OBJECTIVETo investigate the relationship between fasting serum levels of leptin, glucose, insulin resistance, lipids in simple obese children.

METHODSFasting serum levels of leptin and insulin (Fins) were measured by RIA in 42 obese and 42 normally-weighted children matched on age, sex and height, and their total cholesterol (TC), triglyceride (TG), high density lipoprotein-cholesterol (HDL-C) were analyzed with enzymatic methods. HOMA-IR and LDL-C were calculated.

RESULTSSerum level of leptin was (2.74 - 45.12) micro g/L and (0.53 - 10.18) micro g/L in obese and normally-weighted children, respectively, with an average level of leptin (log) significantly higher in obese group than that in control group (P < 0.001). Serum level of leptin was positively correlated with BMI, WHR and percentage of body fat. Of obese children, 83% were leptin resistant. Serum levels of TC, TG, LDL-C and insulin were significantly higher in obese leptin-resistant group than those in normally-weighted control group, but no significant difference in them between obese leptin-sensitive group and its normally-weighted control group was observed. Significantly higher serum levels of TG and lower HDL-C were observed in obese leptin-resistant group, as compared with those in obese leptin-sensitive group.

CONCLUSIONSA big difference in serum level of leptin between obese and normally-weighted children was found, suggesting most obese children were resistant to endogenous leptin. Leptin resistance correlated significantly with the risk of metabolic syndrome and cardiovascular disease, indicating serum level of leptin could be used as an indicator in screening obese children at high risk.

Blood Glucose ; metabolism ; Body Mass Index ; Child ; Cholesterol ; blood ; Female ; Humans ; Insulin Resistance ; Leptin ; blood ; Male ; Obesity ; blood ; Triglycerides ; blood

OBJECTIVETo study DNA and nucleus damage in human embryo lung fibroblast (HLF) exposed to hydroquinone (HQ) and its genotoxicity.

METHODSHLF were treated with HQ (0, 10, 20, 40, 80 micro mol/L, respectively) for 3 h and DNA damage was detected by comet assay. HLF was also treated with the same concentrations of HQ for 1 h and micronucleus test was performed after they were cultured for 24 h.

RESULTSComet assay showed that percentage of cells with tails in each groups treated with varied doses of HQ was 12%, 19%, 42%, 79% and 95%, respectively, with mean tail length of 7.87, 9.35, 11.03, 19.28 and 23.32 micro m, respectively, in an obvious dose-dependent manner (P < 0.05). Very significant increase in percentage of cells with tails and length of their comet tail were observed in those groups treated with HQ of 20, 40 and 80 micro mol/L (P < 0.01). And, proportion of high and severe DNA damage increased with dose of HQ. HQ could also induce formation of micronucleus and abnormal nucleus in all groups treated by varied doses of HQ, with rates of micronucleus and abnormal nucleus of 2%, 3%, 10%, 9% and 15%, and 6%, 7%, 16%, 27% and 28%, respectively, in a significant dose-dependent manner. There was significant increase in rates of micronuclei and abnormal nuclei in cells treated with HQ at doses of 20, 40 and 80 micro mol/L (P < 0.05).

CONCLUSIONSExposure to HQ could cause DNA and nucleus damage inducing genotoxic effects on HLF.

Cell Nucleus ; drug effects ; Comet Assay ; DNA Damage ; drug effects ; Embryo, Mammalian ; Fibroblasts ; cytology ; Humans ; Hydroquinones ; toxicity ; Lung ; cytology ; Micronucleus Tests

OBJECTIVETo study the reproductive toxicity of metadoxine.

METHODSMale and female rats were given metadoxine before pregnancy and early gestation, i.e. to feed metadoxine to male rats for 60 days before copulation and continue feeding during copulation, and feed metadoxine to female rats for 14 days before copulation.

RESULTSNo significant toxic effect was observed in the 400 mg/kg group. A few rats showed paralysis of hind leg in the 800 mg/kg group. The dosage of 1 600 mg/kg caused significant paralysis of hind legs, emaciation, and reduced weight gain. In the 1600 mg/kg group, the mating rate of male rats was significantly affected (P < 0.01). In the 800 and 1 600 mg/kg group, fertility of male rats was markedly reduced (P < 0.01). In the 800 mg/kg group, the effect on sperm counts of epididymis of male rats was markedly reduced (P < 0.05). In the 1 600 mg/kg group, testicle weight and body weight ratio and sperm counts of epididymis rate were significantly (P < 0.001) reduced. In the 1 600 mg/kg group, the fertility rate of female rats was remarkably (P < 0.001) reduced. In the 800 mg/kg group, the weight gain of pregnant rats was significantly reduced (P < 0.001). In both the 800 and 1 600 mg/kg groups, the gestation rate was greatly reduced (P < 0.001). In the 800 mg/kg group, mortality rate before nidation (P < 0.001) and average live fetus number were significantly reduced (P < 0.05). In the 400 mg/kg group, the fetal weight was significantly reduced (P < 0.001). In the 800 mg/kg group, body length, tail length, body weight and sternum development of fetal rats were significantly affected (P < 0.001).

CONCLUSIONUnder the presented experimental conditions, metadoxine has no teratogenic effects on SD rats and the no effect dose is 400 mg/kg. And the no effect dose for the developmental toxicity is less than 400 mg/kg.

Animals ; Dose-Response Relationship, Drug ; Drug Combinations ; Female ; Fertility ; drug effects ; Fetal Weight ; Male ; Organ Size ; Pregnancy ; Pyridoxine ; toxicity ; Pyrrolidonecarboxylic Acid ; toxicity ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Sperm Count ; Testis ; anatomy & histology

OBJECTIVETo investigate the effects of sodium metavanadate (SMV) on blood sugar and glucose phosphorylation in mice, and to discuss the possible mechanism of its hypoglycemic effects.

METHODSDiabetic mice (D) and control mice (V) were randomly allocated to drink SMV (0.2 mg/ml) (CV and DV groups) or NaCl (80 mmol/L) (C and V groups) respectively. The study lasted for 5 weeks. Liver glucokinase, muscle hexokinase, blood glucose and insulin were assayed at the end of each week.

RESULTSBlood glucose was higher in the diabetic groups before the administration of SMV, and the blood glucose level of group DV decreased from (18.77 +/- 1.28) to (8.94 +/- 0.94) mmol/L (P < 0.01) after oral administration of SMV for one week. While liver glucokinase increased from (1.29 +/- 0.64) to (15.36 +/- 1.57) mIU/min/mg protein and muscle hexokinase increased from (1.93 +/- 0.50) to (18.62 +/- 1.71) mIU/min/mg protein (P < 0.01) respectively. There was no continuous change of these parameters during the later weeks. No significant change of serum insulin was observed in the diabetic mice. There was a remarkable negative correlation of blood glucose level with liver glucokinase and muscle hexokinase levels.

CONCLUSIONThe hypoglycemic effects of SMV was independent of insulin level. In consideration of the close relations of the activities of liver glucokinase and muscle hexokinase with diabetes, and the improving of impaired glucose phosphorylation in diabetic mice by oral sodium metavanadate, which might be the mechanism of hypoglycemic effects of SMV.

Animals ; Blood Glucose ; metabolism ; Diabetes Mellitus, Experimental ; blood ; Female ; Glucokinase ; metabolism ; Hexokinase ; metabolism ; Hypoglycemic Agents ; pharmacology ; Insulin ; blood ; Liver ; metabolism ; Mice ; Mice, Inbred ICR ; Muscle, Skeletal ; metabolism ; Phosphorylation ; Random Allocation ; Vanadates ; pharmacology

OBJECTIVETo assess the protective effect of drinking green tea on the development of gastric, liver and esophageal cancers.

METHODSA population based study was conducted in Taixing, Jiangsu province, including 206, 204, 218 cases, respectively, and 415 population controls.

RESULTSGreen tea decreased the development of gastric cancer risk by 40%. Dose-response relationships were observed between the length of time, concentration and quantity of green tea drinking and its protective effects on gastric cancer. For individuals who drink green tea for more than 250 g per month, the risk of gastric cancer reduced about 60%. Green tea might have protective effect on liver cancer. However, no protective effect of green tea was observed on esophageal cancer.

CONCLUSIONGreen tea drinking might be a protective factor for gastric cancer. However, the protective effects of green tea on liver and esophageal cancer were not obvious.

Dose-Response Relationship, Drug ; Esophageal Neoplasms ; prevention & control ; Humans ; Liver Neoplasms ; prevention & control ; Plant Extracts ; therapeutic use ; Stomach Neoplasms ; prevention & control ; Tea ; chemistry

OBJECTIVETo investigate the effect of ERCC1 gene on the repair capability of damaged DNA in lung cancer A549 cells induced by benzo[a]pyrene.

METHODSRecombinant plasmid expressing ERCC1 antisense RNA was constructed and transfected into A549 cells by Lipofectin reagent. The stable-transfected cell colonies were selected by hygromycin. Cell viability was determined by the MTT assay. The level of ERCC1 mRNA was measured by Northern Blot analysis. Single cell gel electrophoresis assay was applied to determine the cellular DNA damage and fifty cells for each group were counted.

RESULTSSeven positive colonies expressing ERCC1 antisense RNA were screened. There was no growth rate difference between the antisense-transfected cells and the parental cells. The endogenous mRNA level in transfected colonies decreased in varied degrees, i.e. 12% approximately 86% of that of the parental cells in Northern Blot assay. After 24 h treatment of 10 micro mol/l benzo[a]pyrene, the repair capability for DNA damage in transfected colonies was reduced to 29% approximately 71% of that of the parental cells. Also, a statistically significant correlation was observed between expression of ERCC1 mRNA and repair capability (r = 0.84).

CONCLUSIONAntisense ERCC1 RNA decreased the repair capability for damaged DNA in lung cancer cells induced by benzo[a]pyrene.

Benzo(a)pyrene ; toxicity ; Cell Line, Tumor ; DNA Damage ; drug effects ; DNA Repair ; drug effects ; DNA-Binding Proteins ; genetics ; metabolism ; pharmacology ; Endonucleases ; genetics ; metabolism ; pharmacology ; Humans ; Lung Neoplasms ; pathology ; Plasmids ; RNA, Antisense ; pharmacology ; RNA, Messenger ; metabolism ; Repressor Proteins ; Transfection

OBJECTIVETo set a quantitative criteria for determining risk for coronary heart disease (CHD) so that potential risk of an individual dying from CHD can be identified and to lay a foundation for predicting individual risk of CHD.

METHODSData of case-control and cohort studies published during 1978 to 2002, as well as data of surveillance of behavior exposure in Sichuan province, were collected by retrieval of literatures. Pooled odds ratios (OR) and relative risks (RR) of all risk factors for CHD were estimated using various statistical models with software for meta-analysis, and attributable risk fractions of varied levels of risk factors could be converted.

RESULTSA risk score conversion table (quantitative criteria for assessment) of main risk factors for CHD were developed for men and women aged 15 - 69 at an interval of five years, including smoking, passive smoking, hypertension, high blood cholesterol level, body mass index, lack of physical activity, alcohol drinking, past history of diabetes, and family history of CHD and hypertension. Individuals with all these risk factors had a risk score beyond 1.00, and risk score for those without them was equal to or below 1.00, which would increase with rise in one's risk level.

CONCLUSIONSEstimation of risk of dying from CHD was based on risk score conversion table of risk factors for CHD, which could be used to predict individual potential risk of dying from CHD in the following 10 years. It lays a foundation for health education to persuade people to change their unhealthy lifestyles and behaviors, and could be used in community health services.

Adolescent ; Adult ; Aged ; Case-Control Studies ; China ; epidemiology ; Cohort Studies ; Coronary Disease ; epidemiology ; etiology ; Feeding Behavior ; Female ; Humans ; Hypertension ; complications ; Life Style ; Male ; Middle Aged ; Odds Ratio ; Risk Assessment ; Risk Factors ; Smoking ; adverse effects ; Urban Health

OBJECTIVETo study the effect of exogenous nucleic acid on physical functions, morphology of hepatic cells and brain neurons in aged rats.

METHODSThirty two aged Wistar rats (20 month-old) were divided randomly into four groups (one aged control group and three aged experimental groups) and eight young rats (3 month-old) was set as young control group. Control groups were fed on standard chow and experimental groups were fed on standard chow supplemented with 93.75 mg/kg (high-dosage group), 46.88 mg/kg (middle-dosage group) and 9.38 mg/kg (low-dosage group) of yeast RNA respectively. SOD, MDA, HDL, sex hormone and growth hormone were determined at the end of a 4-week observation. The microcosmic images of the hepatic cells and brain neurons using the image-pro plus (V.4.0) were also observed.

RESULTSSOD, serum HDL and growth hormone levels in the high dosage group were significantly higher (P < 0.05) than that in the aged control group, and the levels were not different from that in the young control group. MDA level of all yeast RNA supplemented groups was significantly lower than that of aged control group (P < 0.05) and that was not different from the young control group. Serum testosterone of the high and middle dosage groups reached the level of young control group, and that was much higher than the aged control and low dosage group (P < 0.05). Estradiol levels among the aged rats were not different, and those were much lower than the young control group (P < 0.05). Much more number of brain neurons were observed in the high-dose group than other aged rats (P < 0.05). Brain neurons, hepatic cells and karyons in the high-dose group were bigger than that in other aged rats (P < 0.05).

CONCLUSIONExogenous yeast RNA might play an important role in physical functions, the morphology of brain neurons and hepatic cells in natural aged rats. There might have a dose-effect relationship in the process.

Aging ; Animals ; Brain ; physiology ; ultrastructure ; Dose-Response Relationship, Drug ; Hepatocytes ; ultrastructure ; Liver ; physiology ; ultrastructure ; Male ; Neurons ; ultrastructure ; RNA, Fungal ; pharmacology ; Random Allocation ; Rats ; Rats, Wistar ; Yeasts ; chemistry

OBJECTIVEThe objective of this study was to investigate the estrogenic activity of genistein and zearalenone through their effects on the proliferative capacity of human ovarian PEO4.

METHODSEstrogen receptor-positive PEO4 cell was grown in DMEM medium containing 10% bovine serum. Five days before the addition of the test compounds, the cells were washed in phosphate-buffered saline, and the medium was substituted with a phenol red-free DMEM medium containing 5% dextran charcoal-stripped FBS. The respective test compound was added in fresh medium and the control cell received only the vehicle (ethanol). Cell proliferation was detected respectively by MTT assay, (3)H-TdR incorporation and flow cytometry.

RESULTSCompared with vehicle control, 96 x 10(-6) mol/L GS significantly inhibited PEO4 cell proliferation and DNA synthesis as measured by MTT and (3)H-TdR incorporation after treatment for 24 h. Alao, 32 x 10(-6) mol/L GS could exert inhibition on PEO4 cell growth as time extension to 48 h. 32 x 10(-6) mol/L approximately 96 x 10(-6) mol/L GS induced G(2)/M arrest. At low dose (< 8 x 10(-6) mol/L=, GS promoted proliferation in PEO4 cells. ZEA enhanced proliferation, promoted DNA synthesis and increased the S phase population in PEO4 cells.

CONCLUSIONSGenistein possess estrogenic activity and zearalenone have anti-estrogenic activity. They play different effects on the proliferation of human ovarian cancer cell. Genistein enhanced the proliferation of PEO4. Zearalenone inhibited its the proliferation. These results implied that genistein and zearalenone elicit different signal-transduction channel.

Antineoplastic Agents ; pharmacology ; Cell Division ; drug effects ; Estrogens, Non-Steroidal ; pharmacology ; Female ; Genistein ; pharmacology ; Humans ; Ovarian Neoplasms ; pathology ; Receptors, Estrogen ; metabolism ; Tumor Cells, Cultured ; Zearalenone ; pharmacology

OBJECTIVETo explore the effect of environmental estrogens on the proliferation of breast cancer cell line MCF-7.

METHODSThe tested compounds were n-4-nonyphenol, Bisphenol A and dibutylphthalate. Human estradiol-dependent MCF-7 breast cancer cells were grown in DMEM medium containing 10% bovine serum. Five days before the addition of the test compounds, the cells were washed by phosphate-buffered saline, and the medium was substituted with a phenol red-free DMEM medium containing 5% dextral charcoal-stripped FBS. The respective test compound was added in fresh medium and the control cell received only the vehicle (ethanol). The proliferation of MCF-7 was analyzed by the MTT assay, (3)H-TdR incorporation assay and flow cytometry.

RESULTSCompared with the ethanol control, the proliferation and DNA synthesis of the test cells treated with n-4-nonyphenol (8 x 10(-7) mol/L, 96 h), Bisphenol A (8 x 10(-7) mol/L, 96 h) or dibutylphthalate (32 x 10(-6) mol/L, 96 h) treatment was markedly enhanced in a time-dependent and dose-dependent manner.

CONCLUSIONn-4-Nonyphenol, Bisphenol A and dibutylphthalate enhanced the proliferation of human breast cancer cell in vitro, which may demonstrate an estrogenic activity.

Benzhydryl Compounds ; Breast Neoplasms ; pathology ; Cell Division ; drug effects ; Cell Line, Tumor ; Dibutyl Phthalate ; toxicity ; Environmental Pollutants ; toxicity ; Estrogens, Non-Steroidal ; toxicity ; Female ; Humans ; Phenols ; toxicity