131I Induced Hematological Alterations in Rat Blood: Protection by Zinc

The present study was planned to determine the potential of zinc in attenuating the toxicity induced by ¹³¹I in rat blood. Female wistar rats were segregated into four main groups. Animals in Group I served as normal controls; Group II animals were administered a dose of 3.7 Mbq of ¹³¹I (carrier free) intraperitoneally, Group III was supplemented with Zinc in the form of ZnSo₄.7H₂O (227 mg/l drinking water), and Group IV was given a combined treatment of Zinc as well as ¹³¹I, in a similar way as was given to Groups IV and II animals, respectively. The effects of different treatments were studied on various parameters in rat blood including hemoglobin (Hb) levels, % hematocrit, zinc protoporphyrins (ZPP), activities of enzymes which included aminolevulinic acid dehydratase (δ-ALAD) and Na⁺ K⁺ ATPase and uptake of ⁶⁵Zn in blood. The study revealed an increase in the levels of hemoglobin, % hematocrit, activities of δ-ALAD, Na⁺ K⁺ ATPase and uptake of ⁶⁵Zn, 7 days after the ¹³¹I treatment. On the contrary, the levels of ZPP were found to be significantly decreased after ¹³¹I treatment. However, zinc treatment to ¹³¹I-treated animals significantly attenuated the various biochemical and hematological indices. Moreover, zinc treatment to the ¹³¹I-treated animals could significantly decrease the uptake of ⁶⁵Zn, which was increased after ¹³¹I treatment. Based upon these data, the present study suggests that zinc has the potential to attenuate ¹³¹I induced toxicity by restoring the altered hematological indices and biochemical changes.     

Evidence for a secretion of thyroxine by isolated hog thyroid cells.

Isolated thyroid cells prepared from hog thyroid glands by tryptic dispersion were incubated with 131I- for 1--6 h. Free [131I]thyroxine was identified in the incubation medium by three chromatographic methods. Neither [131I]iodotyrosines nor [131I]triiodothyronine were detected. The [131I]thyroxine released in the medium by 100 mul of cells (packed cell volume) after a 6-h incubation period amounted to 1.16% (S.E. = +/- 0.39) of the total radioactivity. The medium [131I]thyroxine represented 15--25% of the total [131I]thyroxine synthesized during the 6 h of incubation. Thyrotropin, 1--60 munits/ml, increased the medium [131I]thyroxine content 2-4 fold. Dibutyryl cyclic AMP mimicked the effect of thyrotropin. The amount of medium [131]thyroxine was strictly related to the amount of incubated cells but was independent of the volume of the incubation medium. When prelabeled cells were incubated in the presence of methimazole the increase in medium [131I]thyroxine was quantitatively related to a decrease in the intracellular [131I]thyroxine. Addition of dinitrotyrosine, an inhibitor of the deiodinase activity, induced the release of iodotyrosines in the incubation medium. That the incubation supernatant of isolated thyroid cells did contain free thyroxine but not iodotyrosines suggests that the normal mechanisms of proteolysis of thyroglobulin and deiodination of iodotyrosines inside the cells are preserved. From these data, it was concluded that the thyroxine release by isolated cells represents a real secretion.     

Diagnostic scintigraphy and effectiveness of 131I radioiodine therapy in differentiated thyroid carcinoma (DTC)

INTRODUCTION: Since the effect of pre-therapeutic scintigraphy on the outcome of DTC treatment is debated, we evaluated factors affecting the effectiveness of (131)I therapy with respect to the delay between diagnostic scintigraphy and the application of radioiodine. MATERIAL AND METHODS: In the studied group of 60 patients with DTC, mean age 54.6 +/- 13.0 years, four weeks prior to the planned diagnostics, L-thyroxine was withdrawn and the following tests performed: (131)I (4 MBq) uptake above the neck, thyroid volume by USG, TSH and hTg level. Wholebody scintigraphy (37 MBq) was performed. The time between this diagnostic scintigraphy and application of (131)I (3657 MBq) was calculated. Based on whole-body 131I scintigraphy (74 MBq) performed 1 year after radioiodine treatment, the patients were divided into: group I - 42 patients with no tracer accumulation, and group II--18 patients who continued to accumulate (131)I in the neck. RESULTS: The differences between the median values of (131)I uptake and of thyroid volumes, and between the TSH and hTg median values in the two groups of patients were found not to be statistically significant. The average times between diagnostic scintigraphy and (131)I treatment in group I and II (9.4 vs. 8.3 weeks, respectively) were not significantly different either. CONCLUSION: Despite the different effectiveness of supplementary (131)I treatment, patients in group I and group II showed no statistically significant differences in the studied parameters. It appears that the diagnostic (131)I activity of 37 MBq and the time between diagnostic scintigraphy and application of (131)I did not have any effect on the results of the treatment in our group of patients.     

Binding of acetylated low density lipoprotein and maleylated bovine serum albumin to the rat liver: one or two receptors?

The liver is the major organ involved in clearance of acetylated low density lipoprotein (acetyl-LDL) and maleylated serum albumin (Mal-BSA). Quantitative analysis of the hepatic uptake by sequential scintigraphy in rats shows that the hepatic uptake capacity for Mal-BSA is at least 15 times larger than for acetyl-LDL particles. A membrane-associated M approximately 250,000 daltons hepatic receptor for acetyl-LDL and Mal-BSA was 1450-fold purified from total membrane by Triton X-114 solubilization, chromatography on polyethylenimine cellulose and gel filtration. This receptor incorporated into liposomes displayed a saturable binding of [131I]Mal-BSA with a dissociation constant Kd = 15 nM and to [131I]acetyl-LDL with a dissociation constant Kd = 0.9 nM. The binding of both ligands was sensitive to poly(vinyl sulfate). The purified scavenger receptor system has a binding capacity for [131I]Mal-BSA 20 times larger than for [131I]acetyl-LDL. This is similar to the maximal removal capacity of the rat liver for both ligands in vivo. Binding studies with Mal-BSA, acetyl-LDL and anti-idiotypic receptor antibodies as competitors for [131I]Mal-BSA and [131I]acetyl-LDL binding demonstrate that [131I]Mal-BSA and [131I]acetyl-LDL compete for a common binding site. However, not all of the Mal-BSA binding sites are capable of interacting with acetyl-LDL.     

Cerebrospinal fluid flow and iodide131 transport in the spinal subarachnoid space

Free Na¹³¹ I and ¹³¹I-Albumin were injected in the cisterna magna of rhesus monkeys. The dynamics of descent into the spinal subarachnoid space and transport out of the cerebrospinal fluid were determined by gamma scintigraphy. ¹³¹I-Albumin moved slowly caudally, reaching the sacral CSF in three hours. Free Na¹³¹I was rapidly absorbed locally and did not descend. When its transport out of cerebrospinal fluid was inhibited by the addition of unlabeled isotonic Na I, ¹³¹I descended slowly at a rate parallel to that of tagged albumin. Injection of Na¹³¹I in hypertonic solutions caused immediate descent. Two minute periods of tumbling activity caused rapid movement of Na¹³¹I and ¹³¹I-Albumin into the lumbar spinal fluid. Na¹³¹I dynamics may serve as a model for other molecules actively transported out of cerebrospinal fluid, such as 5-hydroxy-indoleacetic acid; descent into caudal spinal fluid may depend on the degree of efflux from cerebrospinal fluid and on the animal's activity.     

食盐加碘后甲状腺摄 ~（131）I率的变化及其与尿碘的关系

目的：了解食盐加碘后健康人及甲亢患者甲状腺摄131I率的变化及其与24小时尿碘含量的相关性,探讨甲状腺摄131I率与碘营养状况的关系。方法：对比食盐加碘前后健康体检者及甲亢患者甲状腺摄131I率的变化,分析健康体检者甲状腺摄131I率、晨尿碘浓度及经肌酐校正的尿碘含量与24小时尿碘含量的相关关系。结果：健康人及甲亢患者食盐加碘后3、6及24小时甲状腺摄131I率均显著降低;健康体检者甲状腺摄131I率与24小时尿碘含量呈负相关（r=-0.7651,P〈0.001）,晨尿碘浓度与24小时尿碘含量呈正相关（r=0.8231,P〈0.001）,经肌酐校正的尿碘含量与24小时尿碘含量呈正相关（r=0.9054,P〈0.001）。结论：食盐加碘对甲状腺摄131I率有显著影响,应重新确立甲状腺摄131I率的正常范围及甲亢的诊断标准;经肌酐校正的尿碘含量较晨尿碘浓度能更准确地反映碘营养状况;甲状腺摄131I率可作为评估个体碘营养状况的指标,可以稳定地反映近期的碘营养状况。     

食盐加碘后甲状腺摄131I 率的变化及其与尿碘的关系

目的：了解食盐加碘后健康人及甲亢患者甲状腺摄131I 率的变化及其与24 小时尿碘含量的相关性,探讨甲状腺摄131I 率与 碘营养状况的关系。方法：对比食盐加碘前后健康体检者及甲亢患者甲状腺摄131I 率的变化,分析健康体检者甲状腺摄131I 率、晨 尿碘浓度及经肌酐校正的尿碘含量与24小时尿碘含量的相关关系。结果：健康人及甲亢患者食盐加碘后3、6 及24 小时甲状腺 摄131I 率均显著降低;健康体检者甲状腺摄131I 率与24 小时尿碘含量呈负相关（r=－0.7651, P<0.001）,晨尿碘浓度与24 小时尿碘 含量呈正相关（r=0.8231, P<0.001）,经肌酐校正的尿碘含量与24 小时尿碘含量呈正相关（r=0.9054, P<0.001）。结论：食盐加碘对甲 状腺摄131I 率有显著影响,应重新确立甲状腺摄131I 率的正常范围及甲亢的诊断标准;经肌酐校正的尿碘含量较晨尿碘浓度能更 准确地反映碘营养状况;甲状腺摄131I率可作为评估个体碘营养状况的指标,可以稳定地反映近期的碘营养状况。     

Biological evaluation of ring- and side-chain-substituted m-iodobenzylguanidine analogues

A number of ring- and side-chain-substituted m-iodobenzylguanidine analogues were evaluated for their lipophilicity, in vitro stability, uptake by SK-N-SH human neuroblastoma cells in vitro, and biodistribution in normal mice. As expected, the lipophilicity of m-iodobenzylguanidine increased when a halogen was introduced onto the ring and decreased with the addition of polar hydroxyl, amino, and nitro substitutents. Most of the derivatives showed reasonable stability up to 24 h in PBS at 37 degrees C. While N(1)-hydroxy-N(3)-3-[(131)I]iodobenzylguanidine and 3,4-dihydroxy-5-[(131)I]iodobenzylguanidine generated a more nonpolar product in addition to the free iodide, 3-[(131)I]iodo-4-nitrobenzylguanidine decomposed to a product more polar than the parent compound. The specific uptake of 4-chloro-3-[(131)I]iodobenzylguanidine, 3-[(131)I]iodo-4-nitrobenzylguanidine, and N(1)-hydroxy-N(3)-3-[(131)I]iodobenzylguanidine by SK-N-SH human neuroblastoma cells in vitro, relative to that of m-[(125)I]iodobenzylguanidine, was 117 +/- 10%, 50 +/- 4%, and 12 +/- 2%, respectively. The specific uptake of the known m-iodobenzylguanidine analogues 4-hydroxy-3-[(131)I]iodobenzylguanidine and 4-amino-3-[(131)I]iodobenzylguanidine was 80 +/- 4% and 66 +/- 4%, respectively. None of the other m-iodobenzylguanidine derivatives showed any significant specific uptake by SK-N-SH cells. Heart uptake of 4-chloro-3-[(131)I]iodobenzylguanidine in normal mice was higher than that of m-[(125)I]iodobenzylguanidine at later time points (11 +/- 1% ID/g versus 3 +/- 1% ID/g at 24 h; p < 0.05) while uptake of 3-[(131)I]iodo-4-nitrobenzylguanidine and of N(1)-hydroxy-N(3)-3-[(131)I]iodobenzylguanidine in the heart was lower than that of m-iodobenzylguanidine at all time points. In accordance with the in vitro results, none of the other novel m-iodobenzylguanidine derivatives showed any significant myocardial or adrenal uptake in vivo.     

Synthesis of ring- and side-chain-substituted m-iodobenzylguanidine analogues

With the goal of developing MIBG analogues with improved targeting properties especially for oncologic applications, several radioiodinated ring- and side-chain-substituted MIBG analogues were synthesized. Except for 3-[(131)I]iodo-4-nitrobenzylguanidine and N-hydroxy-3-[(131)I]iodobenzylguanidine, the radioiodinated analogues were prepared at no-carrier-added levels from their respective tin precursors. The radiochemical yields generally were in the range of 70-90% except for 3-amino-5-[(131)I]iodobenzylguanidine for which a radiochemical yield of about 40% was obtained. While the silicon precursor N(1),N(2)-bis(tert-butyloxycarbonyl)-N(1)-(4-nitro-3-trimethylsilylbenzyl)guanidine did not yield 3-[(131)I]iodo-4-nitrobenzylguanidine, its deprotected derivative, N(1)-(4-nitro-3-trimethylsilylbenzyl)guanidine was radioiodinated in a modest yield of 20% providing 3-[(131)I]iodo-4-nitrobenzylguanidine. Exchange radioiodination of 3-iodo-4-nitrobenzylguanidine gave 3-[(131)I]iodo-4-nitrobenzylguanidine in 80% radiochemical yield. No-carrier-added [(131)I]NHIBG was prepared from its silicon precursor N(1)-hydroxy-N(3)-(3-trimethylsilylbenzyl)guanidine in 85% radiochemical yield.     

Radioimmunoassay for Type A Toxin of Clostridium botulinum

A preparation of pure type A toxin of Clostridium botulinum was labeled with (131)I in the presence of chloramine-T and carrier-free isotope. The radioactive toxin ((131)I Tox) was used in a radioimmunoassay procedure similar to that of Berson and Yalow. Dilutions of antibody to the toxin, capable of binding 50% of the added (131)I Tox, were mixed with a sample of the labeled toxin and various concentrations of unlabeled toxin ('Cold' Tox). When concentration of Cold Tox were plotted against the ratio (131)I bound/(131)I not bound, a standard curve was established that could be used to estimate the concentration of Cold Tox in a test mixture. This assay was sensitive to as little as 100 mouse minimum lethal dose and was highly specific for the serological type of the toxin used.     

131I uptake in human thyroid after antidote treatment for mixed fission products contamination

The efficacy of a mixed antidote treatment in blocking 131I uptake in humans was investigated in two volunteers. Simultaneous oral administration of 10 g of calcium alginate, 3 g of ferrihexacyanoferrate (II) and 130 mg of potassium iodide 30 min before 131I administration caused an almost complete block of the 131I thyroid uptake in both subjects. This indicated that calcium alginate and ferrihexacyanoferrate (II) had no influence on the blocking effect of potassium iodide on 131I thyroid uptake. This finding is important because mixed antidote treatment is the recommended treatment in cases of accidental exposure to mixed fission products.     

Diurnal rhythms of thyroid hormones in rooster chicks (Gallus domesticus). 2. Studies on the protein-bound radioiodine and the "free" hormone portion]

In four week old cockerels the plasma was investigated for cyclic changes in total radioactivity, PB131I, PI131I, and "free" thyroid hormones 24 hours after injection of Na131I. Maxima in total radioactivity were observed at 3.00 am and 9.00 pm. They were significant different from the minima at noon (2P less than 0.005). At the same points of the day maxima, resp. minima were found in the PB131I and the "free" hormones. The "free" hormones expressed in per cent of total hormones showed low values at 6.00 am, 3.00 pm, and 9.00 pm. The diurnal changes in haematocrit and albumin concentration were not responsible for the variation of PB131I. In order to eleminate effects of isotope dilution by ingested iodine the PB131I was expressed in per cent of total radioactivity of plasma (= conversion rate) or resp. in per cent of thyroidal radioiodine uptake. The obtained values showed maxima at 6.00 am and 9.00 pm. From that we conclude again on a stimulation of the thyroid at these times.     

Evidence for a secretion of thyroxine by isolated hog thyroid cells

Isolated thyroid cells prepared from hog thyroid glands by tryptic dispersion were incubated with ¹³¹I⁻ for 1–6 h. Free [¹³¹I]thyroxine was identified in the incubation medium by three chromatographic methods. Neither [¹³¹I]iodotyurosines nor [¹³¹I]triiodothyronine were detected. The [¹³¹I]thyroxine released in the medium by 100 μl of cells (packed cell volume) after a 6-h incubation period amounted to 1.16% (S.E. = ± 0.39) of the total radioactivity. The medium [¹³¹I]thyroxine represented 15–25% of the total [¹³¹I]thyroxine synthesized during the 6 h of incubation. Thyrotropin, 1–60 munits/ml, increased the medium [¹³¹I]thyroxine content 2–4 fold. Dibutyryl cyclic AMP mimicked the effect of thyrotropin. The amount of medium [¹³¹I]thyroxine was strictly related to the amount of incubated cells but was independent of the volume of the incubation medium. When prelabeled cells were incubated in the presence of methimazole the increase in medium [¹³¹I]thyroxine was quantitatively related to a decrease in the intracellular [¹³¹I]thyroxine. Addition of dinitrotyrosine, an inhibitor of the deiodinase activity, induced the release of iodotyrosines in the incubation medium. That the incubation supernatant of isolated thyroid cells did contain free thyroxine but no iodotyrosines suggests that the normal mechanisms of proteolysis of thyroglobulin and deiodination of iodotyrosines inside the cells are preserved. From these data, it was concluded that the thyroxine release by isolated cells represents a real secretion.     

Radioiodination of proteins using prosthetic group: a convenient way to produce labelled proteins with in vivo stability.

Radiolabelled peptides can provide new approaches for radiopharmaceutical development. Several prosthetic groups have been developed for radioiodination of proteins in order to minimize in vivo dehalogenation. In this work, the prosthetic group N-succinimidyl 4-[131I]iodobenzoate ([131I]SIB) was obtained by an alternative procedure that employs Cu(I) assisted radioiododebromination to produce p-[131I]iodobenzoic acid with a radiochemical yield of 92.73 +/- 1.51% (N = 6), followed by the reaction with TSTU (O-(N-succinimidyl)-N,N,N'N'-tetramethyluronium) in alkaline medium. The HPLC profile of the final product, revealed that [131I]SIB was obtained with a radiochemical purity of 98.19 +/- 1.14% (N = 6 Swiss mices (normal group) and animals with inflammation focus developed on the right thigh by tupertine injection) were injected with human immunoglobulin (IgG) radioiodinated with [131I]SIB and by direct method (Iodogen). The comparison of results showed a fast blood clearance, better target organ/background relation and low uptake in thyroid and stomach (p < 0.01) for the protein labelled with [131I]SIB, what suggests a greater in vivo stability.     

Meta-iodobenzylguanidine derivatives containing a second guanidine moiety

Radioiodinated meta-iodobenzylguanidine (MIBG) is used in the diagnosis and therapy of various neuroendocrine tumors. To investigate whether an additional guanidine function in the structure of MIBG will yield analogues that may potentially enhance tumor-to-target ratios, two derivatives-one with a guanidine moiety and another with a guanidinomethyl group at the 4-position of MIBG-were prepared. In the absence of any uptake-1 inhibiting conditions, the uptake of 4-guanidinomethyl-3-[(131)I]iodobenzylguanidine ([(131)I]GMIBG) by SK-N-SH cells in vitro was 1.7+/-0.1% of input counts, compared to a value of 40.3+/-1.4% for [(125)I[MIBG suggesting that guanidinomethyl group at the 4-position negated the biological properties of MIBG. On the other hand, 4-guanidino-3-[(131)I]iodobenzylguanidine ([(131)I]GIBG) had an uptake (5.6+/-0.3%) that was 12-13% that of [(125)I]MIBG (46.1+/-2.7%), and the ratio of uptake by control over DMI-treated (nonspecific) cultures was higher for [(131)I]GIBG (20.9+/-0.3) than [(125)I]MIBG itself (15.0+/-2.7). The exocytosis of [(131)I]GIBG and [(125)I]MIBG from SK-N-SH cells was similar. The uptake of [(131)I]GIBG in the mouse target tissues, heart and adrenals, as well as in a number of other tissues was about half that of [(125)I]MIBG. These results suggest that substitution of guanidine functions, especially a guanidinomethyl group, in MIBG structure may not be advantageous.     

~(131)I-Herceptin对HER2过表达乳腺癌细胞Bcl-xL表达的影响

目的:探讨131I-Herceptin对HER2过表达乳腺癌细胞Bcl-x L表达的影响。方法:采用Iodogen法制备131I-Herceptin,超滤法纯化后测定其标记率、放射化学纯度和免疫结合率。通过免疫荧光法检测乳腺癌细胞表面HER2表达水平。131I(4.625 MBq/m L)、Herceptin(125μg/m L)及131I-Herceptin(4.625 MBq/m L)干预乳腺癌BT474细胞后,Western blot检测细胞中Bcl-x L的表达。结果:131I-Herceptin的标记率、放射化学纯度和免疫结合率分别为(89.71±2.93)%、(91.80±1.43)%和(58.84±3.35)%。BT474细胞膜表面HER2表达水平明显高于MDA-MB-231细胞。Herceptin、131I-Herceptin组BT474细胞内Bcl-x L表达水平明显低于对照组及131I组(均P0.01),而Herceptin与131I-Herceptin组之间细胞内Bcl-x L含量差异无统计学意义(P0.05)。结论:131I-Herceptin保留Herceptin对HER2过表达乳腺癌细胞Bcl-x L表达的抑制作用并促进细胞凋亡,进而与131I产生协同作用,较Herceptin更有效地杀伤HER2过表达乳腺癌细胞。     

N-succinimidyl 3-[(131)I]iodo-4-phosphonomethylbenzoate ([(131)I]SIPMB), a negatively charged substituent-bearing acylation agent for the radioiodination of peptides and mAbs

An important criterion in design of acylation agents for the radioiodination of internalizing monoclonal antibodies (mAbs) is to maximize the retention of radioiodine in the tumor following mAb intracellular processing. We have previously shown that labeling methods that generate positively charged catabolites have enhanced tumor retention. Herein we have extended this strategy to investigate the potential utility of labeling internalizing mAbs with an acylation agent that yielded labeled catabolites that would be negatively charged at lysosomal pH. The negatively charged acylation agent, N-succinimidyl 3-[(131)I]iodo-4-phosphonomethylbenzoate ([(131)I]SIPMB), was prepared from its tin precursor, N-succinimidyl 4-di-tert-butylphosphonomethyl-3-trimethylstannylbenzoate (tBu-SPMTB), in 40% radiochemical yield. The free acid, 3-[(131)I]iodo-4-phosphonomethylbenzoic acid ([(131)I]IPMBA), was also prepared from the corresponding precursor, 4-di-tert-butylphosphonomethyl-3-trimethylstannylbenzoic acid (tBu-PMTBA), in 80% radiochemical yield. The rapidly internalizing mAb L8A4 was conjugated to [(131)I]SIPMB in 25-40% yield with preservation of its immunoreactivity. Internalization and processing in the U87DeltaEGFR glioma cell line was studied in a paired label format with L8A4 labeled with (125)I using the Iodogen method. Retention of initially bound radioactivity in these cells at 24 h from [(131)I]SIPMB-labeled mAb was approximately 6-fold higher than that for directly labeled mAb. Catabolite analysis demonstrated that this difference reflected an order of magnitude higher retention of low molecular weight species in these cells. The [(131)I]SIPMB-L8A4 conjugate was intact over the first 2 h; thereafter, lysine-[(131)I]SIPMB was the predominant catabolite. In contrast, L8A4 labeled using Iodogen rapidly gave rise to mono-[(125)I]iodotyrosine within 2 h, which then cleared rapidly from the cells. These results suggest that SIPMB could be a potent candidate for labeling internalizing mAbs and warrant further study.     

Intrathyroidal iodine metabolism in the rat. The influence of diet and the administration of thyroid-stimulating hormone

1. Ratios of mono[¹³¹I]iodotyrosine and di[¹³¹I]iodotyrosine (R values) and the incorporation of ¹³¹I into iodothyronines have been estimated in rat thyroid glands from 30min. to 38hr. after the administration of [¹³¹I]iodide. 2. In rats receiving a powdered low-iodine diet the R values were close to unity and did not change with time after the administration of [¹³¹I]iodide. In rats receiving a commercial pellet diet the R values fell from a mean of 0·8 at 30min. after [¹³¹I]iodide administration to 0·49 at 38hr. 3. Administration of 0·5–2·0i.u. of thyroid-stimulating hormone before giving the injection of [¹³¹I]iodide caused a small diminution in the R value when the time between injecting [¹³¹I]iodide and killing the animal was 16hr. or more. 4. Iodothyronines represented a greater percentage of the total thyroid-gland radioactivity in the iodine-deficient animals than in animals fed on the pellet diet. Thyroid-stimulating hormone had little effect, if any, on the iodothyronine contents.     

Genetic effects of 131I in reproductive cells of male mice

A study was made of the frequencies of dominant lethal mutations (DLM) in pre- and post-meiotic germ cells, reciprocal translocations (RT) in spermatogonia and abnormal sperm heads (ASH) induced by a single intraperitoneal administration of Na131I with an activity of 1.48-740 kBq/g to male mice. The frequency of DLM was shown to increase only when postmeiotic cells were exposed to the radionuclide. The RT frequency increased insignificantly with increases in the dose of 131I. The ASH frequency increased only when maximal doses of 131I were administered. The relative biological efficiency (RBE) of 131I with reference to the indices under study is less than 1.     

Effect of short-term and long-term lithium treatment on uptake and retention of iodine-131 in rat thyroid

No significant change occurred in the uptake by the thyroid of male Wistar rats of a standard dose of carrier-free 131I administered intraperitoneally and its retention by the thyroid, as measured by biological and effective half-life, after feeding these rats a powdered pelleted diet containing lithium carbonate (1.1 g per kg of diet) for 7 days. However, continuing this diet for 10 days inhibited thyroid uptake and increased the retention of 131I. Uptake remained suppressed for up to 4 months after lithium treatment and continuing this treatment for 6 months did not result in any significant change in 131I uptake by the thyroid. Lithium treatment for 10 days increased the biological and effective half-life of 131I in the thyroid and this increase continued for the 6 months treatment period. The dose of 131I delivered to the thyroid was significantly lower after 10 days and 1 month of lithium treatment but there was no change in this dose after 2 and 4 months of treatment. However, there was a significant increase after 6 months.