Expression of relaxin family peptide receptor 1 in the lung tissue of silicosis rats / 中国职业医学

OBJECTIVE: To investigate the potential effect of relaxin family peptide receptor 1( RXFP1) in the process of silica-induced silicosis. METHODS: Sixty-four specific pathogen free male Wistar rats were randomly divided into control group and experimental group. By one time intratracheal infusion,rats in experimental group were treated with 0. 1 m L 500 g / L silica dust suspension while the control group was treated with 0. 1 m L sodium chloride physiological solution. Eight rats from each group were sacrificed on day 1,7,14 and 28 after exposure. Histopathologic changes of the lung tissue were performed with hematoxylin-eosin staining. The expressions of Rxfp1 mRNA and RXFP1 protein in rat lungs were detected by real-time polymerase chain reaction and immunohistochemical staining,respectively. RESULTS: After 28 days of exposure,the grey nodules were observed by naked eye in the lung of the experimental group. The fracture and silicotic nodules could be seen in alveolar interval with light microscope. Compared with the control group,the Rxfp1 mRNA relative expression level in the lungs of experimental group was increased to 145% after 1 day of exposure( P < 0. 01),followed by a decrease on day 7 and 14 and reached similar level of control group( P > 0. 05). By day 28,it dropped to45% of control group( P < 0. 01). The RXFP1 protein relative expression in experimental group was significantly up-regulated since the 7th day compared to that of the control group( P < 0. 01). And it reached to the highest level on the28 th day( P < 0. 01). CONCLUSION: The RXFP1 might play an important role in inhibiting silicosis.

Enhancement effect of polychlorinated biphenyl on benzo (a) pyrene-induced DNA damage in HepG2 cells / 中华预防医学杂志

<p><b>OBJECTIVE</b>To study the effect of polychlorinated biphenyl, Aroclor1254 on benzo (a) pyrene [B (a) P]-induced DNA damage in HepG2 cells.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>

Argyrophil nucleolar organizer regions as biomarker of effect for polycyclic aromatic hydrocarbon exposure / 中华预防医学杂志

<p><b>OBJECTIVE</b>To study whether the argyrophil nucleolar organizer regions (AgNOR) in T lymphocytes of peripheral blood in coke-oven workers can be used as a biomarker of effect for polycyclic aromatic hydrocarbon (PAH) exposure.</p><p><b>METHODS</b>Fifty-two male coke-oven workers were divided into three groups according to exposure levels of coke oven emissions: high-exposure, middle-exposure and low-exposure workers. Additionally 10 men without occupational PAH exposure were chosen as control group. Peripheral blood T lymphocytes were cultured, spread on slides and stained with silver nitrate. The ratio of AgNOR area vs. nuclear area (I/S) in T lymphocytes was analyzed. Urinary 1-hydroxypyrene (1-OHP) was measured as the internal dose of PAH exposure.</p><p><b>RESULTS</b>Mean urinary 1-OHP level in high-exposure group (16.56 +/- 2.77 micromol/mol Cr) was significantly higher than those in low-exposure group (3.30 +/- 2.77 micromol/mol Cr, P < 0.001) and control group (3.04 +/- 1.58 micromol/mol Cr, P < 0.01). The mean I/S of AgNOR in T lymphocytes in high-exposure group (0.056 +/- 0.010) was significantly lower than those in middle-exposure group (0.065 +/- 0.013, P < 0.05), low-exposure group (0.067 +/- 0.008, P < 0.01) and control group (0.076 +/- 0.007, P < 0.001). It was also found that I/S of AgNOR were significantly decreased in middle-exposure group and low-exposure group in comparison with control group (P < 0.01, P < 0.05).</p><p><b>CONCLUSIONS</b>The occupational exposure to PAH resulted in increase of 1-OHP in urine and decrease of AgNOR in T lymphocytes. PAH exposure might lead to damage T lymphocytes function and AgNOR may be considered as a biomarker of effect for PAH exposure.</p>

Analysis of serum glutathione S-transferase and urinary 8-hydroxy-2-deoxyguanosine in coke oven workers / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the application of serum glutathione S-transferase (GST) and urinary 8-hydroxy-2-deoxyguanosine (8-OHdG) as the monitoring biomarkers for coke oven workers exposed to polycyclic aromatic hydrocarbons (PAHs).</p><p><b>METHODS</b>47 male coke oven workers and 31 male control workers were investigated. Urinary 8-OHdG and serum GST were analyzed using high performance liquid chromatography (HPLC) with electrochemical detection and test kit. Urinary 1-hydroxypyrene (1-OHP) as internal exposure of PAHs was also determined simultaneously by alkaline hydrolysis and HPLC.</p><p><b>RESULTS</b>The values of urinary 1-OHP, serum GST and urinary 8-OHdG were reported as median with interquartile range (P(25)-P(75)). Urinary 1-OHP [5.7 (1.4-12.0) micromol/mol Cr], serum GST [22.1 (14.9-31.2) U/ml], and urinary 8-OHdG [1.9 (1.4-15.4) micromol/mol Cr] in coke oven workers were significantly higher than in control workers [3.0 (0.5-6.4) micromol/mol Cr (P < 0.05), 13.1 (9.5-16.7) U/ml (P < 0.01), and 1.3 (1.0-4.0) micromol/mol Cr (P < 0.05) respectively]. Categorizing by smoking status, significant differences in urinary 1-OHP and serum GST were found only in smokers among coke oven workers compared to control workers (P < 0.01), and 8-OHdG levels only in non-smokers (P < 0.01). Additionally, there was significant correlation between urinary 1-OHP and serum GST activity (r(s) = 0.31, P < 0.01, n = 78). The multiple logistic regression analysis showed that coke oven workers were at the higher risk of having GST activities above 16.7 U/ml (OR = 13.2) and 8-OHdG levels above 1.8 micromol/mol creatinine (OR = 4.4). High body mass index was an independent factor to affect urinary 8-OHdG levels.</p><p><b>CONCLUSIONS</b>The elevated serum GST activities and increased oxidative DNA damage were found in the coke oven workers. Occupational exposure and smoking interact on each other. Serum GST may be used as a biomarker for assessing the exposure of PAHs. Assay of urinary 8-OHdG may be useful for evaluating the risk of lung cancer in coke oven workers.</p>

Effects of selenium on benzoa pyrene-induce DNA damage in mouse lung cells / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the effects of selenium on DNA damage induced by benzo[a] pyrene (BaP) in mouse lung cells.</p><p><b>METHODS</b>Sodium selenite was given to Kunming male mice by i.p. and BaP was given by oral gavage. The control group was given solvent only with the same method. DNA damage was detected by single cell gel electrophoresis (or comet assay).</p><p><b>RESULTS</b>The damage degrees in mice treated with 125, 250 and 500 mg/kg of BaP were more severe than that of control (P < 0.01). The rates of comet cells in the BaP-treated groups (43.50%, 84.00%, 95.63%) were significantly higher than that of control (9.75%, P < 0.01), and there was obvious dose-response relationship. 0.75, 1.50 and 3.00 mg/kg of sodium selenite presented antagonistic effects against DNA damage induced by 250 mg/kg of BaP in mouse's lung cells. The antagonistic effect of sodium selenite at the dose of 1.50 mg/kg was better than those of sodium selenite at the doses of 0.75, 3.00 mg/kg.</p><p><b>CONCLUSION</b>BaP at the doses of 125 approximately 500 mg/kg could significantly induce DNA damage of lung cells in mice. 0.75 approximately 3.00 mg/kg of sodium selenite could inhibit DNA damage of lung cells in mice induced by 250 mg/kg of BaP.</p>