[Effect of selenium and arsenic on oxidative stress, DNA oxidative damage and repair in HepG2 cells].

OBJECTIVE: To study alone and combined effect of selenium and arsenic on oxidative stress, DNA oxidative damage and repair. METHODS: HepG2 cells were treated with selenium (2.5, 5.0 and 10.0 micromol/L sodium selenite) alone, arsenic (1.56, 3.13, 6.25, 12.5 and 25.0 micromol/L arsenious acid) alone and combined selenium plus arsenic. The quantitative analysis of malondialdehyde (MDA), 8-OHdG and hOGG1 was carried out by fluorometric method, HPLC-EC and Western Blot to represent oxidative stress, DNA oxidative damage and repair, respectively. RESULTS: Under the condition of alone treatment, sodium selenite (5.0 and 10.0 micromol/L) as well as arsenious acid (6.25, 12.5 and 25.0 micromol/L) resulted in significant increased levels of MDA and 8-OHdG, and inhibition of hOGG1 expression in HepG2 cells compared with solvent control (P < 0.05, P < 0.01). Sodium selenite at the relative low dose (2.5 micromol/L) displayed certain anti-oxidative ability (P > 0.05). Combined treatment of sodium selenite (2.5 micromol/L) and arsenious acid (6.25 micromol/L) caused significant lower levels of MDA and 8-OHdG than those of correspondent arsenic alone treatment (P < 0.05). hOGG1 expression showed no difference between combined treatment (2.5 micromol/L of selenium selenite plus 6.25, 12.5 and 25.0 micromol/L of arsenious acid, respectively) and correspondent arsenic alone treatment (P > 0.05). CONCLUSION: Sodium selenite at the concentrations of 5.0, 10.0 micromol/L and arsenious acid at the concentrations of 6.25, 12.5, 25.0 micromol/L induced enhanced oxidative stress and 8-OHdG production, and inhibition of hOGG1 expression, respectively. Selenium at certain concentration (2.5 micromol/L of selenium selenite) has ameliorative effects on oxidative stress and DNA oxidative damage induced by arsenic, but no effect on repair of DNA oxidative damage.

[Effect of polychlorinated biphenyls on DNA damage induced by benzo[a]pyrene in HepG2 cells].

OBJECTIVE: To explore effects of polychlorinated biphenyl, PCB153 on DNA damage induced by benzo(a) pyrene (B[a]P) in HepG2 cells. METHODS: As target cell, HepG2 cells were treated at the concentrations of 0.1, 1, 10 and 100 micromol/L with PCB153 and at the concentrations of 12.5, 25, 50 and 100 micromol/L B[a]P respectively. DMSO was used as solvent control. Single cell gel electrophoresis (SCGE) was applied for quantitative analysis of DNA damage which was caused by treating alone or co-treating with PCB153 and B[a]P, CYP1A1 (EROD) and CYP2B1 (PROD) activities were detected by using fluorescence spectrophotometry. RESULTS: When compared with the solvent control, the DNA oliver tail moments were increased significantly (P < 0.01) in HepG2 cells treated with all the concentrations of B[a]P, while no significant DNA damage was observed in HepG2 cells treated with all the concentrations of PCB153. When compared with B[a]P treated alone, the DNA oliver tail moments showed a increase tendency in HepG2 cells co-treated with PCB153 (0.1, 1, 10 micromol/L) and B[a]P (50 micromol/L). But DNA oliver tail moments were increased significantly only when co-treated with 10 micromol/L of PCB153 and 50 micromol/L of B[a]P (P <0.01), while decreased significantly after co-exposuring to 100 micromol/L of PCB153 and 50 micromol/L of B[a]P (P <0.01). All concentrations of PCB153 induced significant increase in EROD and PROD activities in HepG2 cells. CONCLUSION: It was suggested that the enhancement of DNA damage induced by B[a]P could be associated with the increases of CYP1A1 and CYP2B1 activities induced by PCB153 in HepG2 cells.

[Oxidative stress of human derived fetal hepatocytes induced by product of chlorinated drinking water (MX)].

OBJECTIVE: To study the oxidative stress induced by 3-chloro-4-( dichloromethyl)-5-hydroxy-2 [5H]-furanone (MX) (a product of chlorinated drinking water) in human derived fetal hepatocytes (L-02) in vitro. METHODS: L-02 cells were treated at the doses of 10, 30, 100 and 300 micromol/L of MX for 24h. Malondialdehyde (MDA), reduced glutathione (GSH) and 8-hydroxydeoxyguanosine (8-OHdG), the representative of antioxidative molecules and the marker of DNA oxidative damage respectively, were detected in L-02 cell treated by MX. Dimethyl sulfoxide (DMSO) was used as solvent control. RESULTS: (1) The content of MDA was significantly increased in L-02 cells etreated by MX at the doses of 30, 100, 300 micromol/L in comparison with solvent control. (2) The level of GSH was significantly decreased and the level of 8-OHdG was significantly increased in L-02 cells treated by MX at the concentration of 100, 300 micromol/L in comparison with solvent control. (3) There was a striking positive association between MDA content and 8-OHdG level (r = 0.767, P < 0.01) and a negative association between GSH level and 8-OHdG level (r = 0.761, P < 0.01) in L-02 cells treated by MX at the doses from 0 to 300 micromol/L. CONCLUSION: MX could induce oxidative stress in L-02 cells including increases of lipid peroxidation and DNA oxidative damage, and weakened effect of antioxidation. DNA oxidative damage in L-02 cells might be associated with lipid peroxidation and the weakening of antioxidation induced by MX.

[Enhancement effect of polychlorinated biphenyl on benzo (a) pyrene-induced DNA damage in HepG2 cells].

OBJECTIVE: To study the effect of polychlorinated biphenyl, Aroclor1254 on benzo (a) pyrene [B (a) P]-induced DNA damage in HepG2 cells. METHODS: HepG2 cells were pretreated with Aroclor1254 (11.5, 23 and 46 micromol/L) for 24 hours and then exposed to B (a) P (50 micromol/L). DMSO (10 ml/L) was used as solvent control. Single cell gel electrophoresis (SCGE) and high-performance liquid chromatography-electrochemical detection (HPLC-EC) assays were applied to detect DNA single-strand breaks and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in HepG2 cells, respectively. RESULTS: Average Oliver tail moment (OTM) and 8-OHdG level in HepG2 cells were significantly increased in B (a) P treated group (1.66 +/- 0.21), (23.31 +/- 6.02) 8-OHdG/10(6)dG than that in solvent control (0.79 +/- 0.15), (12.31 +/- 3.24) 8-OHdG/10(6)dG, respectively. In Aroclor 1254 treated group (11.5, 23.0, 46.0 micromol/L), average OTM were 0.88 +/- 0.20, 1.01 +/- 0.15 and 1.10 +/- 0.16, and 8-OHdG levels were (19.57 +/- 7.57), (22.80 +/- 9.16) and (31.74 +/- 9.25) 8-OHdG/10(6)dG, respectively. A concentration of 46 micromol/L Aroclor1254 caused a significant increase of 8-OHdG level as compared with the solvent control. After pretreatment of HepG2 cells with Aroclor1254 (11.5, 23.0 and 46.0 micromol/L), B (a) P induced more DNA strand breaks (OTM: 2.14 +/- 0.22, 2.43 +/- 0.32 and 2.71 +/- 0.31) and 8-OHdG [(32.50 +/- 3.81), (49.23 +/- 16.66) and (60.36 +/- 18.04) 8-OHdG/10(6)dG] in HepG2 cells than B (a) P alone. CONCLUSION: Aroclor1254 might enhance B (a) P-induced DNA damage in HepG2 cells, which should imply a synergistic effect of Aroclor1254 on the genotoxicity of B (a) P.

Relationship between acne and psychological burden evaluated by ASLEC and HADS surveys in high school and college students from central China.

Previously, acne and its effects on psychological well-being have mostly been studied unilaterally in the western population. This study was aimed to investigate bidirectional relationship between acne and stress using Adolescent Self-Rating Life Events Check (ASLEC) and Hospital Anxiety and Depression Scale (HADS) surveys from inhabitants of central China. An on-line survey of 2,284 high school and college students from central China was conducted using three questionnaires posted on Chinese professional survey website, the Questionnaire Web. The prevalence and severity of acne were determined using the Pillsbury grading, whereas, the role of stress in acne formation was ascertained by the ASLEC scale. The HADS was employed to assess the psychological well-being. A total of 50.61 % of high school and college students in central China were found to be suffering from acne for more than 6 months, and 19.72 % of them were graded as having severe acne. Negative life events were found to accelerate the occurrence and exacerbation of the condition. Acne-affected groups showed significantly higher HADS-A (HADS-anxiety) and HADS-D (HADS-depression) scores than the controls (7.31 and 7.28 vs. 4.37 and 3.85, respectively; p < 0.01). Despite the apparent neglect of acne in Chinese high school and college students, a close bidirectional relationship was found to exist between stress and acne. It is incumbent on the healthcare professional to introduce school-based educational programs to help students with knowledge and management of acne and prevent the consequent psychological disorders.

Ventilator-associated pneumonia in intensive care units in Hubei Province, China: a multicentre prospective cohort survey.

A multicentre prospective cohort study was performed in 17 intensive care units (ICUs) in tertiary care hospitals in Hubei Province, China. Ventilator-associated pneumonia (VAP) was defined according to modified criteria from the published literature. Among 4155 ventilated patients, the crude incidence and incidence rate of VAP were 20.9% and 28.9 cases per 1000 ventilator-days. Multivariate analysis using logistic regression revealed risk factors including male sex [risk ratio (RR): 1.5; P<0.001], coma (RR: 2.1; P<0.001), chronic obstructive pulmonary disease (RR: 1.4; P<0.001), infections at other sites (RR: 1.6; P=0.001), serious disease predating the onset of VAP (RR: 1.6; P<0.001) and interventions including antacid treatment (RR: 1.4; P<0.001), antimicrobial treatment (RR: 5.1; P<0.001), bronchoscopy (RR: 1.5; P=0.041) and tracheostomy (RR: 1.4; P=0.014). The most frequently isolated causative pathogens were Pseudomonas aeruginosa and Acinetobacter baumannii. Of all Staphylococcus aureus isolates, 45.7% were meticillin resistant. Rates, risk factors and causal pathogens of VAP in ICUs in Hubei differ from those reported from developed countries. These data show the need for more effective infection control interventions in Hubei, China.