Studying the damages of mouse retina induced by 2,5-hexanedione / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study toxic effects of 2,5-hexanedione (2,5-HD) on pathology and lipid peroxidation in mouse retina.</p><p><b>METHODS</b>Forty-eight mice were randomly divided into blank control group (12 mice), negative control group exposed to normal solution (12 mice) and group exposed to 2,5-HD for 2. 4 and 8 weeks, respectively (24 mice) by intraperitoneal injection (2.5% 2,5-HD) at the dose of 400 mg/kg. The pathological changes of mouse retina were examined under light microscope. The activity of superoxide dismutase (SOD) and the level of malondialdehyde (MDA) in mouse retina were detected.</p><p><b>RESULTS</b>The retinal structure in the blank and negative control groups was normal. In mice exposed to 2,5-HD for 8 weeks, the swelling of outer and inner segments and disorder arrangement of the segments without clear boundary were found. The staining of outer plexiform layers was uneven and the irregular loose structure appeared. The hyperchromatic pyknotic and necrosis nuclei were presented in ganglion cells layer. Compared with the control and blank groups, the activities of SOD gradually and significantly reduced and the concentrations of MDA increased in group exposed to 2,5-HD (P < 0.05).</p><p><b>CONCLUSION</b>2,5-HD can induce the injury of retina tissues of mice, which may be associated with the lipid peroxidation.</p>

NP9 gene inhibits tumorigenicity of nasopharyngeal carcinoma / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To study the effect of NP9 on the growth of transplanted nasopharyngeal carcinoma (NPC) in nude mice and explore the mechanisms involved.</p><p><b>METHODS</b>Recombinant pRc/CMV2-NP9 plasmid was constructed and transfected into the NPC cell lines by lipofectamine 2000. Cell clones stably expressing NP9 were obtained by detecting the mRNA expression of NP9 in G418-resistant clones with RT-PCR. The tumorigenicity and size of transplanted tumors were assessed after inoculation of NPC cells and their transgene clones into Balb/C mice. The expression of PCNA and cyclin D1 in transplanted tumors was detected by immunohistochemistry.</p><p><b>RESULTS</b>The expression of NP9 was detected in some of NP9 gene-transfected G418-resistant clones of CNE1 and SUNE1. In vivo experiments showed that the tumorigenicity of CNE19 clone was decreased significantly compared to that of CNE1 and its vector control, and the transplanted tumors grew more slowly from SUNE1/NP9 than from SUNE1 and SUNE1/vector. Compared with the vector control, the expression of cyclin D1 and PCNA in CNE1/NP9 transplants was decreased.</p><p><b>CONCLUSION</b>NP9 inhibits tumorigenicity and growth of NPC transplanted tumor by down-regulating the expression of cyclin D1 and PCNA.</p>

A study on lymphocyte DNA damage in traffic policemen in Guangzhou / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the effect of occupational exposure to traffic exhaust and smoking on DNA damage in traffic policemen.</p><p><b>METHODS</b>812 traffic policemen (741 men and 71 women, 130 of office-work and 682 of outside work) from 8 districts in Guangzhou were investigated. Blood samples were taken by venipuncture and lymphocytes were collected by using lymphocyte separation medium and centrifugation. The comet assay was used to measure DNA damage.</p><p><b>RESULTS</b>The office-work policemen [(37.7 +/- 9.5) years] were older than the outside-work ones [(32.3 +/- 8.1) years, P < 0.001]. No significant difference was observed in sex (P = 0.08) and age (P = 0.45). Comet assay showed that occupational exposure to traffic exhaust significantly increased tail length [4.20 micro m, 95% CI: (3.98 - 4.42) micro m vs 3.23 micro m, 95% CI: (2.82 - 3.7) micro m, P < 0.001]. Smokers had longer tail length [4.66 micro m, 95% CI: (4.37 - 4.97) micro m] than ex-smokers [3.28 micro m, 95% CI: (2.57 - 4.17) micro m] and nonsmokers [3.47 micro m, 95% CI: (3.21 - 3.75) micro m, P < 0.001]. In nonsmokers, significant increase in tail length was observed by passive smoking at home (P = 0.004) but not at work (P = 0.22). When out-door nonsmokers were excluded, passive smoking at work also significantly increased tail length (P = 0.007). Analysis of covariance showed that occupational exposure to traffic exhaust, tobacco smoking, and female had independent effect on lymphocyte DNA damage (P < 0.001) after these factors were adjusted. Passive smoking and age had no effect on lymphocyte DNA damage.</p><p><b>CONCLUSIONS</b>Occupational exposure to traffic exhaust and tobacco smoking respectively increase lymphocyte DNA damage. Female traffic policemen may have more severe DNA damage than male.</p>