To study the effects of cadmium chloride on DNA damage of rat liver cells in vivo and in vitro Single cell gel electrophoresis or Comet assay was used At the concentration of 2 185 ?mol/L, 4 375 ?mol/L, 8 75 ?mol/L, 17 50 ?mol/L, 35 00 ?mol/L, cadmium chloride could induce DNA damage of rat liver cells in vitro, and at the doses of 5 ?mol/kg, 10 ?mol/kg, 20 ?mol/kg, cadmium chloride could induce DNA damage of rat liver cells in vivo respectively The in vivo and in vitro results also showed the obvious dose response relationship between the rates of Comet cells and the doses of cadmium chloride [Conclusion]The research infered that at certain dose, cadmium could induce DNA damage and had toxic effects on rat liver cells

Objective This study was conducted to explore the effects of fluorosis on rat renal apoptosis and proliferation, oxidative stress and necrosis. Methods Wistar rats were provided with distilled water containing NaF(50mg/L) for six months. Kidney cell apoptosis and the cell cycle of proliferation were detected by TUNEL (TdT-mediated dUTP Nick End Labelling) and flow cytometry. Rsults TUNEL_positive cells could be detected in fluoride_treated rat kidney. The apoptotic rates of fluoride_treated kidney cells were higher than that of control significantly. Fluorosis could reduce the cell number of G2/M period in cell cycle and decrease DNA relative content significantly. In addition, fluorosis could induce rat renal oxidative stress and necrosis. Cnclusion It was suggested that fluorosis could induce apoptosis and change the cell cycle of rat renal cells in vivo, and also could result in rat renal oxidative stress and necrosis.

Objective To study the antogonistic effects of selenium(Se) on methylmercury (MeHg) induced lipid peroxidation Methods SD rats were purfused perorally with Se and MeHg The effects on lipid peroxidation in rats' brain tissue caused by MeHg and the antagonistic effects of Se were observed Results Se could reduce the accumulation levels of MeHg in brain tissue and increase the GSH contents and GSH Px activities so as to inhibit the lipid peroxidation in brain tissue induced by MeHg and reduce LPO levels Conclusion Se at a certain dose could markedly antagonize MeHg induced lipid peroxidation as a result of reducation of the accumulative levels of MeHg in brain tissue and antagonizing lipid peroxidation induced by Se itself

This study investigated the effect of cadmium on the telomerase activity, the expression of TERT, c-myc and p53 and the apoptosis of rat hepatocytes. The rats were administrated 5, 10 and 20 μmol/kg cadmium chloride intraperitoneally and sacrificed 48 h after the initial treatment. The telomerase activity of the rat hepatocytes was measured by the telomeric repeat amplification protocol (TRAP), and apoptosis was detected by flow cytometry. The mRNA expressions of TERT, c-myc and p53 were measured by reverse transcription-polymerase chain reaction (RT-PCR). C-myc and P53 proteins were determined by immunochemistry. The results showed that cadmium chloride increased the hepatocellular telomerase activity in a dose-dependant manner and induced the apoptosis of hepatocytes significantly. The value of relative coefficient between the telomerase activity and the apoptosis rate was 0.9398. RT-PCR revealed that specific bands corresponding to the TERT mRNA, c-myc mRNA, and p53 mRNA were displayed at 185, 342 and 538 bp respectively. Cadmium chloride could substantially increase the mRNA expressions of TERT, c-myc and p53 in rat hepatocytes, as compared with control. Moreover, cadmium chloride at the doses of 5, 10 and 20 μmol/kg could increase the content of P53 protein in rat hepatocytes obviously, but only that at the doses of 10 and 20 μmol/kg substantially promoted the c-myc protein level in rat hepatocytes. Our study herein suggested that cadmium may contribute to the carcinogenesis by activating telomerase, and overexpressing the mRNAs of TERT, c-myc and p53, and causing apoptosis of normal cells.

Following rapid social and economic development over the past several decades,pollution by heavy metals has been both serious and widespread in many areas of the world,including China.The situations of heavy metal pollution in China were reviewed,and the health risk and control policy of such pollution were also analyzed and discussed in present paper.

OBJECTIVEThis study was conducted to study the effects of sodium fluoride (NaF) on rat renal apoptosis and proliferation, the antagonistic effect of selenium-zinc preparation (Se-Zn) to NaF.

METHODSWistar rats were provided with distilled water containing NaF (50 mg/L) and administered by gavage with different dosed of Se-Zn for six months. Kidney cell apoptosis and the cell cycle of proliferation were detected by TUNEL (TdT-mediated dUTP Nick End Labelling) and flow cytometry.

RESULTSNaF caused rat renal apoptosis, reduce the cell number of G(2)/M period in cell cycle and decrease the relative content of DNA significantly. Se-Zn inhibited the effects of NaF on apoptosis and increased the cell number of G(2)/M period in cell cycle, but failed to increase relative content of DNA.

CONCLUSIONIt was suggested that NaF could induce apoptosis and change the cell cycle in rat renal cells and Se-Zn could antagonize apoptosis and the changes of cell cycle induced by NaF.

Animals ; Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Division ; drug effects ; DNA ; drug effects ; genetics ; metabolism ; Drug Antagonism ; Flow Cytometry ; In Situ Nick-End Labeling ; Kidney ; drug effects ; pathology ; Rats ; Selenium ; pharmacology ; Sodium Fluoride ; pharmacology ; Zinc ; pharmacology

OBJECTIVE: To analyze the influencing factors of suspected occupational noise-induced deafness( ONID) in noise-exposed workers. METHODS: A total of 38 770 noise-exposed workers engaged in occupational health examination were collected as the study subjects from 2012-2016 by judgment sampling method. The data of workers' occupational medical examination was collected,and the incidence and influencing factors of suspected ONID were analyzed. RESULTS: A total of 125 cases of suspected ONID were detected and the detection rate was 0. 32%. The result of multivariate Logistic regression showed that male workers exposed to noise had a higher risk of suspected ONID than female workers( P <0. 01). The odds ratio( OR) and 95% confidence interval( CI) were 1. 98( 1. 22-3. 19). The older the age and the longer service length of workers exposed to noise,the higher the risk of suspected ONID( P < 0. 01). The ORs and 95% CIs were 1. 79(1. 43-2. 25) and 1. 84( 1. 47-2. 30) respectively. The noise-exposed workers had a higher risk of suspected ONID in foreign-funded enterprises than domestic-funded enterprises( P < 0. 01). The noise-exposed workers had a higher risk of suspected ONID in metal manufacturing industries than in non-metal manufacturing industries( P < 0. 01). The ORs and 95% CIs were 1. 83(1. 19-2. 82) and 2. 02(1. 40-2. 94) respectively. CONCLUSION: The incidence of suspected ONID is affected by factors of gender,age,length of service,economy type of enterprises and industry type.

This study investigated the effect of cadmium on the telomerase activity, the expression of TERT, c-myc and p53 and the apoptosis of rat hepatocytes. The rats were administrated 5, 10 and 20 μmol/kg cadmium chloride intraperitoneally and sacrificed 48 h after the initial treatment. The telomerase activity of the rat hepatocytes was measured by the telomeric repeat amplification protocol (TRAP), and apoptosis was detected by flow cytometry. The mRNA expressions of TERT, c-myc and p53 were measured by reverse transcription-polymerase chain reaction (RT-PCR). C-myc and P53 proteins were determined by immunochemistry. The results showed that cadmium chloride increased the hepatocellular telomerase activity in a dose-dependant manner and induced the apoptosis of hepatocytes significantly. The value of relative coefficient between the telomerase activity and the apoptosis rate was 0.9398. RT-PCR revealed that specific bands corresponding to the TERT mRNA, c-myc mRNA, and p53 mRNA were displayed at 185, 342 and 538 bp respectively. Cadmium chloride could substantially increase the mRNA expressions of TERT, c-myc and p53 in rat hepatocytes, as compared with control. Moreover, cadmium chloride at the doses of 5, 10 and 20 μmol/kg could increase the content of P53 protein in rat hepatocytes obviously, but only that at the doses of 10 and 20 μmol/kg substantially promoted the c-myc protein level in rat hepatocytes. Our study herein suggested that cadmium may contribute to the carcinogenesis by activating telomerase, and overexpressing the mRNAs of TERT, c-myc and p53, and causing apoptosis of normal cells.
Animals ; Apoptosis ; drug effects ; Cadmium ; toxicity ; Hepatocytes ; drug effects ; metabolism ; pathology ; Male ; Proto-Oncogene Proteins c-myc ; genetics ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Telomerase ; genetics ; metabolism ; Tumor Suppressor Protein p53 ; genetics ; metabolism

OBJECTIVE: To explore the influencing factors of occupational stress from occupational hazards in employees of a power grid enterprise. METHODS: A total of 972 employees from 3 substations and 1 power dispatch center of a power grid enterprise were selected as research subjects by the cluster sampling method. The Chinese version of the Job Content Questionnaire was used to evaluate the occupational stress using the job demand control(JDC) model. The influence of occupational hazards on occupational stress was analyzed. RESULTS: The median, the 25 th and 75 th percentile scores [M(P_(25), P_(75))] of the 972 research subjects on job demand, job control, and social support dimensions of JDC model occupational stress were 14(12, 15), 25(23, 26), 24(23, 24), respectively. The M(P_(25), P_(75)) of the demand/control(D/C) ratio was 0.99(0.89, 1.13). The incidence of occupational stress was 48.4%(470/972) by the JDC model. The job demand dimension scores, D/C ratios, and incidence of occupational stress by JDC model were higher in employees exposed to electromagnetic radiation, high temperature, high altitude, and visual display terminal(VDT) than in those employees not exposed to the above factors(all P<0.05). The results of multivariate logistic regression analysis showed that the risk of occupational stress increased in those employees exposed to high temperature, high altitude and VDT(all P<0.05) after excluding the influence of confounding factors such as age, length of service, monthly income and exercise. The odds ratio and 95% confidence intervals were 1.91(1.43-2.54) and 1.67(1.26-2.21), respectively. CONCLUSION: The level of occupational stress among employees in power grid enterprise is relatively high by JDC model. High-temperature, high-altitude and VDT operation are the main risk factors of occupational stress by JDC model.

OBJECTIVE: To study the effects of cadmium on the expression of estrogen receptor( ER) and miRAN-155,miRAN-200 c in human breast cancer MCF-7 cells. METHODS: MCF-7cells in logarithmic growth phase were randomly divided into fulvestrant( ICI182780,ICI) group and non-ICI group. The non-ICI group was treated with cadmium chloride(Cd Cl2) at the final concentrations of 0. 0,2. 5,5. 0 and 10. 0 μmol/L for 24 hours. The ICI group was pretreated at a concentration of 1. 0 μmol/L for 12 hours,and then treated with Cd Cl2 at the final concentrations 0. 0,2. 5,5. 0 and 10. 0μmol/L for 24 hours. The cell proliferation activity was measured by methyl thiazolyl tetrazolium assay. Flow cytometry was used to measured cell apoptosis. Western blot was applied to measure the relative expression of ERα and ERβ protein,and the relative expression of miRNA-155 and miRNA-200 c were detected by real-time fluorescence quantitative polymerase chain reaction. RESULTS: The proliferation rates of MCF-7 cells in 2. 5,5. 0 and 10. 0 μmol/L Cd Cl2 groups were significantly decreased than the 0. 0 μmol/L Cd Cl2 group( P < 0. 05). The proliferation rate in ICI group was lower than that of the non-ICI group( P < 0. 05). When Cd Cl2 concentration was 2. 5,5. 0 and 10. 0 μmol/L,the apoptosis rate of MCF-7 cells in non-ICI group increased compared with those cells without exposure to Cd Cl2( P < 0. 05). The relative expression of ERα,ERβ,miRNA-155 and miRNA-200 c increased( P < 0. 05). The proliferation of MCF-7 cells in ICI group decreased( P < 0. 05),and the relative apoptosis rate increased( P < 0. 05); and the relative expression of ERαand ERβ increased( P < 0. 05),the relative expression of miRNA-155 and miRNA-200 c decreased( P < 0. 05). When treated without Cd Cl2,the apoptosis rate of the ICI group increased compared with non-ICI group(P < 0. 05),the relative expression of ERα and ERβ decreased( P < 0. 05),and the relative expression of miRNA-155 and miRNA-200 c were increased( P < 0. 05). When Cd Cl2 concentration was 2. 5,5. 0 and 10. 0 μmol/L,the apoptosis rate and the relative expression of ERα,ERβ,miRNA-155 and miRNA-200 c decreased compared with the non-ICI group treated with same dose Cd Cl2(P < 0. 05). CONCLUSION: Cadmium can induce cell apoptosis and increase expression of miRNAs through the ER signaling pathway.