Assessment of oxidative DNA damage in the oxyR-deficient SOS chromotest strain Escherichia coli PQ300.

The SOS chromotest is a simple short-term genotoxicity assay measuring the induction of gene sfiA in Escherichia coli K-12. The recent availability of SOS tester strains with additional mutations in DNA repair or protection systems allows testing of DNA damaging compounds for genotoxic specificity. E. coli PQ300 differs from the standard SOS tester strain PQ37 in that it contains an additional mutation in gene oxyR that renders it more sensitive to oxidative genotoxins. The generation of reactive oxygen intermediates (ROI) by hydroperoxides (H2O2, t-butyl hydroperoxide, cumene hydroperoxide), gamma-radiation, glucose oxidase, and xanthine oxidase resulted in a more vigorous SOS response in strain PQ300 compared to strain PQ37. PQ300 was also more sensitive than PQ37 for the detection of reducing agents such as ascorbic acid, cysteine, and glutathione, which also alter the redox status of the bacterial cells. However, intercalating agents (adriamycin, bleomycin, and mitomycin C) and the UV- and radiomimetic compound 4-nitroquinoline-1-oxide whose DNA damaging potential are known also to involve ROI did not show significant differences between strains PQ37 and PQ300. It is concluded that the oxyR-deficient strain PQ300 is useful for detecting certain classes of genotoxins that change the oxidative/antioxidative balance of tester bacteria in the SOS chromotest.     

SOS抢救护理小组的组建与实施

介绍了上海交通大学附属一院SOS抢救护理小组的组建、运营和管理,提高了抢救病人的医护应急速度、效率和质量、并有利于护理队伍的培养和急救护理学的发展。     

大豆低聚糖和低聚肽对高脂血症大鼠血管活性物质和血液流变学的影响

目的探讨大豆低聚糖(SOS)和大豆低聚肽(SOP)对高脂血症大鼠血管活性物质和血液流变学的影响。方法60只健康成年SD大鼠随机分为5组:分别饲喂正常饲料(正常对照组,NCG),高脂饲料(高血脂模型组,HCG),高脂饲料 2%SOS(SOS组)、高脂饲料 3%SOP(SOP组)、高脂饲料 2%SOS 3%SOP(SOSP组)8周,测定大鼠血脂、血管活性物质PG I2、TXA2、NO和血液流变学指标。结果各实验组均能显著降低高脂血症大鼠血清TC、TG、LDL-C,升高HDL-C,改善血脂水平。同时升高PG I2、NO,降低TXA2和TXA2/PG I2比值,还能降低血黏度和红细胞压积,并以复合干预组效果最佳。结论SOS和SOP具有良好的调节血脂、影响血管活性物质生成和改善血液流变学的作用,以联合使用效果最为显著。     

Evaluation of mutagenic activity in an extract of pepper tree stem bark (Schinus terebinthifolius Raddi)

An extract (decoction) from pepper tree stem bark (Schinus terebinthifolius Raddi) is widely used in Brazil as a topical antiinflammatory agent and to cicatrize wounds. The extract contains catechin, tannins, terpenes, flavonoids, and saponins; of these components, both mutagenic potential and antioxidant properties have been ascribed to flavonoids. The mutagenicity of some flavonoids is believed to be associated with the formation of reactive oxygen species and seems to depend on the number and position of hydroxyl groups. In the present study, we evaluated an extract of S. terebinthifolius in a series of cell-free and bacterial assays in order to determine its genotoxic potential. The extract was negative in a cell-free plasmid DNA test, indicating that it did not directly break DNA. Positive results, however, were obtained in the SOS chromotest, in a forward mutagenesis assay employing CC104 and CC104mutMmutY strains of Escherichia coli, and in the Salmonella reversion assay, using strains TA97, TA98, TA100, and TA102. All the bacterial tests were performed without exogenous metabolic activation due to the topical use of this preparation. The results indicate that pepper tree stem bark extract produces DNA damage and mutation in bacteria, and that oxidative damage may be responsible for the genotoxicity.     

Vegan Diet and Bone Health—Results from the Cross-Sectional RBVD Study

Scientific evidence suggests that a vegan diet might be associated with impaired bone health. Therefore, a cross-sectional study (n = 36 vegans, n = 36 omnivores) was used to investigate the associations of veganism with calcaneal quantitative ultrasound (QUS) measurements, along with the investigation of differences in the concentrations of nutrition- and bone-related biomarkers between vegans and omnivores. This study revealed lower levels in the QUS parameters in vegans compared to omnivores, e.g., broadband ultrasound attenuation (vegans: 111.8 ± 10.7 dB/MHz, omnivores: 118.0 ± 10.8 dB/MHz, p = 0.02). Vegans had lower levels of vitamin A, B2, lysine, zinc, selenoprotein P, n-3 fatty acids, urinary iodine, and calcium levels, while the concentrations of vitamin K1, folate, and glutamine were higher in vegans compared to omnivores. Applying a reduced rank regression, 12 out of the 28 biomarkers were identified to contribute most to bone health, i.e., lysine, urinary iodine, thyroid-stimulating hormone, selenoprotein P, vitamin A, leucine, α-klotho, n-3 fatty acids, urinary calcium/magnesium, vitamin B6, and FGF23. All QUS parameters increased across the tertiles of the pattern score. The study provides evidence of lower bone health in vegans compared to omnivores, additionally revealing a combination of nutrition-related biomarkers, which may contribute to bone health. Further studies are needed to confirm these findings.     

铁路危险品货运站空气污染物的致遗传毒性作用研究

采用ＳＯＳ／ｕｍｕ 试验和ＳＯＳ 原位试验,对铁路危险品货运站（ 以下简称危货站） 空气污染物的致遗传毒性进行了研究。结果表明：在不加Ｓ９ 活化系统的条件下,危货站空气污染颗粒提取物具有致遗传毒性作用,可使ＴＡ１５３５／ＰＳＫ１００２ 菌株产生β半乳糖苷酶的量增加,并存在剂量—反应关系;加入Ｓ９ 活化系统后,则ＳＯＳ／ｕｍｕ 试验阴性。同时,应用ＳＯＳ 原位法,对危货站空气污染的综合致遗传毒性进行了现场监测。结果显示,随采样体积的增加,β半乳糖苷酶的量也增加,采样体积与酶诱导率之间,存在剂量—反应关系。     

铁路危险品货运站空气污染指标的探讨

铁路危险品货运站（危货站）空气污染物种类多,空气污染严重,为探讨对其监测和评价的综合性能指标和方法,采用空气耗氧量（ＡＯＤ）和ＳＯＳ致遗传毒性原位监测法（ＳＯＳ原位法）,分别对危货站空气污染进行了研究。结果表明,危货站中各点所测ＡＯＤ值与对照区ＡＯＤ值,在统计学上差异均有显著性（Ｐ〈０．０５）。ＳＯＳ原位法显示,随采样体积的增加,β－半乳糖苷酶的量也增加,采样体积与酶诱导率之间存在剂量－反应关系。     

Influence of very short patch mismatch repair on SOS inducing lesions after aminoglycoside treatment in Escherichia coli

Low concentrations of aminoglycosides induce the SOS response in Vibrio cholerae but not in Escherichia coli. In order to determine whether a specific factor present in E. coli prevents this induction, we developed a genetic screen where only SOS inducing mutants are viable. We identified the vsr gene coding for the Vsr protein of the very short patch mismatch repair (VSPR) pathway. The effect of mismatch repair (MMR) mutants was also studied. We propose that lesions formed upon aminoglycoside treatment are preferentially repaired by VSPR without SOS induction in E. coli and by MMR when VSPR is impaired.