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 observe the effect of n-hexane subchronic exposure on the serum level of neuron specific enolase(NSE), neurofilament light chain protein(NF-L) and nerve growth factor(NGF) in rat, and to explore the feasibility of using NSE, NF-L and NGF as biomarkers of n-hexane neurotoxicity. METHODS: Specific pathogen free male SD rats were randomly divided into control group and low-, medium-and high-dose exposure groups, with 6 rats in each group. Rats in the low-, medium-and high-dose exposure groups were given n-hexane solution at doses of 168, 675 and 2 700 mg/kg body mass, respectively, while rats in the control group were gavaged with 0.9% sodium chloride solution, once a day, 5 days a week for 6 weeks. At week 0, 2, 4, and 6 of exposure, the body mass of the rats was weighed, the gait scores were performed, and the serum levels of NSE, NF-L, and NGF were detected.RESULTS: Body mass, gait score and serum levels of NSE and NF-L in rats were statistically significant in terms of the n-hexane exposure dose and exposure time(P<0.01). At the 6 th week of n-hexane exposure, the body mass of the three dose exposure groups was lower than that of the control group(P<0.05), and the gait score was higher than that of the control group(P<0.05). Moreover, the abnormal gait of the rats showed a dose-effect relationship with the increasing n-hexane poisoning dose. At week 2, 4 and 6, the serum levels of NSE and NF-L in these three dose exposure groups were higher than that in the control group(P<0.05). In addition, the serum level of NF-L in rats in the medium-and high-dose exposure groups increased with the n-hexane exposure time increasing and showed a time-effect relationship(P<0.05). The level of serum NGF in rats was statistically significant in the main effects of n-hexane dose and duration of exposure(P<0.05). The serum NGF level in the high-dose exposure group was lower than that in the control group, the low-dose and medium-dose exposure groups(P<0.05). NGF level in serum of rats at week 6 was lower than that at week 0, 2 and 4(P<0.05). CONCLUSION: Both NSE and NF-L in serum can be used as biomarkers for the early effect of n-hexane on peripheral nerve injury. The feasibility of using serum NGF as a biomarker for the early effect of n-hexane on peripheral nerve injury warrants further investigation.