[Environmental and geochemical behaviors of fluorine and its impacts on ecological environment]. / æ°Ÿçš„çŽ¯å¢ƒåœ°çƒåŒ–å­¦è¡Œä¸ºåŠå ¶å¯¹ç”Ÿæ€çŽ¯å¢ƒçš„å½±å“.

In past decades, fluorine exposure of plants and human caused by regional geochemical anomalies of fluorine or environmental pollution has received widespread concerns. Many in-depth researches have been conducted on the geochemical behavior of fluorine in different environmental media, but with disputes and uncertainties. We reviewed the research advances on geochemical behaviors of fluorine in the atmosphere, water and soil, including source, quantity, existence form, migration, transformation, and controlling factors. The observation of correlation between geochemical behaviors of fluorine and plant and human fluoride exposure was also reviewed. Moreover, we proposed that the future research on environmental geochemical behaviors of fluorine should give priority to particular directions.

[Relationship between fluoride exposure, orthopedic injuries and bone formation markers in patients with coal-burning fluorosis]. / ç‡ƒç ¤æ±¡æŸ“åž‹æ°Ÿä¸­æ¯’æ‚£è€ æ°Ÿæš´éœ²ã€éª¨ç›¸æŸä¼¤ç¨‹åº¦ä¸Žéª¨å½¢æˆæ ‡å¿—ç‰©çš„å ³ç³».

Chronic exposure to fluoride is a public health problem worldwide. We explored the relationship between fluoride exposure, orthopedic injuries and bone formation markers alkaline phosphatase (ALP), bone Gla protein (BGP) in participants with coal-burning fluorosis in Hehua Village (coal-burning fluorosis endemic area) in Zhijin County of Guizhou Province and Zhangguan Village (non-fluoride contaminated area) in Anshun City of Guizhou Province. Environmental samples were collected and fluoride contents were examined using a fluoride ion-selective electrode. Dental fluorosis and skeletal fluorosis of 295 participants from Hehua Village and 85 participants from Zhangguan Village were diagnosed with informed consent. Urinary samples and peripheral blood samples were collected from the participants to determine urinary fluoride (UF), ALP acti-vity, and BGP content. The results showed that fluoride contents in rice, pepper, corn, drinking water, clay, vegetable-grown soil, coal and indoor and outdoor air were significantly higher than those in the control area, but lower than the previously reported values. With the increases of UF concentration, the ALP activity and BGP content significantly increased, the severity of skeletal fluorosis was greater, but with no significant changes in dental fluorosis. There was positive correlation between the severity of skeletal fluorosis and ALP activity, BGP content. These results indicated that low fluoride exposure could cause orthopedic injuries. ALP and BGP could be used to eva-luate the bone turnover in patients with skeletal fluorosis, which would be useful in the auxiliary diagnosis and therapeutic evaluation of skeletal fluorosis.

[The mRNA expression of mitogen-activated protein kinase signal pathway related genes in the blood of arseniasis patients caused by burning coal].

OBJECTIVE: To detect the mRNA expression of ERK1, ERK2, JNK1 and P38 gene in mitogen-activated protein kinase(MAPK) path way in the arseniasis patients caused by burning coal. METHODS: 70 arseniasis patients caused by burning coal at Jiaole village XingRen county in December 2006 were selected as case group, and another 30 villagers with similar living habits, matched gender and age, healthy physical condition without history of burning high arsenic coal were selected as control group from 12 km nearby the same village.Silver diethyl dithiocarbamate method (Ag-DDC) was taken to detect the arsenic contents in the environmental media, food, and arsenic level in the urine and hair of arseniasis patients.On the principle of informed consent, the peripheral blood was collected from the patients. The total RNA was extracted with Trizol method and cDNA was reversed from it. The mRNA expression of ERK1, ERK2, JNK1 and P38 gene in MAPK path way were tested by real-time fluorescent quantitative PCR (QT-PCR). RESULTS: A total of 70 cases of arseniasis patients (31 cases of mild, 25 cases of moderate and 14 cases of severe) and 30 cases of control were chosen. The median (quartile) of arsenic contents in the indoor air, outdoor air, coal, chili and corn were 0.079 (0.053-0.117) mg/m(3) ,0.007 (0.002-0.015) mg/m(3) , 93.010 (39.460-211.740) mg/kg, 3.460(0.550-16.760) mg/kg and 1.500(0.300-4.140) mg/kg respectively. They were above the national health standards. The median (quartile) of arsenic contents in the soil, rice and drinking water were separately 12.130(4.230-24.820) mg/kg, 0.650(0.300-0.980) mg/kg and 0.043(0.012-0.089)mg/kg, which were within the national health standards. Compared with the control group ((26.97 ± 9.71)µg/g Cr), arsenic level in the patients' urine ((71.48 ± 22.74)µg/g Cr) increased significantly, the differences were significant (F = 90.38, P < 0.01). Compared with the control group ((1.58 ± 1.07)µg/g), arsenic level in the patients' hair ((4.45 ± 2.78) µg/g) increased significantly, the differences were significant (F = 48.22, P < 0.01). The relative expression amount of the median(quartile) for ERK2, JNK1 mRNA were 0.0667 (0.0378-0.1371) and 0.0013 (0.0009-0.0025), respectively. Compared with the control group 0.1744 (0.1009-0.1985) and 0.0022 (0.0017-0.0030) , only the decreases of ERK2, JNK1 mRNA expression was significant (χ(2) = 15.10, 14.25, P < 0.01), and no significance in the other index. ERK2 mRNA relative expression for mild, medium and severe groups were separately 0.0818 (0.0408-0.1509) ,0.0582 (0.0154-0.1699) and 0.0588 (0.0399-0.1034) . Compared with the control group (0.1744 (0.1099-0.1985) ), there was significant difference (Z = -2.89, -3.19, -2.67, P < 0.01). JNK1 mRNA relative expression were 0.0012 (0.0007-0.001 57), 0.0019 (0.0011-0.0035), 0.0013 (0.0010-0.0026), respectively. Compared with the control group (0.0022 (0.0017-0.0030) ), significances were found in the mild groups (Z = -3.72, P < 0.01). CONCLUSIONS: Arsenic could induce the changes of ERK2 and JNK1mRNA expression in the MAPK path way in arseniasis patients.It suggests that the MAPK signaling pathway take part in the occurrence and development process of arseniasis caused by burning coal.

[Relationship between the methylation and mutation of p53 gene and endemic arsenism caused by coal-burning].

OBJECTIVE: To explore the influence of arsenic pollution caused by coal-burning on methylation (promoter and exon 5) and mutation (exon 5) of human p53 gene, and to analyze the relationship between methylation, mutation and arsenism. METHODS: According to the diagnostic criteria of endemic arsenism, 112 patients with arsenism (including 38 mild cases, 43 moderate cases and 31 severe cases) were selected in the areas with endemic arsenism from Xingren, Guizhou province. Among the subjects, 43 cases were diagnosed by dermatopathological methods, and they were divided into non-cancerous group (24 cases) and cancerous group (19 cases). 90 controls were selected from the non-arsenic polluted areas. Under the principle of informed consent, blood samples were collected from individuals. The methylation of p53 gene in promoter region and exon 5 were detected by extinction enzyme-PCR, the mutation of p53 gene (exon 5) was detected by PCR-SSCP, PCR products cloning and sequencing technology. RESULTS: The positive rates of methylation of p53 gene in promoter region were 13.16% (5/38), 27.91% (12/43) and 45.16% (14/31) respectively among mild, moderate and severe arsenism group, which were obviously higher than the rates in the control group (1.11% (1/90), χ² values were 8.679, 23.690, 41.199, respectively, both P values < 0.017). The positive rates of methylation of p53 gene were 25.00% (6/24) and 63.16% (12/19) in non-cancerous and cancerous group respectively, which were obviously higher than those in the control group (1.11% (1/90), χ² values were 18.762, 57.497, respectively, both P values < 0.025). The positive rates of methylation of p53 gene (exon 5) were 55.26% (21/38), 51.16% (22/43) and 48.39% (15/31) respectively among mild, moderate and severe arsenism group, which were obviously lower than the rates in the control group (88.88% (80/90), χ² values were 18.151, 23.168, 22.420, respectively, both P values < 0.017). The positive rates of methylation of p53 gene (exon 5) were 54.17% (13/24) and 42.11% (8/19) in non-cancerous and cancerous group respectively, which were obviously lower than those in the control group (88.88% (80/90), χ² values were 15.201, 22.075, respectively, both P values < 0.025). The mutation rates of p53 gene (exon 5) were respectively 5.26% (2/38), 16.28% (7/43) and 25.81% (8/31) among mild, moderate and severe arsenism group; while the results in moderate and severe arsenism group were obviously higher than in the control group (0.00%, χ² values were 15.465, 24.870, respectively, both P values < 0.017). The positive rate of mutation of p53 gene (exon 5) were respectively 16.67% (4/24) and 31.58% (6/19) in non-cancerous and cancerous group, which were obviously higher than it in the control group (0.00%, χ² values were 15.545, 30.077, both P values < 0.025). The hypermethylation of p53 gene in promoter region was related with the mutation of p53 gene (exon 5) (coefficient of association was 0.294, P value < 0.05); and the hypomethylation of p53 gene (exon 5) was related with the its mutation (coefficient of association was 0.410, P value < 0.05). CONCLUSION: Arsenic pollution caused by coal-burning can cause the hypermethylation of p53 gene in promoter region, hypomethylation and mutation of p53 gene (exon 5), and the changes of methylation of p53 gene are related with its mutation and might be one of the important etiological factors of arsenic pathogenicity or carcinogenesis.

Analysis of p16 gene mutation, deletion and methylation in patients with arseniasis produced by indoor unventilated-stove coal usage in Guizhou, China.

The aim of this study was to determine p16 gene mutation, deletion, and promoter 5' CpG island hypermethylation in peripheral blood mononuclear leukocyte of patients with arseniasis as attributed to exposure to indoor unventilated coal stove. The role of the aberrant change of p16 gene in the induction and development of carcinogenesis in endemic arsenisiasis region in China was also examined. Polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP), multiplex PCR (mPCR), methylation-specific PCR (MSP), and sequencing techniques were performed to detect (1) mutation of the p16 gene exon 2, (2) homozygous deletion of the p16 gene exon 1 and exon 2, and (3) hypermethylation of the promoter CpG island in peripheral blood mononuclear leukocyte of patients with arseniasis. Results showed no mutation was found in exon 2 of p16 gene. The homozygous deletion frequency of p16 gene was 5 and 15% in control and arseniasis patients, respectively. The homozygous deletion occurred mainly in exon 2, with significant deletion frequencies of 9, 13, and 20% in mild, intermediate, and severe arseniasis groups. The significant homozygous deletion frequency was 9 and 39% in noncarcinoma and carcinoma individuals. The positive rate of p16 gene promoter CpG island hyermethylation was 42 and 2% in the exposed group and the control group, respectively. The positive rate was 26, 42, and 50% in mild, intermediate, and severe arseniasis. The marked different positive rate was 22 and 56% in noncarcinoma and carcinoma individuals, respectively. In conclusion, homozygous deletion and hypermethylation of p16 gene may play an important role in the initiation and development of manifestations seen in endemic arseniasis including carcinogenesis.