Objective To determine the iodine content of common foods in different geographical areas (coastal city,coastal rural area,mountainous city and rural area) in Fujian Province and provide basic data for evaluation of dietary iodine intake.Methods In 2010,based on the types of food of the total diet study,one food sample(consumption rate is greater than 1％) was collected in coastal city(Taijiang),coastal rural area(Xiang'an),mountainous city (Sanyuan) and rural area(Mingxi).These foods including cereal,beans,potato,meat,eggs,milk,aquatic products,vegetables,fruits,sugar,beverages,liquor and seasoning,and so on 184 kinds of common foods.The iodine content of these food was tested by As (Ⅲ)-Ce4+ catalytic spectrophotometry.Results Among the 184 kinds of food tested,164 were not indicated food iodine content in the Chinese Food Composition Tables (2004).The iodine content of common food in Fujian Province in descending order were salt (30 000 μg/kg),aquatic products(341.4 μg/kg),eggs(255.9 μg/kg),dairy(106.7 μg/kg),meat(103.2 μg/kg),cereals (40.7 μg/kg),vegetables(30.7 μg/kg),beans(12.9 μg/kg),sugar(8.5 μg/kg),fruits(6.7 μg/kg),potatoes(2.4 μg/kg) and alcohol(2.1 μg/kg).The iodine content of kelp and laver was the highest in all the food,which was 314 780.1,176 956.5 μg/kg,respectively.The iodine content of food from animal(241.4 μg/kg) was much higher than that of the food from plant(25.4 μg/kg).The iodine content of common cereals,potatoes,beans,sea algae,meat,eggs and aquatic products was compared in the four areas,and the difference was not statistically significant (M =135.5,20.0,42.0,16.0,54.0,4.0,x2 =1.4,all P ＞ 0.05).The iodine content of vegetables and fruits was compared,and the difference was statistically significant (x2 =8.5,M =204.5,all P ＜ 0.05).Conclusion The iodine content of different foods is different.

Objective To analyze the monitoring results of patients with iodine deficiency disorders,and to find out the eliminating process of iodine deficiency disorders and the iodine nutritional status of population before adjustment of iodine level in edible salt in Fujian Province.Methods Thirty counties(cities,districts) were sampled by population proportion probability sampling in the whole Province in 2011; one primary school was selected from each of those 30 counties(cities,districts) ; 40 children aged 8-10 were selected from each of those 30 primary schools; thyroid volume of these children was examined by type-B ultrasound and the iodine level in edible salt from those 40 households was tested by the method of direct titration.Twelve urine samples of those 40 children were collected randomly,and urinary iodine level was tested by arsenic cerium catalytic spectrophotometry.Resident's per capita salt intake was calculated by the three-day-weighing method.In the village(where the school was in),5 drinking water samples were collected in the north,the south,the east,the west and the center of the village.If the water supply was centralized in the village,then 2 tap water samples were collected.Water iodine level was determined by arsenic cerium catalytic spectrophotometry.Three townships(towns,street offices)were selected in the vicinity of those schools; 5 pregnant and 5 lactating women were selected in each of those 3 townships (towns,street offices).Their urinary iodine level was determined by arsenic cerium catalytic spectrophotometry.Results Totally 1219 children aged 8 to 10 were examined,and their goiter rate was 4.92％(60/1219).Three hundred and sixty three urine samples were tested,and the median urinary iodine level was 223 μg/L.Among them,urinary iodine ＜ 50 μg/L accounted for 5.2％ (19/363),and ＜ 100 μg/L accounted for 14.6％ (53/363).The median urinary iodine level of pregnant women was 147.2 μg/L,and 52.0％(235/452) of them were less than 150 μg/L.The median urinary iodine level of lactating women was 134.1 μg/L.The consumption rate of qualified iodized salt was 94.4％ (1143/1211).Per capita daily salt intake was 6 g,and 81.4％ (293/360) of the residents' intake was less than 9 g.The median iodine content of drinking water was 6.2 μg/L,and 89.5％ (68/76) of them was less than 10 μg/L.Conclusions All indicators have met the national standard of eliminating iodine deficiency disorders in Fujian Province in 2011.But there is an iodine deficiency problem in pregnant women,and these women should be given extra iodine supplement.

Objective To investigate the expression and distribution of the downstream substrate of extracellular regulated protein kinase(ERK1/2) pathway, ternary complex factor phospho-Elk-1, in rat brains with chronic fluorosis, and reveal the mechanism of the impaired learning and memory ability caused by chronic fluorosis. Methods Seventy-two SD rats, weighing 100 - 120 g, were randomly divided into 3 groups, 24 in each group (half male and half female). The rats in control group were fed with tap water (fluoride < 0.5 mg/L); low- and high-dose fluoride groups were fed with tap water with different concentrations of NaF(5.0,50.0 mg/L F-, respectively). After 6 months, body weight was weighed, dental fluorosis was determined by observation and urinary fluoride and bone fluoride were detected by fluorine ion-selective electrode; the learning ability of rats was measured by navigation test of Morris water maze, and memory ability by spatial probe test in Morris water maze; the expression and distribution of phospho-Elk-1 in different brain regions were detected by immunohistochemistry method. Results In low- and high-fluoride groups, the body weight of rat[(449.2 ± 77.1), (312.8 ± 89.7)g] was significantly decreased than that of control [(635.5 ± 76.2 )g, all P< 0.05], the varying degrees of dental fluorosis were observed(x2 = 7.83, P<0.05), urinary fluoride[(2.56 ±0.91),(5.73 ±3.14)mg/L] and bone fluoride[(709.2 ± 37.4) ,(1306.3 ± 102.4) mg/kg] were significantly higher than those in controls[(0.92 ± 0.30)mg/L,(348.5 ± 89.2)mg/kg, all P< 0.05]. The escape latency of low- and high-fluoride groups[ (7.4 ± 4.1), (12.2 ± 5.7)s] was longer than that of control [(4.8 ± 2.7 )s, all P < 0.05] and the escape latency in high-fluoride group was significantly longer than that in other groups (all P < 0.05); in spatial probe test, the time of first crossing platform was longer in rats with fluorosis [(4.18 ± 1.10),(5.89 ± 0.56)s] as compared to control[(1.17 ± 0.75)s, all P< 0.05]. Expressions of phospho-Elk-1 in the hippocampus CA1(167.4 ± 8.3,163.2 ± 9.4), CA2(175.7 ± 5.0,183.3 ± 4.2), CA3(165.2 ± 11.6,162.9 ± 4.4), CA4(168.7± 6.9,169.5 ±5.3), fascia dentate (185.2 ±4.0,193.1 ±6.1) and caudate putamen( 181.4 ± 3.8, 179.8 ± 5.5) in low- and high-fluoride groups were higher than those of controls(142.4 ± 8.1,144.9 ± 8.4,143.6 ± 5.8, 116.8 ± 9.1,140.2 ± 7.8,163.1 ± 13.1, all P< 0.05). Conclusion Chronic fluorosis can cause increased expression of phospho-Elk-1 in the hippocampus and caudate putamen region of rat brains, which might be related to the mechanisms of decreased learning and memory ability of rats overexposed to fluoride.

Objective To investigate the changes of reactive oxygen species(ROS) level and mitochondria fission-fusion-balance in cortical neurons of rats with chronic fluorosis and reveal the correlation between these two factors. Methods One hundred and twenty rats were randomly divided into 3 groups(control group, low-dose fluorosis group, high-dose fluorosis group) and 40 rats were in each group according to body weight and the experiments were carried out for 3 months or 6 months. The rats were fed with different concentrations of fluoride (NaF) to establish fluorosis models. Controls were fed with tap water( < 0.5 mg/L), experimental animals in low- or high-dose group were fed with water containing NaF 10.0,50.0 mg/L, respectively. The level of ROS and the morphology in mitochondria fission-fusion balance in neurons of the cortex of rat brains prepared with cortical frozen sections were detected with ROS fluorescent probe and MitoTracker RED probe, respectively. Results Significant differences of the level of ROS and the numbers of abnormal mitochondria in morphology in the cortical neurons were found between 3 groups at the experiment period of 3 month and 6 month(F= 3.07,3.06,3.05,3.07, all P < 0.05). As compared with control group(10.43 ± 5.98,4.12 ± 3.86) at the experiment period of 3 month, the level of ROS and the numbers of abnormal mitochondria in morphology in the cortical neurons were obviously increased in high-dose fluorosis group(25.48 ± 6.09,20.47 ± 6.09, all P < 0.05), whereas no significant changes were found in low-dose fluorosis group(11.67 ± 3.49,6.68 ± 3.48, all P> 0.05). Furthermore, the increases in both ROS level and abnormal numbers of mitochondria were significant observed in the cortical neurons of low-dose fluorosis group (63.02 ± 8.15, 49.33 ± 8.61) and high-dose fluorosis group(65.60 ± 7.40,53.10 ± 6.95) as compared with the control group (25.26 ± 6.41,20.26 ± 6.41) at the experimental period of 6 month (all P < 0.05). The abnormal numbers of mitochondria correlated with ROS level(r = 0.93,0.81, all P < 0.05). Conclusions Taking excessive amount of fluoride results in high level of oxidative stress and impaired the balance of mitochondrial fission-fusion,which is dependent on the feeding times and doses of fluoride. The mechanism of the mitochondrial abnormalities might be associated with the high level of oxidative stress induced by chronic fluorosis.

Objective To observe the expression of mitochondrial fission protein locus Fis1 and ultrastructural changes in the renal cells of rats with chronic fluorosis,and to reveal the mechanism in mitochondrial damage of the renal cells.Methods Sixty SD rats were randomly divided into 3 groups according to sex and body mass(20 in each group):control group,lower fluoride group and higher fluoride group.All the rats were fed with different doses of sodium fluoride in drinking water(0,10 and 50 mg/L,respectively).Six-month later,the expression of Fisl in renal cells was determined by real-time fluorenscence quantitative PCR and immunohistochemistry technology,the mitochondrial morphology of renal cells was observed under transmission electron microscopy (TEM).Results As compared with the control group(28.70 ± 12.41),Fis1 mRNA levels(91.48 + 34.83 and 582.09 ± 184.69) in renal cells of the lower fluoride and the higher fluoride groups were increased(all P ＜ 0.05).As compared with the control group(10.49 ± 7.66),Fisl protein levels(16.33 ± 10.26 and 21.50 ± 5.24) in renal cells of the lower fluoride and the higher fluoride groups showed a trend of increasing,the higher fluoride group was higher than that of the control group(P ＜ 0.05).By TEM,mitochondrial crest in renal cells of the lower fluoride and the higher fluoride groups was vague or disappeared,mitochondrial division section appeared.Conclusions Fluoride is a kind of toxicant that can cause damage to mitochondrion of renal cells,induce the expression of Fis1 in transcriptional and protein level,and lead to the obstacles of mitochondrial fusion-fission and ultrastructural abnormality of mitochondrion,which may play an important role in mechanism of mitochondrial damage in the renal cells of rats with chronic fluorosis.

Animals ; Female ; Fluorosis, Dental ; blood ; etiology ; Glutathione Peroxidase ; blood ; Male ; Malondialdehyde ; blood ; Myocytes, Cardiac ; pathology ; ultrastructure ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Sinoatrial Node ; pathology ; ultrastructure ; Sodium Fluoride ; poisoning ; Superoxide Dismutase ; blood

OBJECTIVETo investigate the function of luxS in sulfurmetabolism of Streptococcus mutans (Sm).

METHODSThe growth with absorbency (A) of the standards and mutant strains was measured and analyzed in the sulfur-limited defined medium at different periods. The laser scanning confocal microscopy (LSCM) was used to observe and compare the biofilm thickness of the two kinds of strains at different culture conditions.

RESULTSThe significant increases in the thickness of mutant strain biofilm and its growth were observed after the addition of cysteine, but did not reach the standards strain levels (P < 0.05). The growth and the biofilm thickness of the mutant strains were (1.301 ± 0.009) and (45.009 ± 0.429) µm. When methionine and S-adenosylhomocysteine of certain concentrations were respectively added, the biofilm thickness and the growth of mutant strain were raised but did not reach the level of the standards strain at 24 h (P < 0.05), but at 48 h they did. When the methionine was added in the mutant strains for 24 h, the biofilm thickness and the growth of mutant strain were (0.448 ± 0.028) and (37.068 ± 2.392) µm, as for the adding of S-adenosylhomocysteine were (0.460 ± 0.005) and (27.343 ± 1.107) µm. When adding the supernatant fluid of standard strains, the biofilm thickness and the growth levels of mutant strain were much higher than those of the standards strain. The biofilm thickness and growth of both kinds of strains decreased after the addition of S-adenosylmethionine.

CONCLUSIONSluxS gene plays not only a role in quorum sensing but also a role in sulfurmetabolism.

Bacterial Proteins ; genetics ; metabolism ; Biofilms ; growth & development ; Carbon-Sulfur Lyases ; genetics ; metabolism ; Culture Media ; Culture Techniques ; Cysteine ; metabolism ; Gene Expression Regulation, Bacterial ; Methionine ; metabolism ; Microscopy, Confocal ; Quorum Sensing ; S-Adenosylhomocysteine ; metabolism ; S-Adenosylmethionine ; metabolism ; Streptococcus mutans ; genetics ; growth & development ; metabolism ; Sulfur ; metabolism

OBJECTIVETo construct double gene deletions at the htrA and clpP loci on the chromosome of Streptococcus mutans (Sm) and to remove the antibiotic resistance markers with the Cre-loxP(*) site-specific recombination system.

METHODSThe htrA gene was cloned into the pGEM-T-Easy TA cloning vector and then inactivated via the insertion of a kanamycin resistance cassette (lox71-Km-lox66), yielding pGEM-T-ΔhtrA/Km for deleting the htrA gene. Using the same method, the pGEM-T-ΔclpP/Sp was constructed for deleting the clpP gene. Following the transformation of pGEM-T-ΔhtrA/Km in Sm, the homologous recombination event was selected. One such mutant was transformed with a cre expression plasmid (pCrePA). The kanamycin resistance gene was then excised. The pCrePA was then easily eliminated at nonpermissive temperatures, resulting in a mutant strain (MSΔhtrA) carrying a deletion at the htrA loci without a selectable marker. This mutant was verified by PCR and DNA sequencing. Then, the clpP and spectinomycin resistance gene were deleted from MSΔhtrA, yielding markerless mutant strain lacking clpP and htrA.

RESULTSThe deletion of htrA, clpP and antibiotic resistance markers were confirmed by PCR analysis and DNA sequencing.

CONCLUSIONSA mutant of Sm was constructed successfully which contained a deletion of the htrA and clpP gene without selectable marker. The Cre-loxP(*) system can be applied to Sm, which provides experimental evidence for generating markerless multiple gene deletion mutants.

Drug Resistance, Microbial ; genetics ; Gene Deletion ; Gene Expression Regulation, Bacterial ; Genes, Bacterial ; Genetic Vectors ; Integrases ; genetics ; Plasmids ; Streptococcus mutans ; genetics

ObjectiveTo investigate the transcriptional changes of nitochondria fission and fusion gene loci and reactive oxygen species (ROS) level in cortical neurons of rats with chronic fluorosis,and to reveal their roles in mitochondria damage due to chronic fluorosis.MethodsSD rats were fed with different doses of fluoride through drinking water[＜ 0.5(control),10,50 mg/L,respectively] for 3 and 6 months.The level of ROS and mRNA contents of mitochondria fission gene loci Drp1/Fis1 and fusion gene locus Mfn1 in the cortical neurons of rat brains were detected with ROS fluorescent probe and real-time PCR,respectively.ResultsAs compared with control group [10.43 ± 5.98,(3.4 ± 0.6) × 103,(8.8 ± 1.4) × 10,(1.2 ± 0.2) × 102] at the experiment period of 3 months,the level of ROS and mRNA contents of mitochondria fusion gene locus Mfn1 and fission gene loci Drp1/Fis1 in the cortical neurons were obviously increased in the rats fed with 50 mg/L fluoride through drinking water[25.48 ± 6.09,(1.0 ± 0.2) × 1011,(3.0 ± 1.6) × 103,(8.9 ± 3.6) × 102,all P ＜ 0.05],whereas no significant changes were found in the rats fed with 10 mg/L fluoride[11.67 ± 3.49,(3.1 ± 0.3) × 104,(6.7 ± 2.7) × 10,(5.0 ± 0.9) × 10,all P ＞0.05].Furthermore,at 6 months of the experiment the increases in ROS level(63.02 ± 8.15,65.60 ± 7.40) and mRNA contents of mitochondria fission gene loci Drp1/Fis1 [(2.0 ± 0.8) × 106,(4.0 ± 0.6) × 105,(3.8 ± 1.3) × 103,(1.3 ± 0.2) × 103] and the decrease in mitochondrial fusion gene locus Mfn1[(3.0 ± 0.4) × 106、(4.0 ± 0.9) × 104]were observed in the cortical neurons of the rats fed with 10 mg/L and 50 mg/L fluoride as compared with the control group[25.26 ± 6.41,(3.0 ± 0.8) × 109,(5.1 ± 0.8) × 103,(2.8 ± 0.7) × 102,all P ＜ 0.05].Conclusions Excessive intake of fluorine leads to elevated ROS levels,and decreased transcription of mitochondrial fusion gene loci Mfn1,which is positively correlated with the time and dose-exposed to fluoride.The changes of mitochondrial fission and fusion gene loci in the cortical neurons may be related to high level of oxidative stress induced by chronic fluorosis.