were incorporated into the crude nuclear and mitochondrial fractions as stable complexes. The transport of these complexes to the kidneys seems to be limited. In addition, gel filtration of supernatant fractions of liver and kidney through a Sephadex G-75 column indicated that the proportion of mercury bound to metallothionein fraction decreased depending on the dose of selenium administered simultaneously with the mercury. This reduction was attributed to the decreased synthesis of mercury-thionein due to a reduction in the activity of Hg2+ which results from binding between mercury and selenium in the cells.

Animals↗
PubMed1991

Asphyctic lesion: proliferation of tyrosine hydroxylase-immunoreactive nerve cell bodies in the rat substantia nigra and functional changes in dopamine neurotransmission.

Asphyxia was induced in male rat pups by performing a delayed cesarean section on pregnant Sprague-Dawley rats. Oxygen saturation and heart rate were recorded during induction of asphyxia. Animals were sacrificed at 3 weeks of age. Brain sections were stained for tyrosine-hydroxylase (TH), dopamine-and-cyclic-AMP-regulated-phosphoprotein-32 (DARPP-32) immunoreactivity (IR) and thionein. Increasing time of asphyxia caused a reduction in the number of nerve cell bodies in the CA1 and CA3 regions of the hippocampus reflecting neuronal death. Furthermore, asphyxia resulted in an increased number of TH-IR nerve cell bodies indicative of a proliferation of dopaminergic neurons in the zona compacta of the substantia nigra. Finally, a significant decrease in rearing was observed in asphyctic animals during the habituation phase, as well as following apomorphine-induced (1 mg/kg s.c.) postsynaptic dopamine receptor stimulation. On the other hand, the apomorphine-induced increase in locomotion was enhanced in asphyctic animals. The implications of these findings for hyperkinesia and attention deficits in disorders resulting from asphyxia are discussed.

Animals↗
PubMed1992

Angiotensin II binding sites in the hamster brain: localization and subtype distribution.

This study was designed to characterize the distribution of angiotensin II (AII) binding sites in the hamster brain. Brain sections were incubated with [125I][sar1,ile8]-angiotensin II in the absence and presence of angiotensin II receptor subtype selective compounds, losartan (AT1 subtype) and PD123177 (AT2 subtype). Binding was quantified by densitometric analysis of autoradiograms and localized by comparison with adjacent thionein stained sections. The distribution of AII binding sites was similar to that found in the rat, with some exceptions. [125I][sar1,ile8]-angiotensin II binding was not evident in the subthalamic nucleus and thalamic regions, inferior olive, suprachiasmatic nucleus, and piriform cortex of the hamster, regions of prominent binding in the rat brain. However, intense binding was observed in the interpeduncular nucleus and the medial habenula of the hamster, nuclei void of binding in the rat brain. Competition with receptor subtype selective compounds revealed a similar AII receptor subtype profile in brain regions where binding is evident in both species. One notable exception is the medial geniculate nucleus, predominately AT1 binding sites in the hamster but AT2 in the rat. Generally, the AII binding site distribution in the hamster brain parallels that of the other species studied, particularly in brain regions associated with cardiovascular and dipsogenic functions. Functional correlates for AII binding sites have not been elucidated in the majority of brain regions and species mismatches might provide clues in this regard.

Angiotensin II↗
PubMed1978

Maleate induced change in the kidney binding of mercury in rats pretreated with cadmium.

The kidney uptake of Hg2+ was increased by Cd2+-pretreatment when Hg2+ was given intraperitoneally but not subcutaneously. Subsequent s.c. administration of maleate increased Hg2+ release from the kidneys only if Hg2+ was given subcutaneously. Neither the effect of Cd2+, nor that of maleate, on the distribution of Hg2+ among the renal soluble protein fractions was affected by the route of Hg2+ administration. The protective effect of Cd2+-pretreatment against the nephrotoxic effect of Hg2+ was also independent of the route of Hg2+ administration. Maleate given in nephrotoxic doses removed Hg2+ and copper, but not Cd2+ from the renal metallothionein fraction. Mercury in the urine, however, was not complexed by proteins with the molecular weight of thionein, but was bound to high molecular weight proteins and diffusible molecules. These findings are discussed in relation to the role of metallothionein in the interaction between Cd2+ and Hg2+.

Animals↗
PubMed1980

The interaction of cadium-induced rat renal metallothionein with bivalent mercury in vitro.

Addition of Hg2+ in vitro to metallothionein (Cd : Cu : Zn = 6.5 : 4 : 1) from the kidneys of Cd2+ exposed rats appears to result initially in the replacement of Zn2+, then Cd2+ and finally copper. The ionic stoichiometries between Hg2+-binding and the release of Cd2+ (or Zn2+) and copper are 3 : 2 and 1 : 1 respectively. After treatment with amounts of Hg2+ sufficient to displace completely either the bound Zn2+ and Cd2+, or all of the original cations, the metallothionein has little or no negative charge at pH 8.0 and is not resolved into the two isometallothioneins, which characterize the (Cd, Cu, Zn)-thionein, by ion exchange chromatography at this pH. Cation substitution occurs in both isometallothioneins and there is no evidence that Hg2+ interacts preferentially with one of them. Treatment of the metallothionein with increasing amounts of Hg2+, equivalent to approx. 25% and 50% of the bound cations gives rise to a range of molecular species of progressively decreasing negative charge. The consistent stiochiometry between Hg2+ uptake and Cd2+ or Zn2+ release at all concentrations of Hg2+ indicates that free thiol groups are not formed during the substitution reaction.

Animals↗
PubMed1980

The in vivo effects of maleate on the cation-distribution in rat kidney metallothionein sub-fractions after induction by cadmium and/or mercury.

The metallothionein fractions, isolated by gel filtration from the kidneys of rats that have been dosed with Cd2+, Hg2+ or Cd2+ followed by Hg2+, yield very different elution profiles on ion-exchange chromatography. The metallothionein from Cd2+-treated animals is resolved into the isomethallothioneins I and II and a minor, less negatively-charged species (B), which contains Cd2+ and copper, but little Zn2+. The corresponding fraction from the kidneys of rats doses with Hg2+ yields five components, all of which contain Hg2+, Zn2+ and Cu, but in different ratios. Three of these compounds correspond in their elution characteristics from DE-cellulose with the above-mentioned isometallothioneins I and II and fraction B. The last of these, which also is rich in Cu, is the major Hg2+-binding component. The distribution of Hg2+ and of other cations between these five sub-fractions, but not the number of sub-fractions, is altered by Cd2+-pretreatment of the animals. Treatment of Cd2+-dosed rats with sodium maleate has no significant effect on the distribution of cations (Cd2+, Zn2+ and copper) amongst the renal metallothionein subfractions. The same treatment, applied to animals dosed with either Hg2+ only, or Cd2+ followed by Hg2+, causes the elimination of 70--75% of the Hg2+ from the metallothionein fraction. Loss occurs from all subfractions, but is greatest in subfraction B, which also loses copper. Whilst it is possible that Hg2+ may induce metallothionein and other metalloproteins in the kidney, Hg2+ appears to bind to both isometallothioneins I and II, when these are induced by Cd2+-pretreatment. The loss of Hg2+, but not of Cd2+, from these metalloproteins after treatment with sodium maleate may be related to differences in the relative binding affinities of the two cations for thionein and other cellular proteins.

Animals↗
PubMed1985

Synthesis of a nonacosapeptide (beta-fragment) corresponding to the N-terminal sequence 1-29 of human liver metallothionein II and its heavy metal-binding properties.

A nonacosapeptide (beta-fragment) corresponding to the N-terminal sequence 1-29 of human liver metallothionein II was synthesized by the fragment condensation method. The Cd-binding ability of the beta-fragment was much stronger than that of cysteine as thionein and synthetic alpha-fragment corresponding to the C-terminal sequence 30-61 of human liver metallothionein II. Both the alpha- and beta-fragments bound preferentially to Cu ions rather than Cd ions.

Amino Acid Sequence↗
PubMed1985

An arsenic-binding protein in rainbow trout.

A pulse dose of 5 microCi 74As-labeled arsenic acid was given in diet contained in No. 4 gelatin capsules to two groups of rainbow trout (90 +/- 6 g). These groups consisted of the control and the treatment group which was preexposed to 22.8 mg As/kg diet for 2 weeks. An extract of cytosol prepared from the liver of both control and pretreated fish sacrificed 48 hr after the pulse dose was found to contain an arsenic-binding protein with molecular weight of about 19,000. This protein accounted for less than 25% of the extracted cytosol in both the control and preexposed fish. Arsenic may not induce the synthesis of thionein in the liver as the molecular weight of 19,000 is outside the range previously reported for metallothionein. The binding of arsenic to this protein may not be of any adaptive significance.

Animals↗
PubMed1992

Membrane structure, toxins and phospholipase A2 activity.

The phospholipid-hydrolyzing enzyme phospholipase A2 (PLA2) (EC 3.1.1.4) exists in several forms which can be located in the cytosol or on cellular membranes. We review briefly cellular regulatory mechanisms involving covalent modification by protein kinase C and the action of Ca2+, cytokines, G proteins and other cellular proteins. The major focus is the role of phospholipid structure on PLA2 activity, including (1) the mechanism of PLA2 action on synthetic phospholipid bilayers, (2) perturbation of synthetic and cellular membranes with lipophilic agents and membrane-interactive peptides and (3) the ability of these agents to activate endogenous PLA2 activity, with emphasis on the venom and plant toxins melittin, cardiotoxin and Pyrularia thionein.

Animals↗
PubMed1991

The distribution of myelinated nerve fibers in the mature opossum esophagus.

Myelination of nerve fibers could be important in establishing normal esophageal peristalsis. We therefore examined the general distribution and the age of appearance of myelinated nerve fibers in the smooth-muscle part of the esophagus of the American opossum. Tissues stained with thionein and Sudan black B were examined by light microscopy. Other tissues were prepared for electron microscopy and examined in the light microscope in Toluidine blue stained sections as well as at electron microscopy. In mature animals (weight greater than 2.0 kg, age greater than or equal to 1 year), myelinated nerve fibers, oriented mainly craniocaudally, were most abundant at the striated muscle-smooth muscle junction, and declined in density distally along the organ. They were nearly absent at the esophagogastric junction. They were more abundant in the stomach just below the esophagogastric junction. The myelinated nerve fibers commonly lay within sheathed fascicles that had the appearance of peripheral nerves, like the shunt fascicles of the stomach and colon. In immature animals myelinated fibers did not appear until a weight of about 1 kg was reached, 50 days after weaning and about 150 days after birth. Since the younger animals are presumably swallowing normally, myelination of the extrinsic nerves is not essential for esophageal motor function.

Animals↗
PubMed1985

Cadmium found in non-soluble fraction of kidney homogenates and its relation to renal dysfunction after cadmium-cysteine administration.

The critical concentration of cadmium (Cd) in the kidney after acute administration of Cd-cysteine (Cys) is 10 micrograms/g wet wt in whole kidney and is equal to that following Cd-thionein (Th) injection. This fact suggests that the nephrotoxicity of Cd-Th may be due to the Cd ions liberated from Cd-Th. To clarify the mechanism of the nephrotoxicity, the subcellular distribution of Cd injected as Cd-Cys was determined between supernatant and sediment fractions. Renal Cd level observed at 4 h increased with dose, but the Cd concentration in the supernatant fraction was kept almost constant at higher doses. Renal dysfunction measured by urinary protein and glucose levels was seen at the higher doses. This suggested that Cd in the sediment fraction of the kidney homogenates may be the ultimate cause for the nephrotoxicity of Cd-Cys. The sedimental Cd was eliminated from the kidney by 24 h. Much of the Cd found in the supernatant fraction was bound to high-molecular-weight proteins (HMWP) at 4 h, and almost all Cd ions were found to be bound to metallothionein at 24 h. Therefore, the HMWP-bound Cd in the supernatant fraction also may be a cause for the renal dysfunction. It is concluded that in addition to the HMWP-bound Cd in the supernatant fraction, CD distribution into the sediment fraction should be considered as a factor in causing nephrotoxicity after Cd-Cys and possibly Cd-Th administration.

Animals↗