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PubMed2004

Synthesis of radioiodine labeled dibenzyl disulfide for evaluation of tumor cell uptake.

Benzyl 4-halobenzyl and ally benzyl disulfide were synthesized as diallyl disulfide analogues and their tumor growth inhibitory effects on the cancer cells (SNU C5 and MCF-7) were comparable to that of diallyl disulfide, indicating that the disulfide functional group was responsible for the tumor growth inhibitory effects. Cu(I)-assisted radioiodination of benzyl 4-bromobenzyl disulfide gave benzyl 4-[123I/125I]iodobenzyl disulfide in 30-40% radiochemical yield. The radiolabeled disulfide was taken up by the cancer cells in a time-dependent manner, and the uptake was inhibited by the pretreatment of S-methyl methanethiosulfonate (MMTS), phorone and diallyl disulfide. This study suggested that the radiolabeled dibenzyl disulfide was taken up by the cancer cells via thiol-disulfide exchange and retained inside the cells.

Antineoplastic Agents↗
PubMed1994

[Preparation and characteristics of a tritiated derivative of CP-96,345--a nonpeptide antagonist of the substance P receptor with a high specific radioactivity].

[3H]CP-96.345 with the specific radioactivity of 84.2 Ci/mmol has been prepared from CP-96.345 by the high-temperature solid state isotopic exchange. The tritiated compound was equipotent with the parent antagonist in inhibiting the iodinated substance P binding to brain membranes from various species. Direct binding of [3H]CP-96.345 was detected by radioligand analysis using the striatum-enriched membranes from the guinea-pig brain.

Animals↗
PubMed1976

USAN assigned to radioactive pharmaceutical.

The United States Adopted Names (USAN) applicable to radioactive pharmaceuticals are composed of the names of the basic compound serving as the carrier for the radioactivity, the symbol for the radioactive isotope, and the atomic weight (since several radioactive isotopes of a given element may be in use--see listing under iodine). The following listing of nonproprietary names (shown in boldface type) is arranged in alphabetical order according to the English name of the radioactive element. The isotopes of hydrogen are listed under their specific names, deuterium and tritium. Radioactive pharmaceuticals are often supplied by the manufacturers under a designation equivalent to the adopted nonproprietary name and are listed as such; specific trademarks are given in brackets when they exist. Basic information relative to these lists was given in the editorial that accompanied the first such listing.

Pharmaceutical Preparations↗
PubMed1986

[Organ distribution of ruthenocenyl biogenic amine derivatives--radiodiagnostic agents for the adrenals and ovaries?].

The organ distribution of 103Ru labelled ruthenocenyl derivatives of tyramine, histamine, benzylamine, phenylethylamine and homoveratrylamine were measured in rats. The derivatives of tyramine, histamine and benzylamine showed a high affinity for the adrenal and ovar. Adrenal/muscle ratios up to 2000:1 were gained but only if the dose was administered i.v. and was below 0.1 mumol/kg. The ruthenocenyl derivatives of tyramine labelled with 103Ru in the ruthenocene moiety or with 14C in the tyramine moiety showed a parallel distribution pattern but completely different from the distribution of 103RuCl3. This indicates that the tyramine derivatives are not destroyed in the body yielding Ru-ions. The advantages of the ruthenocenyl derivatives in comparison with the known amphetamine derivatives labelled with radioactive iodine are discussed.

Adrenal Glands↗
PubMed1999

Long-term palliation in metastatic carcinoid tumours with various applications of meta-iodobenzylguanidin (MIBG): pharmacological MIBG, 131I-labelled MIBG and the combination.

Carcinoid tumours are rare, but well known for their characteristic presentation with diarrhoea and flushes due to overproduction of serotonin in the case of liver metastases. Treatment is mainly based on the reduction of vasoactive peptide hypersecretion and symptomatic improvement Octreotide and interferon are widely applied and effective treatment options to induce symptomatic improvement and, to a lesser extent, biochemical response. The main drawbacks, however, are the need for frequent injections and/or the occurrence of side effects. A rather new approach is the application of meta-iodobenzylguanidine (MIBG), which resembles noradrenalin and serotonin. In carcinoid patients, MIBG is taken up in the tumour cells and stored in the neurosecretory granules. When labelled with 131 iodine, radionuclide imaging is positive in up to 70% of the patients. In these patients, two cycles of a therapeutic dose of radioactive MIBG may induce long-lasting palliation (8 months) by internal irradiation. Also, the non-radioactive MIBG compound may be effective in palliation, even in patients with a negative scan. The mode of action is based on specific tumour acidification as found in animal models, and/or based on its effect as a false neurotransmittor. Three case reports demonstrate different therapeutic possibilities of MIBG: 1) symptomatic relief with unlabelled MIBG, which is a safe and simple treatment; 2) the longterm palliation following radioactive treatment; and 3) an additional new aspect of predosing with unlabelled MIBG followed by radioactive MIBG led to improved tumour targeting and impressive clinical response.

3-Iodobenzylguanidine↗
PubMed2000

Studies on thyroid function in rats subjected to repeated oral administration with kojic acid.

To elucidate the effects of kojic acid on thyroid function, the compound was given orally to male rats for 4 weeks at 0, 4, 15, 62.5, 250 and 1,000 mg/kg. In 1,000 mg/kg treatment of kojic acid, the rats showed a slight decrease in motility, inhibition of body weight gain, and a decrease in food consumption. An increase in thyroid weight and a morphological change, i.e., hypertrophy of epithelial cells of the thyroid gland follicles, were observed after 1 week of administration. In addition, the uptake of radioactive iodine from blood into the thyroid gland was enhanced and the TCA-precipitable radioactive iodine in the thyroid gland increased in those rats. However, the rates of the iodination in the thyroid gland did not change during the experiment period. Although serum T4 concentration was low in the rats treated with 1,000 mg/kg kojic acid, it was not observed in any changes in TSH concentration. None of these changes were found in the other groups. These observations suggest that massive administration of kojic acid may decrease blood T4 concentration and that thyroid function may be enhanced compensatorily. On the other hand, the absorption of kojic acid was rapid as manifested by the Tmax of blood concentrations of radioactivity, which was as short as 1.0 +/- 0.0 hr, and the t1/2 was 4.8 +/- 0.3 hr. Blood concentrations of radioactivity disappeared nearly completely at 24 hr after administration. This result indicates that the toxic effect observed on the thyroid gland treated with only the largest dosage of kojic acid may depend on a fast decrease following a transient increase of concentration of the compound in the blood.

Animals↗
PubMed1985

Application of O-(4-diazo-3-[125I]iodobenzoyl)sucrose for the detection of the catabolic sites of low density lipoprotein.

The sites of degradation of human low density lipoprotein (LDL), are analyzed using the novel labelling compound O-(4-diazo-3-[125I]iodobenzoyl)sucrose (D125IBS). The decay from rat serum of D125IBS-labelled LDL is identical to the serum decay of conventionally iodinated (ICI method) LDL. The radioactivity derived from D125IBS-labelled LDL accumulates predominantly in the liver after intravenous injection and the hepatic radioactivity remains associated with the lysosomal compartment for an extended period of time, when compared to the radioactivity derived from conventionally iodinated LDL. It is concluded that the D125IBS labelling procedure is an interesting new tool to study the sites of catabolism of serum lipoproteins.

Affinity Labels↗
PubMed2000

Toxicological and cytophysiological aspects of lanthanides action.

Lanthanides, also called rare-earth elements, are an interesting group of 15 chemically active, mainly trivalent, f-electronic, silvery-white metals. In fact, lanthanides are not as rare as the name implies, except for promethium, a radioactive artificial element not found in nature. The mean concentrations of lanthanides in the earth's crust are comparable to those of life-important elements like iodine, cobalt and selenium. Many lanthanide compounds show particular magnetic, catalytic and optic properties, and that is why their technical applications are so extensive. Numerous industrial sources enable lanthanides to penetrate into the human body and therefore detailed toxicological studies of these metals are necessary. In the liver, gadolinium selectively inhibits secretion by Kupffer cells and it decreases cytochrome P450 activity in hepatocytes, thereby protecting liver cells against toxic products of xenobiotic biotransformation. Praseodymium ion (Pr3+) produces the same protective effect in liver tissue cultures. Cytophysiological effects of lanthanides appear to result from the similarity of their cationic radii to the size of Ca2+ ions. Trivalent lanthanide ions, especially La3+ and Gd3+, block different calcium channels in human and animal cells. Lanthanides can affect numerous enzymes: Dy3+ and La3+ block Ca2+-ATPase and Mg2+-ATPase, while Eu3+ and Tb3+ inhibit calcineurin. In neurons, lanthanide ions regulate the transport and release of synaptic transmitters and block some membrane receptors, e.g. GABA and glutamate receptors. It is likely that lanthanides significantly and uniquely affect biochemical pathways, thus altering physiological processes in the tissues of humans and animals.

Animals↗
PubMed1997

[Biological effects of the iodine 131 radionuclide].

Radionuclides released into the biosphere by local sources are added to artificial radionuclides introduced by atmospheric nuclear weapon tests or nuclear accidents. The main polluters are nuclear industry reprocessing plants and nuclear power stations. Other sources are hospitals using radionuclides for diagnostics and therapy. This article presents the effects of radioisotope iodine-131 on a living organism, on the cell and on the genetic material within the cell. Beside the accident iodine-131 contamination, its wide diagnostic and therapeutic application attributes to the total radiation dose. The biological distribution of this radiopharmaceutical in the body depends on the way of use and on the and physical and chemical shape of this radiopharmaceutical. A few minutes after the administration, all iodine ingested or inhaled is rapidly absorbed by blood. The irradiation dose in blood depends on the administered amount of 131I and the fraction passing into the plasma as protein-bound 131I. After entering the organism, iodine mostly accumulates in the thyroid gland. The effect of ionized radiation on living cells are proportional to the dosage of 131I. Intracellular radioactive decay occurs in cytoplasm, in karyoplasm, and in the DNA molecule incorporated fraction. Beside the damage resulting from the deposition of radiation energy, 131I causes biological damage when it decays while the isotope is incorporated into the DNA of human cells. Certain beta/gamma-emitting isotopes such as 131I may be particularly hazardous when incorporated into DNA. Incorporation of radioactively labeled compounds into the DNA leads to highly selective irradiation of the nucleus of the proliferating cells. This produces pronounced biological damage as the genetic material in the cell nucleus constitutes the most radiosensitive target within the cell.

Animals↗
PubMed1973

Studies on mono- and diiodohistidine. II. Congenital goitrous hypothyroidism with thyroglobulin defect and iodohistidine-rich iodoalbumin production.

Butanol-insoluble iodinated compounds in the urine of patients with congenital goiters have been generally regarded as iodopeptides. Monoiodohistidine (MIH) and diiodohistidine (DIH) were identified from the urine of four patients with congenital goitrous hypothyroidism. From radioiodine studies, 40-70% of the urinary radioactivity was in the iodide-free fraction from which about 40% was identified as MIH and DIH by crystallizations to a constant specific activity. Iodotyrosines were simultaneously identified in the urine. However the presence of an iodotyrosine-deiodinase activity was demonstrated in the two removed goiters with a normal K(m) for MIT. In vivo iodotyrosine deiodination was normal for hypothyroid subjects. No thyroglobulin was identified in the thyroids from these patients. The major iodoprotein was iodoalbumin which, after in vivo labeling, contained 84-89% of the total soluble protein radioactivity. The thyroxine content of the goiter iodoalbumins and other iodoproteins was extremely low. Iodohistidines were identified in comparable proportions in the iodoalbumin and in the other iodoproteins isolated from each goiter. The average iodohistidine content of these proteins as crystallizable MIH and DIH was in the individual cases 15 and 4% of the in vivo incorporated radioiodine. DIH was identified in all iodoprotein fractions. The mean DIH/MIH ratios from the individual cases were 1.16 and 0.35. The corresponding DIT/MIT ratios were 3.19 and 1.45, respectively. The major consequence of this thyroglobulin defect is the iodination of inappropriate proteins (mainly albumin) resulting in low yields of thyroxine and high yields of iodohistidines. Iodohistidines from the goiter iodoproteins were not deiodinated and, at least for MIH, were quantitatively excreted in the urine of these patients. From the MIH iodoalbumin content and the MIH urinary excretion, goiter iodoalbumin turnover estimates were made and, although elevated, could not maintain a normal thyroxine secretion. The urinary excretion of iodohistidines easily demonstrated by column chromatography is offered as a test for detecting this variety of congenital goiter.

Adult↗
PubMedDate not supplied

Synthesis and biologic evaluation of a radioiodinated quinazolinone derivative for enzyme-mediated insolubilization therapy.

We have developed a new strategy that aims to concentrate therapeutic radionuclides within solid tumors. This approach, which we have named EMIT (enzyme-mediated insolubilization therapy), is a method for enzyme-dependent, site-specific, in vivo precipitation of a radioactive molecule (from a water-soluble precursor) within the extracellular space of solid tumors. The prodrug, ammonium 2-(2'-phosphoryloxyphenyl)-6-iodo-4-(3H)-quinazolinone, labeled with iodine-125 ((125)IPD) and its authentic compound labeled with iodine-127 (IPD) have been synthesized, purified, and characterized. The alkaline phosphatase (ALP)-mediated conversion of these water-soluble nonfluorescent prodrugs to the water-insoluble fluorescent species, iodine-125-labeled 2-(2'-hydroxyphenyl)-6-iodo-4-(3H)-quinazolinone ((125)ID) and its iodine-127-labeled derivative (ID), has been demonstrated in vitro. Biodistribution studies in mice indicate that both (125)IPD and (125)ID are minimally retained by most tissues and organs. In addition, following its intravenous injection in mice, (125)IPD is localized in ALP-rich regions and converted to (125)ID, which remains indefinitely within the tissues where it is produced. We believe that EMIT is a strategy that will lead to the active and specific concentration and entrapment of therapeutic radionuclides within solid tumors, the consequent protracted irradiation of tumor cells within the range of the emitted particles, and the effective therapy of solid tumors.

Alkaline Phosphatase↗
PubMedDate not supplied

Targeted delivery of DNA using YEE(GalNAcAH)3, a synthetic glycopeptide ligand for the asialoglycoprotein receptor.

In vivo gene therapy shows promise as a treatment for both genetic and acquired disorders. The hepatic asialoglycoprotein receptor (ASGPr) binds asialoorosomucoid-polylysine-DNA (ASOR-PL-DNA) complexes and allows targeted delivery to hepatocytes. The tris(N-acetylgalactosamine aminohexyl glycoside) amide of tyrosyl(glutamyl) glutamate [YEE(GalNAcAH)3] has been previously reported to have subnanomolar affinity for the ASGPr. We have used an iodinated derivative of YEE(GalNAcAH)3 linked to polylysine and complexed to the luciferase gene (pCMV-Luc) in receptor-binding experiments to establish the feasibility of substituting ASOR with the synthetic glycopeptide for gene therapy. Scatchard analyses revealed similar Kd values for both ASOR and the glycopeptide. Binding and internalization of 125I-Suc-YEE(GalNAcAH)3 were competitively inhibited with either unlabeled ASOR or glycopeptide. The reverse was also true; 125I-ASOR binding was competed with unlabeled YEE(GalNAcAH)3 suggesting specific binding to the ASGPr by both compounds. Examination of in vivo delivery revealed that the 125I-labeled glycopeptide complex mimicked previous results observed with 125I-ASOR-PL-DNA. CPM in the liver accounted for 96% of the radioactivity recovered from the five major organs (liver, spleen, kidney, heart, and lungs). Cryoautoradiography displayed iodinated glycopeptide complex bound preferentially to hepatocytes rather than nonparenchymal cells. In vitro, as well as in vivo, transfections using the glycopeptide-polylysine-pCMV-luciferase gene complex (YG3-PL-Luc) resulted in expression of the gene product. These data demonstrate that the YEE(GalNAcAH)3 synthetic glycopeptide can be used as a ligand in targeted delivery of DNA to the liver-specific ASGPr.

Animals↗
PubMed1978

A simple methods for labeling BSP with 131I.

BSP was labeled with 131I using the Greenwood and Hunter method, which was rapid and simple. The chromatoelectrophoresis of the labeled compound showed that the labeling efficiency was 100%. Scintigraphic studies gave good results in accordance with radioactive BSP distribution reported in the literature.

Electrophoresis↗
PubMed2006

Synthesis of 131I-labeled glucose-conjugated inhibitors of O6-methylguanine-DNA methyltransferase (MGMT) and comparison with nonconjugated inhibitors as potential tools for in vivo MGMT imaging.

O(6)-Substituted guanine derivatives are powerful agents used for tumor cell sensitization by inhibition of the DNA repair enzyme O(6)-methylguanine-DNA methyltransferase (MGMT). To provide targeted accumulation of MGMT inhibitors in tumor tissue as well as tools for in vivo imaging, we synthesized iodinated C(8)-alkyl-linked glucose conjugates of 2-amino-6-(5-iodothenyl)-9H-purine (O(6)-(5-iodothenyl) guanine, ITG) and 2-amino-6-(3-iodobenzyloxy)-9H-purine (O(6)-(5-iodobenzyl) guanine, IBG). These compounds have MGMT inhibitor constants (IC(50) values) of 0.8 and 0.45 microM for ITGG and IBGG, respectively, as determined in HeLa S3 cells after 2-h incubation with inhibitor. To substantiate that the (131)I-(hetero)arylmethylene group at the O(6)-position of guanine is transferred to MGMT, both the glucose conjugated inhibitors ITGG and IBGG and the corresponding nonglucose conjugated compounds ITG and IBG were labeled with iodine-131. The radioiodinations of all compounds with [(131)I]I(-) were performed with radiochemical yields of >70% for the destannylation of the corresponding tri-n-butylstannylated precursors. The binding ability of [(131)I]ITGG, [(131)]IBGG, [(131)I]ITG, and [(131)I]IBG to purified MGMT was tested. All radioactive compounds were substrates for MGMT, as demonstrated using a competitive repair assay. The newly synthesized radioactive inhibitors were utilized to study ex vivo biodistribution in mice, and the tumor-to-blood ratio of tissue uptake of [(131)I]IBG and [(131)I]IBGG was determined to be 0.24 and 0.76 after 0.5 h, respectively.

Animals↗