[Effects of iodine excess on islet ß cells(ß-TC-6) function and the mechanism].

OBJECTIVE: To explore the influences of iodine excess on insulin secret function of mouse insulinoma cells ß-TC-6 and the mechanism. METHODS: ß-TC-6 cells were treated with excessive iodine( Na I) in vitro. After 24 hour of exposure, the MTT assay was used to measure the cell viabilities. ß-TC-6 cells, after 24 hour of exposure in excessive iodine, were stimulated with Krebs-Ringer bicarbonate buffer containing 5. 6mmol/L glucose for 1 hour at 37 ℃, then the supernatant was collected for insulin determination by ELISA kit. Western blot was used to detect the expression of Bcl-2, Bax, GRP78 and IRE1α. RESULTS: The rate of cell viability decreased from 1 mmol/L to 100mmol/L iodine excess group by a dose-dependent manner and was significantly lower than the control group and as follow by 73. 3%, 71. 2% and 55. 8% of that of control group. Iodine excess impaired the insulin secret function of ß-TC-6 cells in 1 mmol/L and 100 mmol/L iodine excess groups. The expression of Bcl-2 decreased while the expressionof Bax increased significantly when compared with control group( P < 0. 05). From 1mmol/L iodine excess group, the expression of GRP78 and IRE1α were increased significantly when compared with control group( P < 0. 05). CONCLUSION: Iodine excess decreased the cell viabilities and impaired insulin secret function, which might be related to endoplasmic reticulum stress and Bcl-2 families.

Leucine facilitates the insulin-stimulated glucose uptake and insulin signaling in skeletal muscle cells: involving mTORC1 and mTORC2.

Leucine, a branched-chain amino acid, has been shown to promote glucose uptake and increase insulin sensitivity in skeletal muscle, but the exact mechanism remains unestablished. We addressed this issue in cultured skeletal muscle cells in this study. Our results showed that leucine alone did not have an effect on glucose uptake or phosphorylation of protein kinase B (AKT), but facilitated the insulin-induced glucose uptake and AKT phosphorylation. The insulin-stimulated glucose uptake and AKT phosphorylation were inhibited by the phosphatidylinositol 3-kinase inhibitor, wortmannin, but the inhibition was partially reversed by leucine. The inhibitor of mammalian target of rapamycin complex 1 (mTORC1), rapamycin, had no effect on the insulin-stimulated glucose uptake, but eliminated the facilitating effect of leucine in the insulin-stimulated glucose uptake and AKT phosphorylation. In addition, leucine facilitation of the insulin-induced AKT phosphorylation was neutralized by knocking down the core component of the mammalian target of rapamycin complex 2 (mTORC2) with specific siRNA. Together, these findings show that leucine can facilitate the insulin-induced insulin signaling and glucose uptake in skeletal muscle cells through both mTORC1 and mTORC2, implicating the potential importance of this amino acid in glucose homeostasis and providing new mechanistic insights.

The relationship between plasma nickel concentrations and type 2 diabetes mellitus risk: A protective effect within a specific range.

BACKGROUND: Nickel is considered an essential nutrient for certain microbial, plant, and animal species, but its role in human health remains controversial. Some studies have reported the relationship between nickel and type 2 diabetes mellitus (T2DM), but the results are not consistent and the mechanism is not clear, which needs further exploration. AIM: To investigate the possible correlation between nickel and T2DM. METHODS: We conducted a case-control study of 192 patients with T2DM and 189 healthy controls at a hospital in central China. Plasma concentrations of nickel and six other trace elements were measured with inductively coupled plasma mass spectrometry. Logistic regression models, restricted cubic spline models (RCS), and Bayesian kernel machine regression (BKMR) were used to evaluate the relationship between plasma nickel and T2DM and its metabolic risk factors, as well as the presence or absence of interactions between nickel and other elements. RESULTS: The T2DM group exhibited considerably lower plasma nickel levels than the control group (P < 0.001). Whether using a crude or adjusted model, logistic regression analysis finds a negative correlation between nickel levels and the risk of T2DM (P trend < 0.001). According to the RCS, the risk of T2DM reduces with rising nickel levels when the value is below 6.1 µg/L; nickel has a negative linear correlation with fasting plasma glucose (FPG), an inverse U-shaped connection with superoxide dismutase (SOD), and a positive linear correlation with malondialdehyde (MDA) (all P overall < 0.05). The plasma nickel concentration was positively correlated with zinc, vanadium, and chromium (r = 0.23, 0.11, and 0.19, respectively; all P < 0.05) and negatively correlated with copper (r = - 0.11, P < 0.05). In the BKMR model, interactions of nickel with zinc on T2DM and SOD, nickel with chromium on T2DM and homeostasis model assessment of ß cell (HOMA-ß), and nickel with copper on FPG, homeostasis model assessment of insulin (HOMA-IR), and MDA were observed. CONCLUSION: Nickel may have a dual effect on the risk of T2DM, with a protective range of less than 6.1 µg/L. Potential interactions between nickel, copper, zinc, and chromium existed in their associations with T2DM and its metabolic risk factors.

Patterns of sleep quality and its influence factors: A latent class model among students of medical university in Hubei Province, China.

BACKGROUND: Sleep problem among undergraduate students has become one of the most pressing public health problems. This study aimed to explore the latent class of sleep patterns and the factors affecting sleep in Chinese students of medical university. METHODS: 3423 students participated in the cross-sectional study. The survey consisted of the reduced Morningness-Evening Questionnaire, the Pittsburgh Sleep Quality Index, and Health-Promoting Lifestyle Profile-II. Latent profile analysis and multinominal logistic regression analysis were performed. RESULTS: Three potential sleep categories were identified: "sleep disorder group" (1.87 %), "daytime dysfunction group" (24.42 %), and "good sleep group" (73.71 %). Compared with the "good sleep group," the "sleep disorder group" showed monthly living expenses (RMB) ≥ 3000 yuan (OR) = 13.04), interpersonal relationships as poor (OR = 3.71), health status as poor (OR = 45.09), circadian rhythm as eveningness (OR = 6.17), and poor health-promoting lifestyles (OR = 2.090) as its risk factors (all p < 0.05). Meanwhile, sophomore (OR = 1.75), junior (OR = 1.52), interpersonal relationships as poor (OR = 1.88), health status as poor (OR = 4.62), intermediate-chronotype (OR = 2.19), eveningness chronotype (OR = 5.66), and health-promoting lifestyles as poor (OR = 1.55) were identified as risk factors for the "daytime dysfunction group" (all p < 0.05). LIMITATIONS: Causal conclusions can not be drawn and recall bias in data collection. CONCLUSIONS: Significant population heterogeneity was found in the sleep quality. Implementing targeted interventions focusing on circadian rhythm and lifestyle is crucial to improve the sleep quality of students with different conditions.

Methylisothiazolinone pollution inhibited root stem cells and regeneration through auxin transport modification in Arabidopsis thaliana.

Methylisothiazolinone (MIT) is a widely used preservative and biocide to prevent product degradation, yet its potential impact on plant growth remains poorly understood. In this study, we investigated MIT's toxic effects on Arabidopsis thaliana root growth. Exposure to MIT significantly inhibited Arabidopsis root growth, associated with reduced root meristem size and root meristem cell numbers. We explored the polar auxin transport pathway and stem cell regulation as key factors in root meristem function. Our findings demonstrated that MIT suppressed the expression of the auxin efflux carrier PIN1 and major root stem cell regulators (PLT1, PLT2, SHR, and SCR). Additionally, MIT hindered root regeneration by downregulating the quiescent center (QC) marker WOX5. Transcriptome analysis revealed MIT-induced alterations in gene expression related to oxidative stress, with physiological experiments confirming elevated reactive oxygen species (ROS) levels and increased cell death in root tips at concentrations exceeding 50 µM. In summary, this study provides critical insights into MIT's toxicity on plant root development and regeneration, primarily linked to modifications in polar auxin transport and downregulation of genes associated with root stem cell regulation.

p38 mitogen-activated protein kinase (MAPK) promotes cholesterol ester accumulation in macrophages through inhibition of macroautophagy.

p38 MAPK has been strongly implicated in the development of atherosclerosis, but its role in cholesterol ester accumulation in macrophages and formation of foam cells, an early step in the development of atherosclerosis, has not been investigated. We addressed this issue and made some brand new observations. First, elevated intracellular cholesterol level induced by the exposure to LDL-activated p38 MAPK and activation of p38 MAPK with anisomycin increased the ratio of cholesterol esters over free cholesterol, whereas inhibition of p38 MAPK with SB203580 or siRNA reduced the LDL loading-induced intracellular accumulation of free cholesterol and cholesterol esters in macrophages. Second, exposure to LDL cholesterol inhibited autophagy in macrophages, and inhibition of autophagy with 3-methyladenine increased intracellular accumulation of cholesterol (free cholesterol and cholesterol esters), whereas activation of autophagy with rapamycin decreased intracellular accumulation of free cholesterol and cholesterol esters induced by the exposure to LDL cholesterol. Third, LDL cholesterol loading-induced inhibition of autophagy was prevented by blockade of p38 MAPK with SB203580 or siRNA. Neutral cholesterol ester hydrolase was co-localized with autophagosomes. Finally, LDL cholesterol loading and p38 activation suppressed expression of the key autophagy gene, ulk1, in macrophages. Together, our results provide brand new insight about cholesterol ester accumulation in macrophages and foam cell formation.

Circadian rhythms and sleep quality among undergraduate students in China: The mediating role of health-promoting lifestyle behaviours.

BACKGROUND: Poor sleep quality have become one of the most pressing public health problems for undergraduate students. The aim of this cross-sectional study was to investigate the relationship between circadian rhythms and sleep quality and the meditating role of health-promoting lifestyles in the relationship of Chinese undergraduate students. METHODS: A total of 3423 students participated. The online survey consisted of the reduced Morningness-Evening Questionnaire (rMEQ), the Pittsburgh Sleep Quality Index (PSQI) and Health-Promoting Lifestyle Profile-II (HPLP-II). Logistic regression models were employed. RESULTS: The prevalence of poor sleep quality is 43.03 %. The total mean scores of HPLP - II, PSQI, and rMEQ are 96.94 ± 17.26, 5.20 ± 2.70 and 14.83 ± 2.10, respectively. A significant negative correlation exists between the rMEQ and PSQI scores (r = -0.262, p < 0.001), but a positive correlation exists between the rMEQ and HPLP scores (r = 0.232, p < 0.001). The total and sub-domain scores of HPLP are also negatively correlated with the PSQI scores (r = -[0.166, 0.291], p < 0.001). Mediation analysis demonstrates the mediation of HPLP (indirect effect = -0.036, p < 0.001) on the effect of the rMEQ on PSQI scores that accounts for 13.30 % of the total effect. LIMITATIONS: Cross-sectional design and recall bias in data collection. CONCLUSIONS: The effect of circadian rhythm on sleep quality is partially mediated by the health-promoting lifestyle. In addition to maintaining a normal circadian rhythm, helping undergraduate students develop a healthy lifestyle is also an effective measure to improve sleep quality.

Structural Genomic Analysis of SARS-CoV-2 and Other Coronaviruses.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative agent of the coronavirus disease 2019 (COVID-19) pandemic. In this study, we conducted a comparative analysis of the structural genes of SARS-CoV-2 and other CoVs. We found that the sequence of the E gene was the most evolutionarily conserved across 200 SARS-CoV-2 isolates. The E gene and M gene sequences of SARS-CoV-2 and NC014470 CoV were closely related and fell within the same branch of a phylogenetic tree. The absolute diversity of E gene and M gene sequences of SARS-CoV-2 isolates was similar to that of common CoVs (C-CoVs) infecting other organisms. The absolute diversity of the M gene sequence of the KJ481931 CoV that can infect humans was similar to that of SARS-CoV-2 and C-CoVs infecting other organisms. The M gene sequence of KJ481931 CoV (infecting humans), SARS-CoV-2 and NC014470 CoV (infecting other organisms) were closely related, falling within the same branch of a phylogenetic tree. Patterns of variation and evolutionary characteristics of the N gene and S gene were very similar. These data may be of value for understanding the origins and intermediate hosts of SARS-CoV-2.

Occurrence of two NDM-1-producing Raoultella ornithinolytica and Enterobacter cloacae in a single patient in China: probable a novel antimicrobial resistance plasmid transfer in vivo by conjugation.

OBJECTIVES: To identify the general features of acquisition of drug-resistance genes in two multi-drug resistant Enterobacteriaceae strains isolated from a single patient in China. METHODS: The whole-plasmid was sequenced by Illumina Hiseq 4000 and Pacbio RSII procedures. The plasmid conjugation transfer experiment were performed by the mating-out assay. Drug-resistance genes were amplified by PCR assay. RESULTS: We identified two New Delhi metallo-ß-lactamase type 1(NDM-1)-producing isolates, named Raoultella ornithinolytica B1645-1 and Enterobacter cloacae B1645-2, which shared the same sulfonamide-resistant dihydropteroate synthase sul2 gene and aminoglycoside O-phosphotransferase aph(3'')-Ib gene. A novel antimicrobial resistance plasmid pCYNDM01 was first discovered from the multi-drug resistant R. ornithinolytica B1645-1. Interestingly, plasmid pCYNDM01 carried a Gifsy-2 prophage gene. The blaNDM-1 gene was located on a novel complex class 1 integron with a structure of sul1-qacEΔ1-ΔISAba125-blaNDM-1-blaMBL-trpC-ISCR1-catb8-aacA4-IS1-IS6100-dfrA14-intI1. The carrying the blaNDM-1 gene plasmid pCYNDM01 was transferred to the E. cloacae B1645-2 recipient strain. This 149.44 kb plasmid pCYNDM01 belonged to the IncFII type. CONCLUSIONS: A novel antimicrobial resistance plasmid pCYNDM01 was first recovered from a multi-drug resistance R. ornithinolytica B1645-1 isolated from China. The novel complex sul1-type class 1 integron might play an essential role in the mobilization of the blaNDM-1 gene among different enterobacterial species. The occurrence of plasmid pCYNDM01 transfer from R. ornithinolytica to E. cloacae in vitro by conjugation showed that plasmid pCYNDM01 was a self-conjugative plasmid and might cause dissemination of drug-resistance genes within different enterobacterial species from a single patient in vivo by conjugation. The novel variant F-like T4SS of plasmid pCYNDM01 might be as a tool of R. ornithinolytica B1645-1 for resistance genes transfer. The emergence of the two NDM-1-producing Enterobacteriaceae strains should be attracted China attentions and required to prevent its future prevalence.

2,3,5,4'-tetrahydroxystilbene-2-O-ß-D-glucoside induces autophagy of liver by activating PI3K/Akt and Erk pathway in prediabetic rats.

BACKGROUND: 2,3,5,4'-tetrahydroxystilbene-2-O-ß-D-glucoside (TSG) is an active compound derived from Polygonum multiflorum Thunb., a Chinese Taoist herbal medicine, which exerts lipid lowering, anti-cancer, anti-aging, anti-inflammatory and hepatoprotective effects. However, its role in protecting hepatocytes under pre-diabetic condition remains unclear. METHODS: In this study, we developed prediabetic SD rats by feeding high-fat and high-sugar diet. The body weight, blood lipid, blood glucose, and fasting insulin (FINS) and insulin resistance index (HOMA-IR) were detected and calculated to assess the potential risk of prediabetes. HE and Oil Red O staining was used, and blood level of biochemical index was detected to observe the liver injury. The autophagic cell death-associated signaling proteins, and the potential signaling factors p-Akt/Akt and p-Erk/Erk were detected using western blot to explore the potential effects of TSG on pre-diabetic liver and the underlying mechanisms. RESULTS: The results showed that the body weight in TSG-treated group was significantly decreased vs. the model group. The blood glucose, the level of FINS and HOMA-IR, TC and TG were decreased in TSG-treated group as well. Furthermore, TSG treatment significantly ameliorated lipid droplet accumulation, enhanced liver anti-oxidative response which may be associated with an increased activity of SOD and GSH-Px, and a decrease of LDLC and MDA. The autophagic cell death-associated proteins, p-AMPK, ATG12, LC3 II, and Beclin 1 were up-regulated in the TSG-treated group, while the upstream signaling pathway, PI3K/Akt and Erk, were activated. CONCLUSIONS: TSG induced liver autophagic cell death to protect liver from prediabetic injury by activating PI3K/Akt and Erk.

[Intervention of selenium on injured thyroid hormone metabolism by excessive iodine].

OBJECTIVE: To study the mechanism of the disorder of thyroid hormone metabolism resulted from iodine excess in order to seek suitable selenium intervention dosage. METHODS: 140 Balb/c mice were randomly divided into seven groups, the normal control group, the excessive iodine group (drank the water containing potassium iodate 3000 microg/L) and five selenium intervention groups (drank the water containing 3000 microg/L of potassium iodate and 0.1, 0.2, 0.3, 0.4 and 0.5 mg/L of selenium). All of the mice were cultivated for 16 weeks and the thyroid hormone in plasma were assayed by radioimmunoassay. The iodine in urine and thyroid were analyzed by Cer-Arsenite colormetric method. The activities of glutathione peroxidase, superoxide dismutase and thyroid peroxidase and the level of malondialdehyde in thyroid were analyzed. RESULTS: The level of thyroid hormone of selenium intervention groups had no significant difference with that of normal control group (P > 0.05). Compared with excessive iodine group, the iodine in thyroid of 0.2 mg/L selenium intervention group increased significantly (P < 0.05). Compared with the normal control group, the activities of glutathione peroxidase and superoxide dismutase and the level of malondialdehyde of 0.2-0.3 mg/L selenium intervention groups in thyroid were not significantly different. Compared with the normal control group, the activity of thyroid peroxidase of 0.1-0.3 mg/L selenium intervention groups were not significantly different. CONCLUSION: The results indicated that the optimal dose of selenium could restrain the disorder of thyroid hormone metabolism induced by excessive iodine in mice.

[Intervention of selenium on neurogranin expression in filial cerebrum of mice with excess iodine].

OBJECTIVE: To study the effects of excess iodine intake on neurogranin expression in cerebrum of filial mice and the intervention of selenium. METHODS: Sixty BALB/c mice were divided randomly into four groups with different drinking water: control group (tap water, NC), excess iodine group (3000 microg/L I, EL +), supplementing selenium group (200 microg/L Se, Se +) and the excess iodine plus selenium (3000 microg/L + I 200 microg/L Se, EI + Se +) group. The mice were mated at the end of the fourth month. Serum T4 and T3 were determined on postnatal day 14 and 28. The expression level of neurogranin in filial cerebrum was measured by immunohistochemistry and Western blot. RESULTS: Serum T4 level in EI (68.78 +/- 11.10 nmol/ L) + was lower significantly than that in NC (100.85 +/- 11.47 nmol/ L) and EI + Se + (93.15 +/- 12.10 nmol/ L) on postnatal day 14. Western blot analysis showed that the relative level of neurogranin in EI + (0.621 +/- 0.041) was lower than that in NC (0.841 +/- 0.039) and EI + Se + (0.781 +/- 0.029) on postnatal day 14 (P < 0.05). No significant difference in serum T4 and neurogranin level between four groups on postnatal day 28. CONCLUSION: Excess iodine intake might change the expression of neurogranin in filial cerebrum and the selenium supplementation might alleviate it.

[Intervention of selenium on injured type 1 deiodinase by excessive iodine in mice].

OBJECTIVE: To study the mechanism of the damage resulted from iodine excess and to seek suitable selenium intervention dosage. METHOD: 160 BALB/c mice were divided into eight groups, the normal control group, the excessive iodine group (drunk the water containing potassium iodate 3000 microg/L) and six selenium groups (drunk the water containing potassium iodate 3000 microg/L and selenium 0.1, 0.2, 0.3, 0.4, 0.5 and 0.75 mg/L). The type 1 deiodinase (D1) activities and the levels of mRNA in liver, kidney and thyroid were determined by RT-PCR. RESULTS: The mRNA levels of D1 restored to normal levels in all of the IS groups, while only 0.1-0.4 mg/L selenium supplement groups had normal activities of D1 in liver, kidney and thyroid. CONCLUSION: Decline of D1 activities in liver, kidney and thyroid seems to be one of the reasons of the damage and should be chosen for effective intervention.

[Effects of iodine excess and selenium supplement on the levels of thyroid hormone and its receptor expression in filial cerebrum of mice].

OBJECTIVE: To study effects of iodine excess on the levels of serum T4 and T3 and TRalpha1 and TRbeta1 expression in the cerebrum of filial mice and the supplement of selenium. METHODS: Sixty BALB/c mice were divided randomly into four groups: control group (tap water, NC), iodine excess group (3000 microg/L I, EI +), selenium supplement group (200 microg/L Se, Se +) and iodine excess plus selenium (3000 microg/L + I 200 microg/L Se, EI + Se +) group. The mice were mated at the end of the fourth month. Serum T4 and T3 were determined on postnatal day 14 and 28. The expression levels of TRalpha1 and TRbeta1 mRNA in filial mice cerebrum were detected by fluor scent real time PCR. RESULTS: Serum T4 level in EI + was lower significantly than that in NC and EI + Se + on postnatal day 14. mRNA levels of TRalpha1 and TRbeta1 in EI + were higher than those in other groups on postnatal day 0 and 28. No significant difference in serum T4 level and TRalpha1 and TRbeta1 mRNA expression level between four group on postnatal day 28. CONCLUSION: The expression of TRalpha1 and TRbeta1 infilial mice cerebrum could be up-regulated by iodine excess intake and could be alleviated by selenium supplement.

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.

Selenium supplement alleviated the toxic effects of excessive iodine in mice.

The relationship between the iodine intake level of a population and the occurrence of thyroid diseases is U-shaped. When excessive iodine is ingested, hypothyroidism or hyperthyroidism associated with goiter might develop. The aim of the study was to evaluate the effect of Se supplementation on the depression of type 1 deiodinase (D1) and glutathione peroxidase (GSHPx) activities caused by excessive iodine. D1 activity was assayed by the method with 125I-rT3 as a substrate. Compared to the effect of iodine alone, iodine in combination with selenium increased the activities of D1 and GSHPx. The addition of selenium alleviated the toxic effects of iodine excess on the activities of D1 and GSHPx.

Effect of selenium supplementation on activity and mRNA expression of type 1 deiodinase in mice with excessive iodine intake.

OBJECTIVE: To investigate the effect of selenium supplementation on the selenium status and selenoenzyme, especially the activity and mRNA expression of type 1 deiodinase (D1) in mice with excessive iodine (EI) intake and to explore the mechanism of selenium intervention on iodine-induced abnormities. METHODS: Weanling female BALB/c mice were given tap water or 3 mg/L of iodine or supplemented with 0.5 mg/L or 1.0 mg/L of selenium in the presence of excessive iodine for 5 months. Selenium status, thyroid hormone level, hepatic and renal D1 activity and mRNA expression were examined. RESULTS: Excessive iodine intake significantly decreased the selenium concentration in urine and liver, and the activity of glutathione peroxidase (GSH-Px) in liver. Meanwhile, serum total T4 (TT4) increased while serum total T3 (TT3) decreased. Hepatic D1 enzyme activity and mRNA expression were reduced by 33% and 86%, respectively. Renal D1 enzyme activity and mRNA were reduced by 30% and 55%, respectively. Selenium supplementation obviously increased selenium concentration, activity of GSH-Px and Dl as well as mRNA expression of D1. However, increasing the supplementation of Se from 0.5 to 1.0 mg/L did not further increase selenoenzyme activity and expression. CONCLUSION: Relative selenium deficiency caused by excessive iodine plays an essential role in the mechanism of iodine-induced abnormalities. An appropriate dose of selenium supplementation exercises a beneficial intervention.

[Influences of excess iodine on thyroid hormone concentrations in cerebrum of filial mice and intervention of selenium].

OBJECTIVE: To study the influence of excessive iodine intake on thyroid hormones in cerebrum of filial mice and intervention of selenium. METHODS: 60 Balb/c mice were divided randomly into 4 groups: control group, iodine group, selenium group and iodine plus selenium group and given tap water, tap water containing iodine 3000 microg/L, tap water containing selenium 200 microg/L and tap water containing iodine plus selenium 200 microg/L respectively as drinking water. At the end of the fourth month, the mice mated. Thyroid hormones and TSH in serum and in cerebrum of filial mice were determined at the postnatal 0, 14th and 28th day. RESULTS: At the postnatal 14th day, serum TT4 level was lower significantly, and serum TSH was higher in iodine group than those in control group and in the iodine plus selenium group. At the postnatal 0 day and 14th day, thyroid hormone concentrations in the cerebrum of progeny of mice were lower significantly in iodine group than those in control group, selenium group and iodine plus selenium (P < 0.05). No significant difference was observed among the four groups in TT4, TT3 and rT3 concentrations in serum and cerebrum at the postnatal 28th day. CONCLUSION: Excessive iodine intake can change thyroid hormone concentrations in the cerebrum of progeny of mice and selenium supplementation exerted favorable effects on it.

[Effect of selenium supplement on the disordered lipid metabolism induced by the overdose of iodine in mice].

OBJECTIVE: To explore the effect of selenium supplement on the disordered lipid metabolism induced by the overdose of iodine in mice. METHODS: The 80 Balb/c mice were randomly divided into eight groups, the normal control group, the high iodine group (drunk the water containing iodine 3000 microg/L) and six selenium groups (drunk the water containing iodine 3000 microg/L and selenium 0.1, 0.2, 0.3, 0.4, 0.5, 0.75 mg/L). The total cholesterol and triglyceride in serum and liver were determined. RESULTS: The total cholesterol in serum, the total cholesterol and triglyceride in liver of high-iodine group increased significantly compared with normal control group. There is no difference between normal control group and the group drunk the water contained 0.2 mg/L selenium. CONCLUSION: It suggests that it is an effective intervention dosage to drunk water containing 0.2 mg/L selenium.

[Effect of excessive iodine exposure on the serum TC and TG level in rats].

OBJECTIVE: To study effect of excessive iodine exposure on the serum TC and TG level in rate. METHODS: According to body weight, 60 Wistar rats were divided into 6 groups and given drinking water including different doses of iodine. The iodine concentrations were 0 (control), 1800, 3600, 7200, 14000 and 28000 microg/L, respectively. Three months later, related indices were determined. RESULTS: In excessive iodine groups, no obvious changes of thyroid morphology was observed. Urinary iodine level increased dose-dependently. Excessive iodine intake resulted in a significant reduce of serum TT4 level and an obvious increase of serum TC level in a dose-dependent manner. The positive correlation was observed between serum TC and urinary iodine. There was the negative correlation between serum TC and serum T4. CONCLUSION: Excessive-iodine exposure resulted in an increase in serum TC level. And serum lipids, together with urinary iodine and serum thyroid hormones, could be used as biomarkers for excessive iodine exposure.