Supplemental Selenium Alleviates the Toxic Effects of Excessive Iodine on Thyroid

As excessive iodine intake is associated with a decrease of the activities of selenocysteine-containing enzymes, supplemental selenium was hypothesized to alleviate the toxic effects of excessive iodine. In order to verify this hypothesis, Balb/C mice were tested by giving tap water with or without potassium iodate and/or sodium selenite for 16 weeks, and the levels of iodine in urine and thyroid, the hepatic selenium level, the activities of glutathione peroxidase (GSHPx), type 1 deiodinase (D1), and thyroid peroxidase (TPO) were assayed. It had been observed in excessive iodine group that hepatic selenium, the activities of GSHPx, D1, and TPO decreased, while in the groups of 0.2 mg/L, 0.3 mg/L and 0.4 mg/L supplemental selenium, the urinary iodine increased significantly. Compared with the group of excessive iodine intake alone, supplemental selenium groups had higher activities of GSHPx, D1, and TPO. We could draw the conclusion that supplemental selenium could alleviate toxic effect of excessive iodine on thyroid. The optimal dosage of selenium ranges from 0.2 to 0.3 mg/L which can protect against thyroid hormone dysfunction induced by excessive iodine intake.     

Effect of selenium on thyroid hormone metabolism in filial cerebrum of mice with excessive iodine exposure

The effects of supplementing selenium on thyroid hormone metabolism were studied on mice with excessive iodine exposure. The serum concentrations of thyroxine (T₄) and triiodothyronine (T₃) and the activities of iodothyronine 5′ and 5-deiodinase (D2, D3) were measured in the brain of filial mice to study the influence of selenium on thyroid hormone metabolism. Measurements were carried out on postnatal day 0, 14, and 28. It was found that selenium supplementation alleviated the adverse effects of excessive iodine on progeny. The serum TT₄ level as well as TT₄ and TT₃ concentrations and D3 activity in cerebrum of progeny decreased, whereas D2 activity increased in the cerebrum of progeny on postnatal day 0 and 14. Selenium supplementation exerted some favorable effects on thyroid hormone metabolism in cerebrum of progeny of dam with excessive iodine intake.     

The role of selenium in thyroid hormone metabolism and effects of selenium deficiency on thyroid hormone and iodine metabolism

Selenium deficiency impairs thyroid hormone metabolism by inhibiting the synthesis and activity of the iodothyronine deiodinases, which convert thyroxine (T₄) to the more metabolically active 3,3′-5 triiodothyronine (T₃). Hepatic type I iodothyronine deiodinase, identified in partially purified cell fractions using affinity labeling with [¹²⁵I]N-bromoacetyl reverse triiodothyronine, is also labeled with⁷⁵Se by in vivo treatment of rats with⁷⁵Se-Na₂SeO₃. Thus, the type I iodothyronine 5′-deiodinase is a selenoenzyme. In rats, concurrent selenium and iodine deficiency produces greater increases in thyroid weight and plasma thyrotrophin than iodine deficiency alone. These results indicate that a concurrent selenium deficiency could be a major determinant of the severity of iodine deficiency.     

Selenoenzyme activities in selenium- and iodine-deficient sheep

This study was conducted to evaluate the effects of single and combined deficiencies of selenium and iodine on selenoenzyme activities in sheep. Twenty-four male lambs were assigned to one of four semisynthetic diets: combined deficient A (Se⁻I), Se-deficient B (Se⁻I⁺), I-deficient C (Se⁺I⁻), and basal diet D (Se⁺I⁺). Thyroid hormones (T₃, T₄), thyroid stimulating hormone (TSH), and inorganic iodine (PII) were determined in plasma. Selenium and glutathione peroxidase activity (GSH-Px) were determined in erythrocytes, and tissue samples, including the thyroid, liver, kidney, and brain, were taken for selenoenzyme analysis. Plasma T₃, T₄, and TSH concentrations were similar in all groups. Type I deiodinase (ID-I) activity in liver and kidney remained unchanged in Se or I deficiency. In contrast, hepatic ID-I activity was increased by 70% in combined Se-I deficiency. Thyroidal cystolic GSH-Px (c-GSH-Px) and phospholipid GSH-Px (ph-GSH-Px) activities remained constant in both Se-deficient groups, whereas thyroidal c-GSH-Px activity increased (57%) in I deficiency. Type II deiodinase (ID-II) activity was not detectable in the cerebrum and cerebellum, whereas cerebellum Type III deiodinase (ID-III) activity was decreased in I deficiency and combined Se-I deficiencies. The results of the present study support a sensitive interaction between Se and I deficiencies in sheep thyroid and brain. Furthermore, the lack of thyroidal ID-I activity, the presservation of the thyroidal antioxidant enzymes, and the increases in hepatic ID-I indicate that a compensatory mechanism(s) works toward retaining plasma T₃ levels, mostly by de novo synthesis of T₃ and peripheral deiodination of T₄ in Se- and I-deficient sheep.     

The role of selenium in thyroid hormone metabolism and effects of selenium deficiency on thyroid hormone and iodine metabolism

Selenium deficiency impairs thyroid hormone metabolism by inhibiting the synthesis and activity of the iodothyronine deiodinases, which convert thyroxine (T₄) to the more metabolically active 3,3′–5 triiodothyronine (T₃). Hepatic type I iodothyronine deiodinase, identified in partially purified cell fractions using affinity labeling with [¹²⁵I]N-bromoacetyl reverse triiodothyronine, is also labeled with⁷⁵Se by in vivo treatment of rats with⁷⁵Se−Na₂SeO₃. Thus, the type I iodothyronine 5′-deiodinase is a selenoenzyme. In rats, concurrent selenium and iodine deficiency produces greater increases in thyroid weight and plasma thyrotrophin than iodine deficiency alone. These results indicate that a concurrent selenium deficiency could be a major determinant of the severity of iodine deficiency.     

Na+/I− Symporter and Type 3 Iodothyronine Deiodinase Gene Expression in Amniotic Membrane and Placenta and Its Relationship to Maternal Thyroid Hormones

Placental type 3 iodothyronine deiodinase (D3) potentially protects the fetus from the elevated maternal thyroid hormones. Na⁺/I^? symporter (NIS) is a plasma membrane glycoprotein, which mediates active iodide uptake. Our objectives were to establish the distribution of NIS and D3 gene expressions in the placenta and the amniotic membrane and to investigate the relationship between placental D3 and NIS gene expressions and maternal iodine, selenium, and thyroid hormone status. Thyroid hormones, urinary iodine concentration (UIC), and selenium levels were measured in 49 healthy term pregnant women. NIS and D3 gene expressions were studied with the total mRNA RT-PCR method in tissues from maternal placenta (n?=?49), fetal placenta (n?=?9), and amniotic membrane (n?=?9). NIS and D3 gene expressions were shown in the fetal and maternal sides of the placenta and amniotic membrane. Mean blood selenium level was 66?±?26.5 μg/l, and median UIC was 143 μg/l. We could not demonstrate any statistically significant relationship of spot UIC and blood selenium with NIS and D3 expression (p?>?0.05). Positive correlations were found between NIS and thyroxine-binding globulin (TBG) (r?=?0.3, p?=?0.042) and between D3 and preoperative glucose levels (r?=?0.4, p?=?0.006). D3 and NIS genes are expressed in term placenta and amniotic membrane; thus, in addition to placenta, amniotic membrane contributes to regulation of maternofetal iodine and thyroid hormone transmission. Further studies are needed to clarify the relationship between maternal glucose levels and placental D3 expression and between TBG and placental NIS expression.     

Oxidative DNA base damage, antioxidant enzyme activities and selenium status in highly iodine-deficient goitrous children

The objective of this study was to investigate oxidative DNA damage, and the levels of antioxidant enzymes (AOE) and selenium (Se) in relation to iodine deficiency and/or goiter in children. The study was performed in a group of goitrous high school children (15-18 years of age) ( n =14) with severe or moderate iodine deficiency. Thyroid hormones (TSH, FT 4 , TT 4 , FT 3 , TT 3 ), urinary iodine (UI) and plasma Se levels, and erythrocyte glutathione peroxidase (GSHPx), superoxide dismutase (SOD) and catalase (CAT) activities were determined and compared with those of a control group consisting of non-goitrous high school children ( n =14) with normal UI levels or mild iodine deficiency. In the goitrous group, concentrations of FT 4 , TT 4 , plasma Se and UI, and activities of GSHPx and SOD were found to be significantly lower. Six typical hydroxyl radical-induced base lesions in genomic DNA of peripheral blood were identified and quantified by gas chromatography/isotope-dilution mass spectrometry (GC/IDMS), and higher levels of DNA base lesions were observed in the goitrous group. The results suggest that highly iodine-deficient goitrous children may be under oxidative stress, which may lead to greater level of oxidative damage to DNA. This study supports the evidence for the reported relationship between iodine deficiency and the increased incidence of thyroid malignancies.     

Control of doxorubicin-induced,reactive oxygen-related apoptosis by glutathione peroxidase 1 in cardiac fibroblasts

Reactive oxygen formation plays a mechanistic role in the cardiotoxicity of doxorubicin, a chemotherapeutic agent that remains an important component of treatment programs for breast cancer and hematopoietic malignancies. To examine the role of doxorubicin-induced reactive oxygen species (ROS) in drug-related cardiac apoptosis, murine embryonic fibroblast cell lines were derived from the hearts of glutathione peroxidase 1 (Gpx-1) knockout mice. Cells from homozygous Gpx-1 knockout mice and parental animals were propagated with (Se+) and without (Se-) 100 nM sodium selenite. Activity levels of the peroxide detoxifying selenoprotein glutathione peroxidase (GSHPx) were marginally detectable (<1.6 nmol/min/mg) in fibroblasts from homozygous knockout animals whether or not cells were supplemented with selenium. GSHPx activity in Se- cells from parental murine fibroblasts was also <1.6 nmol/min/mg, whereas GSHPx levels in Se+ parental murine fibroblasts were 12.9 ± 2.7 nmol/min/mg (mean ± SE; P < 0.05). Catalase, superoxide dismutase, glutathione reductase, glutathione S-transferase, glucose 6-phosphate dehydrogenase, and reduced glutathione activities did not differ amongst the four cell lines. Reactive oxygen production increased from 908 ± 122 (arbitrary units) for untreated control cells to 1668 ± 54 following exposure to 1 μM doxorubicin for 24 h in parental fibroblasts not supplemented with selenium (P < 0.03); reactive oxygen formation in doxorubicin-treated parental fibroblasts propagated in selenium was 996 ± 69 (P = not significant compared to untreated control cells). Reactive oxygen levels in homozygous Gpx-1 knockout fibroblasts, irrespective of selenium supplementation status, were increased and equivalent to that in selenium deficient wild type fibroblasts. When cardiac fibroblasts were exposed to doxorubicin (0.05 μM) for 96 h and examined for cell cycle alterations by flow cytometry, and apoptosis by TUNEL assay, marked G2 arrest and TUNEL positivity were observed in knockout fibroblasts in the presence or absence of supplemental selenium, and in parental fibroblasts propagated without selenium. Parental fibroblasts propagated with selenium and exposed to the same concentration of doxorubicin demonstrated modest TUNEL positivity and substantially diminished amounts of low molecular weight DNA. These results were replicated in cardiac fibroblasts exposed to doxorubicin (1–2 μM) for 2 h (to mimic clinical drug dosing schedules) and examined 96 h following initiation of drug exposure. Doxorubicin uptake in cardiac fibroblasts was similar irrespective of the mRNA expression level or activity of GSHPx. These experiments suggest that the intracellular levels of doxorubicin-induced reactive oxygen species (ROS) are modulated by GSHPx and play an important role in doxorubicin-related apoptosis and altered cell cycle progression in murine cardiac fibroblasts.     

Glutathione Peroxidase (GSHPx) Activity in the Liver of Red Deer in Relation to Hepatic Selenium Concentrations, Sex, Body Weight and Season of the Year

The purpose of this study was to determine glutathione peroxidase (GSHPx) activity in the liver of red deer in relation to selenium concentrations in the liver, as well as to evaluate changes in GSHPx activity according to sex, body weight and season of the year. Total selenium concentration in the liver of red deer averaged 0.095?±?0.018?μg/g of wet weight. GSHPx activity in the liver of red deer ranged widely from 4.4 to 45.8?U/g of protein. Females were characterized by higher GSHPx activity compared to males (21.2 vs. 17.0?U/g protein). The highest GSHPx activity was recorded in autumn and the lowest in summer. The lowest GSHPx activity in the liver was found in the heaviest animals (>100?kg body weight), averaging 14.0?U/g protein. Animals weighing <66?kg and 66-100?kg were characterized by similar activity of 25.1 and 24.5?U/g, respectively. Despite the differences in GSHPx activity according to sex, body weight and season of the year, these factors had no significant effect on the activity of this enzyme. The main factor regulating GSHPx activity in the liver of examined red deer was selenium concentration.     

The Impact of Iodine Excess on Thyroid Hormone Biosynthesis and Metabolism in Rats

Thyroid function ultimately depends on appropriate iodine supply to the gland. There is a complex series of checks and balances that the thyroid uses to control the orderly utilization of iodine for hormone synthesis. The aim of our study is to evaluate the mechanism underlying the effect of iodine excess on thyroid hormone metabolism. Based on the successful establishment of animal models of normal-iodine (NI) and different degrees of high-iodine (HI) intake in Wistar rats, the content of monoiodotyrosine (MIT), diiodotyrosine (DIT), T₄, and T₃ in thyroid tissues, the activity of thyroidal type 1 deiodinase (D1) and its (Dio1) mRNA expression level were measured. Results showed that, in the case of iodine excess, the biosynthesis of both MIT and DIT, especially DIT, was increased. There was an obvious tendency of decreasing in MIT/DIT ratio with increased doses of iodine intake. In addition, iodine excess greatly inhibited thyroidal D1 activity and mRNA expression. T₃ was greatly lower in the HI group, while there was no significant difference of T₄ compared with NI group. The T₃/T₄ ratio was decreased in HI groups, antiparalleled with increased doses of iodine intakes. In conclusion, the increased biosyntheses of DIT relative to MIT and the inhibition of thyroidal Dio1 mRNA expression and D1 activity may be taken as an effective way to protect an organism from impairment caused by too much T₃. These observations provide new insights into the cellular regulation mechanism of thyroid hormones under physiological and pathological conditions.     

Selenium Modulates Oxidative Stress-Induced Cell Apoptosis in Human Myeloid HL-60 Cells Through Regulation of Calcium Release and Caspase-3 and -9 Activities

Selenium is an essential chemopreventive antioxidant element to oxidative stress, although high concentrations of selenium induce toxic and oxidative effects on the human body. However, the mechanisms behind these effects remain elusive. We investigated toxic effects of different selenium concentrations in human promyelocytic leukemia HL-60 cells by evaluating Ca²⁺ mobilization, cell viability and caspase-3 and -9 activities at different sample times. We found the toxic concentration and toxic time of H₂O₂ as 100 μm and 10 h on cell viability in the cells using four different concentrations of H₂O₂ (1 μm–1 mm) and six different incubation times (30 min, 1, 2, 5, 10, 24 h). Then, we found the therapeutic concentration of selenium to be 200 nm by cells incubated in eight different concentrations of selenium (10 nm–1 mm) for 1 h. We measured Ca²⁺ release, cell viability and caspase-3 and -9 activities in cells incubated with high and low selenium concentrations at 30 min and 1, 2, 5, 10 and 24 h. Selenium (200 nm) elicited mild endoplasmic reticulum stress and mediated cell survival by modulating Ca²⁺ release, the caspases and cell apoptosis, whereas selenium concentrations as high as 1 mm induced severe endoplasmic reticulum stress and caused cell death by activating modulating Ca²⁺ release, the caspases and cell apoptosis. In conclusion, these results explained the molecular mechanisms of the chemoprotective effect of different concentrations of selenium on oxidative stress-induced apoptosis.     

Red elemental selenium (Se0) improves the immunoactivities of EPC cells,crucian carp and zebrafish against spring viraemia of carp virus

Selenium, as an essential trace element, interferes through selenoproteins in many physiological processes of plants and mammals. Its antiviral activity has recently attracted much attention because selenium improves the antiviral capacity of animal cells against a few viruses relevant to human diseases. In this study, the red elemental selenium was purified from the fermentative culture of Herbaspirillum camelliae WT00C and then used to culture epithelioma papulosum cyprinid (EPC) cells or feed crucian carp and zebrafish. Finally, its antiviral effects were investigated at the cell level and living fishes after spring viraemia of carp virus infection. At the cell level, 5, 10 and 20 μg ml^–1 red elemental selenium significantly induced the expression of interferon (IFN) and ISG15 genes in EPC cells. The viral TCID₅₀ (50% tissue culture infective dose) values in the EPC cells incubated with 5, 10 and 20 μg ml^–1 red elemental selenium were significantly less than those of the control. More expression of IFN and ISG15 genes and less TCID₅₀ values indicate that red elemental selenium indeed improves the antiviral capability of EPC cells. In the crucian carp fed with the food containing 5 and 10 μg g^–1 red elemental selenium, IFN expressions showed 13- and 39-fold increases at the 16th day of post-injection, and its expression was dependent on selenium concentrations. Meanwhile, no fish death occurred in all the experimental groups. In the zebrafish fed with the red worm containing 5 μg g^–1 red elemental selenium, IFN and Mx expressions and survival rate were significantly higher than those of the control. The results of this study show that red elemental selenium indeed improves the antiviral activity of fish. The antiviral effects of selenium mainly come from its immune regulation through its incorporation into selenoproteins. The optimum level of selenium contributes to improving fish immunity, whereas excess selenium causes excessive immune and inflammatory responses.     

Trace elements status in multinodular goiter

Importance of iodine and selenium in thyroid metabolism is well known, but the roles of other essential trace elements including copper, zinc, manganese and iron on thyroid hormone homeostasis remain unclear. The aim of this study was to investigate the status of those trace elements in benign thyroid diseases and evaluate possible links between trace element concentrations and thyroid hormones.The study group was composed of 25 patients with multinodular goiter. Concentrations of thyroid hormones (plasma-free thyroxine, FT₄; free triiodothyronine, FT₃; and thyrotropin, TSH), selenium, copper, zinc, manganese and iron in plasma, and urinary iodine were determined. The results were compared with those of a healthy control group (n=20) with no thyroid disorder.A mild iodine deficiency was observed in the patients with multinodular goiter whereas urinary iodine levels were in the range of “normal” values in healthy controls. All patients were euthyroid, and their thyroid hormone concentrations were not significantly different from the control group. Plasma selenium, zinc and iron concentrations did not differ from controls, while copper and manganese levels were found to be significantly higher in the patients with multinodular goiter indicating links between these trace elements and thyroid function and possibly in development of goiter. Besides iodine, there was a significant correlation between plasma copper concentration and FT₃/FT₄ ratio.     

Effects of 17β-Estradiol and Vitamin E Treatments on Blood Trace Element and Antioxidant Enzyme Levels in Ovariectomized Rats

We investigated the effect of 17β-estradiol (E₂) alone and separately vitamin E treatment on trace element status of rats following an ovariectomic operation. Forty rats were equally divided into four groups: Group 1, control, non-ovariectomized rats; Group 2, (OVX) rats, ovariectomized under general anesthesia; Group 3, (OVX+E₂) rats, the group received a 40 μg kg⁻¹ subcutan dose of E₂ per day after ovariectomy; and Group 4, (OVX + E₂ + vitamin E) rats, received the same E₂ treatment, but with an additional 100 mg kg⁻¹ intraperitoneal dose of vitamin E per day after ovariectomy. At the end of the 30-day experiment, the rats were sacrificed and their blood was collected for the measurement of zinc, copper, iron, phosphorus, selenium, magnesium, calcium, manganese, and chromium; copper–zinc superoxide dismutase (SOD); manganese-superoxide dismutase (Mn-SOD); glutathione peroxidase (Se-GSH-Px); and catalase (CAT). The levels of zinc, copper, iron, phosphorus, selenium, calcium, chromium, and manganese and activities of SOD, Mn-SOD, Se-GSH-Px, and CAT were lower in the OVX than in the control group, but magnesium level was unaffected. However, zinc, copper, iron, phosphorus, selenium, calcium, chromium, and manganese levels and SOD, Mn-SOD, Se-GSH-Px, and CAT activities were higher under separate E₂ and E₂ + vitamin E treatments. The level of magnesium in the treated-OVX groups was not different than in the OVX group. In conclusion, E₂ treatment has an ameliorating effect on the trace element status in OVX, and this effect may be enhanced with the addition of vitamin E.     

Iodine and selenium carry over in milk and cheese in dairy cows: effect of diet supplementation and milk yield

Iodine and selenium are essential trace elements involved in the regulation of thyroid metabolism and antioxidant status. Two experiments were undertaken on lactating cows to determine the milk concentrations of iodine and selenium, carry over (CO) in milk, the fraction in curdle portion and how milk yield affects the milk iodine and selenium concentrations and CO. Sources of elements were potassium iodide and sodium selenite. In Experiment 1, 12 cows were randomly allotted to three diet groups in a completely randomized design: control group (CTR) - total mixed ration (TMR) containing 1.71 and 0.08 mg/kg dry matter (DM); Group 1 (T1) - TMR plus 23.8 and 2.2 mg; Group 2 (T2) - TMR plus 45.5 and 4.3 mg, respectively, for iodine and selenium. In Experiment 2, 30 cows were allotted to three groups according to milk yield: high (H), average (A) and low (L). Within each group, cows were randomly assigned two levels of iodine and selenium: Level 1: TMR containing 1.55 and 0.15 mg/kg DM; Level 2: TMR plus 47.2 mg and 8.0 mg, respectively, iodine and selenium. In both experiments, individual milk samples were collected and analyzed for iodine and selenium contents. In Experiment 1, Grana Padano cheese was obtained at lab scale and the iodine and selenium fractions in the curd were measured. In Experiment 1, the iodine intake increased (P < 0.001) the concentration and total excretion in milk. The CO increased (P < 0.05) from 16 (CTR) to 27 (T1) and 26% (T2); the sampling time was significant (P < 0.05) with no interaction with treatments. Concentration of selenium in milk was increased (P < 0.05) by treatment and CO decreased (P < 0.01) from 26 (CTR) to 12 (T1) and 9% (T2). The iodine showed a mild enrichment factor in the curdle (about 1.7-fold), whereas selenium enriched five- to sevenfold. In Experiment 2, the level of iodine supplementation affected (P < 0.05) the concentration and total excretion in milk. No effects on milk iodine concentration were related to milk yield or milk yield × treatment interaction; however, the iodine excretion in milk was major (P < 0.05) in higher yielding groups. The iodine CO was affected (P < 0.05) by the milk yield in supplemented groups. The selenium milk concentration and excretion were affected (P < 0.01) by the milk yield, whereas the CO was affected (P < 0.05) by the milk yield and selenium supplementation. Results highlight the possibility of fortification with iodine in milk and selenium in cheese through animal feeding.     

Antioxidant Responses of Wheat Seedlings to Exogenous Selenium Supply Under Enhanced Ultraviolet-B

The paper reports the effects of selenium (Se) supply on growth and antioxidant traits of wheat (Triticum aestivum L. cv Han NO.7086) seedlings exposed to enhanced ultraviolet-B (UV-B) stress. Antioxidant responses of seedlings were different depending on the Se concentration. Compared with the control, the lower amount used (0.5 mg Se kg⁻¹ soil) had no significant effect on biomass accumulation. The treatments with 1.0, 2.0, and 3.0 mg Se kg⁻¹ promoted biomass accumulation of wheat seedlings, and the increased amount in biomass was the most at 1.0 mg Se kg⁻¹ treatment. Se treatments with 1.0, 2.0, and 3.0 mg kg⁻¹ also significantly increased activities of peroxidase (POD) and superoxide dismutase (SOD) and reduced the rate of superoxide radical (O₂⁻) production and malondialdehyde (MDA) content of wheat seedlings. In addition, anthocyanins and phenolic compounds content in wheat seedlings evidently increased by the treatments with 1.0 and 2.0 mg Se kg⁻¹. The lower Se treatment had no significant effect on MDA content, although it increased activities of antioxidant enzymes (POD, SOD, and catalase activities) and reduced the rate of O₂⁻ production in wheat seedlings. These results suggest that optimal Se supply is favorable for the growth of wheat seedlings and that optimal Se supply can reduce oxidative stress of seedlings under enhanced UV-B radiation.     

Protective effects of selenium-glutathione-enriched probiotics on CCl4-induced liver fibrosis

Hepatic fibrosis is a common pathological basis of liver cirrhosis and hepatocellular carcinomas. So, prevention and treatment of liver fibrosis is one of the crucial therapeutic goals in hepatology. Organic selenium, glutathione or probiotics supplementation could ameliorate hepatic fibrosis, respectively. The purpose of this study is to develop a novel selenium-glutathione-enriched probiotics (SGP) and to investigate its protective effect on CCl₄-induced liver fibrosis in rats. Yeast strains with the high-yield glutathione were isolated and identified by analysis of 26S ribosomal DNA sequences. The fermentation parameters of SGP were optimized through single-factor, Plackett–Burman (PB) design and response surface methodology (RSM). The final SGP contained 38.4 μg/g of organic selenium, 34.1 mg/g of intracellular glutathione, approximately 1×10¹⁰ CFU/g live Saccharomyces cerevisiae and 1×10¹² CFU/g live Lactobacillus acidophilus. SGP had better protective effects on liver fibrosis than selenium, glutathione or probiotics, respectively. The hepatic silent information regulator 1 (SIRT1) level was down-regulated and oxidative stress, endoplasmic reticulum (ER) stress, inflammation and phosphorylated MAPK was increased in CCl₄-treated rats. However, SGP can significantly reverse these changes caused by CCl₄. Our findings suggest that SGP was effective in attenuating liver fibrosis by the activation of SIRT1 signaling and attenuating hepatic oxidative stress, ER stress, inflammation and MAPK signaling.     

Radiotracer Experiments on Biological Volatilization of Organic Iodine from Coastal Seawaters

Biological volatilization of iodine from seawaters was studied using a radiotracer technique. Seawater samples were incubated aerobically in serum bottles with radioactive iodide tracer (¹²⁵I), and volatile organic and inorganic iodine were collected with activated charcoal and silver wool trap, respectively. Iodine was volatilized mainly as organic iodine, and inorganic iodine volatilization was not observed. Influence of light intensity on the volatilization was determined, but no significant differences were observed under light (70,000 lux) and dark conditions. The effect of the chemical form of iodine on the volatilization was determined, and the results suggested that volatilization preferentially occurs from iodide (I^?) but not from iodate (IO₃ ^?). Volatilization did not occur when the samples were autoclaved or filtered through a 0.22-μm pore size membrane filter. Incubation of the samples with antibiotics caused decreased volatilization. Conversely, enhanced volatilization was observed when the samples were incubated with yeast extract. Fifty-nine marine bacterial strains were then randomly isolated from marine environments, and their iodine-volatilizing capacities were determined. Among these, 19 strains exhibited significant capacities for volatilizing iodine. 16S ribosomal RNA gene comparisons indicated that these bacteria are members of Proteobacteria (α and γ subdivisions) and Cytophaga-Flexibacter-Bacteroides group. One of the strains, strain C-19, volatilized 1 to 2% of total iodine during cultivation, and the gaseous organic iodine was identified as methyl iodide (CH₃I). These results suggest that organic iodine volatilization from seawaters occurs biologically, and that marine bacteria participate in the process. Considering that volatile organic iodine emitted from the oceans causes atmospheric ozone destruction, biological iodine volatilization from seawater is of great importance. Our results also contribute to prediction of movement and diffusion of long-lived radioactive iodine (¹²⁹I) in the environment.     

Mechanism of Iodine Uptake by Cabbage: Effects of Iodine Species and Where It is Stored

Iodine-enhanced vegetable has been proven to be an effective way to reduce iodine deficiency disorders in many regions. However, the knowledge about what mechanisms control plant uptake of iodine and where iodine is stored in plants is still very limited. A series of controlled experiments, including solution culture, pot planting, and field experiments were carried out to investigate the uptake mechanism of iodine in different forms. A new methodology for observing the iodine distribution within the plant tissues, based on AgI precipitation reaction and transmission electron microscope techniques, has been developed and successfully applied to Chinese cabbage. Results show that iodine uptake by Chinese cabbage was more effective when iodine was in the form of IO₃ ⁻ than in the form of I⁻ if the concentration was low (<0.5 mg L⁻¹), but the trend was opposite if iodine concentration was 0.5 mg L⁻¹ or higher. The uptake was more sensitive to metabolism inhibitor in lower concentration of iodine, which implies that the uptake mechanism transits from active to passive as the iodine concentration increases, especially when the iodine is in the form of IO₃ ⁻. The inorganic iodine fertilizer provided a quicker supply for plant uptake, but the higher level of iodine was toxic to plant growth. The organic iodine fertilizer (seaweed composite) provided a more sustainable iodine supply for plants. Most of the iodine uptake by the cabbage is intercepted and stored in the fibrins in the root while the iodine that is transported to the above-ground portion (shoots and leaves) is selectively stored in the chloroplasts.     

SELENIUM STIMULATES GROWTH OF MARINE MACROALGAE IN AXENIC CULTURE1

The marine brown alga Fucus spiralis L. and the red alga Goniotrichum alsidii (Zanard) increase their growth upon the, addition of SeO₃^2- or SeO₄^2- when cultivated axenically in the artificial seawater ASP6 F2. In the concentration range 1 · 10^?10-1 · 10^?7 M there are two optima, one at 3.3 · 10^?10 M and another at 3.3 · 10^?8 M. α-To-copherol, often administered together with selenium to mammals suffering from selenium deficiency, gives no additive effect with selenium, but α-tocopherol in the concentration range 1 × 10^?7-1 × 10^?6 M does influence the morphology of the Fucus plants. Organically bound selenium has no effect.