Application of 1H-NMR-based metabolomics for detecting injury induced by long-term microwave exposure in Wistar rats' urine.

There has been growing public concern regarding exposure to microwave fields as a potential human health hazard. This study aimed to identify sensitive biochemical indexes for the detection of injury induced by microwave exposure. Male Wistar rats were exposed to microwaves for 6 min per day, 5 days per week over a period of 1 month at an average power density of 5 mW/cm(2) (specific absorption rate of 2.1 W/kg). Urine specimens were collected over 24 h in metabolic cages at 7 days, 21 days, 2 months, and 6 months after exposure. (1)H NMR spectroscopy data were analyzed using multivariate statistical techniques. Urine metabolic profiles of rats after long-term microwave exposure were significantly differentiated from those of sham-treated controls using principal component analysis or partial least squares discriminant analysis. Significant differences in low molecular weight metabolites (acetate, succinate, citrate, ketoglutarate, glucose, taurine, phenylalanine, tyrosine, and hippurate) were identified in the 5 mW/cm(2) microwave exposure group compared with the sham-treated controls at 7 days, 21 days, and 2 months. Metabolites returned to normal levels by 6 months after exposure. These data indicated that these metabolites were related to the perturbations of energy metabolism particularly in the tricarboxylic acid cycle, and the metabolism of amino acids, monoamines, and choline in urine represent potential indexes for the detection of injury induced by long-term microwave exposure.

[Influence of microwave radiation on synapsin I expression in PC12 cells and its mechanism].

AIM: To investigate the effect of microwave radiation on expression and phosphorylation of synapsin I and to discover the mechanism by research on the change of expression of BDNF and its receptor, TrkB. METHODS: PC12 cells were exposed to microwave with average power density being 30 mW/cm(2). HPLC was used to detect the release of amino acids; RT-PCR, Western blot and immunocytochemistry were used to detect the expressions of synapsin I, BDNF and TrkB; immune co-precipitation was used to study the interaction of BDNF and TrkB. RESULTS: It resulted in the decrease of the release of Asp, Glu, GABA and Gly at 1 h (P<0.01) after radiation. Protein of synapsin I was decreased in 9 h-2 d (P<0.01 or P<0.05); its mRNA was decreased in 3-9 h and increased at 1 d (P<0.01 or P<0.05); its phosphorylation was decreased at 3 h, increased at 1 d, and decreased at 2 d again (P<0.01 or P<0.05) after radiation. Protein of BDNF was decreased at 3 h and increased in 1-2 d (P<0.01 or P<0.05); its mRNA were decreased in 3-9 h, increased at 1d, and decreased at 2 d again (P<0.01 or P<0.05) after radiation. Protein of TrkB was increased in 3 h-1 d (P<0.01 or P<0.05); its mRNA decreased at 3 h and 2 d (P<0.01) after radiation. The interaction between BDNF and TrkB was increased in 3-9 h, but decreased in 1-2 d (P<0.01 or P<0.05) after radiation. CONCLUSION: Microwave radiation can induce the decrease of the release of amino acids and the expression and phosphorylation of synapsin I, and the abnormality of expressions and interaction of BDNF and TrkB in PC12 cells. The factors might play a role in the injury and repair of information transmission in PC12 cells.

[Influence of microwave radiation on synaptic structure and function of hippocampus in Wistar rats].

OBJECTIVE: To investigate the effect of microwave radiation on synaptic structure, characteristic of synaptosome, the contents and release of neurotransmitters in hippocampus in Wistar rats. METHODS: Wistar rats were exposed to microwave radiation with average power density of 30 mW/cm(2). Electron telescope was used to study the change of the synaptic structure at 6 h after radiation and to identify synaptosome. Flow cytometry and electron spin resonance were used to study the change of the concentration of Ca(2+) in synapse and the fluidity of membrane proteins of synaptosome. High performance liquid chromatography (HPLC) and spectrophotometer were used to study the changes of contents and release of amino acids and acetylcholine in hippocampus. RESULTS: Microwave radiation of 30 mW/cm(2) caused deposits of synapse vesicle, elongation of active zone, the increase of thickness of postsynaptic density (PSD) and curvature, and perforation of synapse. The concentration of Ca(2+) in synapse (P<0.01) and tc of membrane proteins (P<0.01) of synaptosome increased contents of glutamic acid and glycine (P<0.01) and release of GABA increased the increase of contents and release of acetylcholine, and activity of acetyl cholinesterase (P<0.01) increased. CONCLUSION: Microwave radiation can induce the injure of synaptic structure and function of hippocampus, and then induce the disorder of the ability of learning and memory in rats.

Distribution of the alleles at loci D16S539, D7S820, and D13S317 in hydatidiform mole genome from Chinese women and its relationship with clinical prognosis.

Using polymerase chain reaction and denaturating polyacrylamide gel electrophoretic techniques, we studied 53 cases of hydatidiform moles. Of these, 41 cases were genetically complete hydatidiform moles (g-CHM) whose genome were totally paternally derived. We investigated the distribution of the alleles in the short tandem repeat sequences at loci D16S539, D7S820, and D13S317 in these cases. In particular, we analyzed the allelic distribution and potential significance in cases with traceable benign and invasive moles (i.e., persistent trophoblastic tumor [PTT]). Among 41 g-CHM cases, there were six alleles at D16S539, five alleles at D7S820 (the frequencies of alleles 9 and 10 were respectively lower and higher than those in Beijing population), and seven alleles at D13S317; the heterozygosity of loci D16S539, D7S820, and D13S317 was 0.0732, 0.0976, and 0.0732, respectively. Among 23 benign cases, there were six alleles at D16S539, four at D7S820, and six at D13S317; among 11 PTT cases, there were five alleles at D7S820 and four alleles each at D16S539 and D13S317. The frequencies of allele 9 at D16S539 and allele 10 at D7S820 were higher than in benign cases (P < 0.05). There were significant differences in frequencies of alleles 9 and 10 at D7S820 between the cases and the Beijing population, and heterozygosity at the three loci was lower in the cases than in the population. In addition, invasiveness of hydatidiform mole correlated to the frequency of allele 9 at loci D16S539 and allele 10 at D7S820.

[Study of gene differential display of hydatidiform moles].

OBJECTIVE: To screen the specific molecular maker of invasive hydatidiform moles (HM) by differential display analysis. METHODS: For dot hybridization, about 1.0 microg of each cDNA sample of invasive and non-invasive HM were labeled as probes using the Dig DNA labeling and Detection Kit (Boehringer Mannheim). The specific expression fragments of invasive HM recovered from PAGE gel were re-amplified by PCR, and the PCR products were dotted onto nylon membrane and hybridized by two probes of invasive and non-invasive HM cDNA respectively. Some fragments with a strong positive hybridization signal were cloned into the polylinker of lasmid PUC19 and were sequenced. The fragments' sequences were searched for homology in the NCBI data using the BLAST (Database: GenBank Human EST entries; Posted date:Aug 31, 2004; Number of letters in database: 1,697,659,032; Number of sequences in database: 3,677,722). RESULTS: The 20 fragments in 28 bands with specific expression in invasive HM were re-amplified, of which 13 showed positive hybridization signals, and 3 were cloned into the polylinker of lasmid PUC19. A fragment in the 3 was a new expressed sequence tag (EST) and the sequence was submitted to NCBI data (dbEST_Id: 10875704; GenBank_Accn: BM403211). CONCLUSION: There are more differences in gene expression between invasive and non-invasive HMs, and differential display analyses are of a potential significance to early diagnosis of invasive HM.

[The relationship between malignant transformation and fertilization types of hydatidiform moles].

OBJECTIVE: To study the relationship between malignant transformation and fertilization types of hydatidiform moles (HM). METHODS: Fifty four HM specimens were analyzed by using multiplex STR-PCR (9 loci) to determine the fertilization types and all patients were followed-up for the human chorionic gonadotropin (hCG) over 1 year. RESULTS: Total malignant transformation cases were 10 in all the 54 HM. Ggenetics complete hydatidiform moles (g-CHM) with DNA from only paternal origin, were observed in 38 cases including 28 homozygote and 10 heterozygote cases. In homozygote and heterozygote cases,malignant transformation occurred in 8 cases of the empty eggs fertilized by single sperms and 2 by double sperms respectively. In all the 54 HMs, 16 cases of DNA from parents were genetic partial hydatidiform moles (g-PHM), and no malignant transformation occurred in each haploidy egg fertilized by double sperms. CONCLUSION: (1)Genetic complete hydatidiform moles (g-CHM) showed a higher malignant transformation risk than genetic partial hydatidiform moles (g-PHM) (P=0.024 2); (2)There was no significant difference in malignant transformation between homozygote and heterozygote of g-CHM (P=0.699).