苯并（a）芘染毒大鼠血、肺中SOD、LPO及SOD／LPO变化的研究

用苯并（ａ）芘对大鼠经气管内染毒，在染毒后９０、１８０、２７０、３６０和５４０天时动态观察肺组织和血中超氧化物歧化酶（ＳＯＤ）、脂质过氧化物（ＬＰＯ）及ＳＯＤ／ＬＰＯ比值的变化．结果表明，苯并（ａ）芘可诱发大鼠血和肺组织中自由基反应增强，ＳＯＤ活性降低，脂质过氧化反应增高，ＬＰＯ含量升高，抗氧化能力降低，ＳＯＤ／ＬＰＯ比值降低．体内抗氧化和脂质过氧化平衡失调．     

青石棉、苯并(a)芘气管染尘大鼠血中SOD和LPO变化的研究

为了观察青石棉、苯并（ａ）芘染尘大鼠血中超氧化物歧化酶（ＳＯＤ）和脂质过氧化物（ＬＰＯ）的变化，以探讨其致癌机制，用气管内染尘法，在染尘后９０，１８０，２７０，３６０和５４０天时观察大鼠ＳＯＤ、ＬＰＯ及ＳＯＤ／ＬＰＯ比值的变化，采用方差分析处理数据。结果提示，青石棉、苯并（ａ）芘可致ＳＯＤ活性降低、ＬＰＯ含量升高、ＳＯＤ／ＬＰＯ比值降低的趋势。表明体内抗氧化和脂嵵使趸胶馐У鳌     

甲醛对大鼠的氧化性损伤

大鼠吸入不同剂量甲醛１０天，其血、肺、肝、肾、睾丸、脑和眼球脂质过氧化物（ＬＰＯ）均有增加趋势．肝和睾丸ＬＰＯ增加有统计学意义。肾ＧＳＨＰＸ活性随甲醛浓度加大而显著升高。肝和睾丸组织ＬＰＯ／ＧＳＨＰＸ比值显著升高。表明甲醛吸入可造成大鼠肝脏和睾丸的脂质过氧化损伤，并使它们的抗氧化能力降低。     

镁对实验性动脉粥样硬化家兔机体抗氧化体系机能的影响

用高脂膳食诱导的动脉粥样硬化家兔心肌组织和肝脏抗氧化体系机能的改变规律及镁对机体抗氧化机能的影响。提示：动脉粥样硬化家兔心脏超氧化歧化酶（ＳＯＤ）及ＳＯＤ／ＬＰＯ比值显著降低，而过氧化脂质（ＬＰＯ）明显升高。肝组织ＬＰＯ含量升高显著，而谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）、ＳＯＤ活性及ＳＯＤ／ＬＰＯ和ＧＳＨ－Ｐｘ／ＬＰＯ显著降低。补充镁显著降低心脏ＬＰＯ含量，并使肝脏的ＳＯＤ、ＧＳＨ－Ｐｘ及ＳＯＤ／ＬＰＯ、ＧＳＨ－Ｐｘ／ＬＰＯ与心脏ＳＯＤ／ＬＰＯ比值明显升高。提示：动脉粥样硬化家兔机体抗氧化机能明显减低，这种变化可能在动脉粥样硬化的发生、发展中起重要作用。而镁对机体抗氧化机能产生一定的影响。     

吸入苯产生自由基对外周血毒作用的实验研究

在本研究中，大鼠吸入三个不同浓度（６．３ｐｐｍ，７１．８ｐｐｍ，４５９．５ｐｐｍ）苯３０天以及吸入７１．８ｐｐｍ不同时间（１０，２０，３０天）后，测定了反应血中自由基活性的指标如白细胞过氧化脂质（ＬＰＯ），血浆过氧化脂质、红细胞超氧化物歧化酶（ＳＯＤ）、红细胞谷胱甘肽（ＧＳＨ）。结果显示各染毒组在３０天后白细胞ＬＰＯ均较对照组明显升高，而白细胞显著减少仅发生在中、高剂量组。大鼠吸入７１．８ｐｐｍ２０天和３０天后白细胞ＬＰＯ异常升高，白细胞数明显下降。红细胞ＳＯＤ、ＧＳＨ以及血浆ＬＰＯ在所有染毒组均未见异常变化。结果提示大鼠吸入苯后外周血白细胞的下降可能与其膜脂质过氧化有关，白细胞过氧化脂质升高比白细胞减少更为敏感。     

急性高海拔地区对大鼠某些组织中Mn—SOD,CuZn及LPO的影响

将大鼠快速由平原带至高原，其肺，肾组织Ｍｎ－ＳＯＤ，ＣｕＺｎ－ＳｏＤ活性明显降低，心脏ＳＯＤ活性也呈下降趋势；心、肺、肾组织的ＬＰＯ含量显著升高。结果提示：急进高海拔地区、可引起体内抗氧化能力减弱，脂质过氧化反应增强。     

吸入苯产生自由基对外周血毒作用的实验研究

在本研究中，大鼠吸入三个不同浓度苯３０天以及吸入７１．８ｐｐｍ不同时间后，测定了反应血中自由基活性的指标如白细胞过氧化脂质（ＬＰＯ），血浆过氧化脂质、红细胞超氧化物歧化酶（ＳＯＤ）、红细胞谷胱甘肽（ＧＳＨ）。结果显示各染毒组在３０天后白细胞ＬＰＯ均较对照组明显升高，而白细胞显著减少仅发生在中、高剂量组，大鼠吸入７１．８ｐｐｍ２０天和３０天后白细胞ＬＰＯ异常升高，白细胞数明显下降，红细胞ＳＯＤ、ＧＳ     

天然矿泉水对大鼠LPO含量和SOD活力的影响

观察了广西某矿泉水对正常大鼠和染尘大鼠体内过氧化脂质（ＬＰＯ）含量和全血中超氧化物歧化酶（ＳＯＤ）活力的影响。结果表明，该矿泉水能在一定程度上降低大鼠体内ＬＰＯ含量和提高ＳＯＤ活力，对锡矿尘诱致大鼠体内ＬＰＯ水平的升高和ＳＯＤ活力下降具有一定的拮抗作用。     

慢性氟中毒大鼠氟、抗氧化酶类变化及硒的影响

Ｗｉｓｔａｒ大鼠饮１．５８、２．６３ｍｍｏｌ／Ｌ高氟水１４个月造成慢性氟中毒，另２组大鼠在饮高氟水同时加饲２．０ｍｇ／ｋｇ硒饲料。在氟中毒不同时期分３批测其血清、尿液氟（Ｆ）、硒（Ｓｅ）含量；全血、血清、肝、肾脏谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）、超氧化物歧化酶（ＳＯＤ）活性；还原、氧化型谷胱甘肽（ＧＳＨ、ＧＳＳＧ）和脂质过氧化物（ＬＰＯ）含量。结果：氟中毒大鼠尿、血Ｆ升高；血清、组织ＬＰＯ在氟中毒早、中、晚期持续升高；ＧＳＨ－Ｐｘ、ＳＯＤ和ＧＳＨ早期上升，中、晚期明显下降。提示氟中毒大鼠存在明显脂质过氧化损伤，抗氧化酶类和抗氧化剂表现为从代偿到失代偿，最终造成自由基代谢紊乱。补Ｓｅ后氟中毒大鼠尿Ｆ排泄，血Ｆ下降；ＧＳＨ－Ｐｘ、ＳＯＤ和ＧＳＨ恢复，ＬＰＯ下降。此与Ｓｅ拮抗高Ｆ及对抗氧化酶类、抗氧化剂和脂质过氧化物产生直接或间接作用有关。     

高血压病患者血浆von Wilebrand因子含量与脂质过氧化的关系

观察６０例高血压病（ＥＨ）患者血浆ｖｏｎＷｉｌｅｂｒａｎｄ因子（ｖＷＦ）含量与血浆脂质过氧化物（ＬＰＯ）、超氧化物歧化酶（ＳＯＤ）的关系。结果：ＥＨ患者血浆ｖＷＦ及ＬＰＯ含量明显高于对照组，且Ⅱ期患者高于Ⅰ期患者；ＳＯＤ／ＬＰＯ比值低于对照组，但Ⅰ期与Ⅱ期之间差异无显著性。各组间ＳＯＤ含量无明显变化。ＥＨ患者血浆ｖＷＦ含量与ＬＰＯ浓度呈显著正相关，与ＳＯＤ／ＬＰＯ比值呈负相关。提示脂质过氧化是ＥＨ内皮损伤的一个重要原因。     

Experimental asbestos carcinogenesis

Laboratory rodents were exposed to one of three mineralogical types of asbestos dust, amosite, crocidolite, or chrysotile. Inhalation exposures were accomplished in chambers where ballmilled specimens of these dusts were disseminated for 4 hours daily, 4 days weekly, at a mean atmospheric concentration of about 48 mg/m³. Additional animals were injected with these dusts intratracheally, intrapleurally, or intraperitoneally. Histopathologic studies showed a fibrotic reaction in all species to all three types of dusts, with amosite provoking the strongest such response especially in guinea pigs. Two pulmonary cancers were produced in rats exposed to the inhalation of crocidolite. Local injection into the pleural or peritoneal cavities caused 5 mesotheliomas in rats after chrysotile treatment and 6 mesotheliomas in rats and rabbits after crocidolite treatment. Guinea pigs and hamsters developed no tumors in this experiment, and with the dose used, there were no tumors in any species in the amosite group.     

Recovery of ingested asbestos fibers from the gastrointestinal lymph in rats

Using the transmission electron microscope, asbestos fibers have been assessed in lymph fluid collected from the thoracic lymph duct in five groups of rats previously exposed to asbestos fibers (by ingestion). Ten rats were gavaged a single dose weighing approximately 20 mg. Five were given pure UICC chrysotile A while another group of five had pure UICC crocidolite. All the rats of the chrysotile group were positive animals with recovery rate values ranging from 6.9 × 10^?7 to 3 × 10^?5 (90% of the fibers being recovered during the first 16 hr following the gavage). The crocidolite group had only three positive animals and lower recovery rate values of 5.7 × 10^?8 to 5.6 × 10^?7. A third group was fed a synthetic diet containing 1%, by weight, chrysotile with a majority of short fibers (90% below 4 μm). Of the 15 rats comprising this group, 13 were positive with maximum daily recovery rates ranging from 2.1 × 10^?7 to 2.1 × 10^?6. A group of eight rats fed the same kind of diet but containing a higher proportion of long fibers, showed only four positive animals, however, they had higher daily recovery rates ranging from 1.9 × 10^?5 to 2.1 × 10^?4. No fibers were encountered in the samples of the two control rats. This study demonstrates the passage of chrysotile and crocidolite fibers across the gastrointestinal wall, with the passage rate being higher for long fibers than short ones.     

Enhanced lipid peroxidation and lysosomal enzyme activity in the lungs of rats with prolonged pulmonary deposition of crocidolite asbestos.

The interaction of UICC crocidolite asbestos with biological membranes in vivo was studied in rats after a single intratracheal dose of a suspension of 20 mg of fibres per rat. Development of lung fibrosis (increased level of hydroxyproline, a collagen index together with corresponding pathomorphological alteration) confirmed the penetration of crocidolite fibres into the lungs in the course of seven months exposure. The pulmonary deposition of crocidolite affected the lysosomal membranes of lung cells as manifested by (1) enhanced lipid peroxidation with (2) stimulation (release) of activity of beta-glucuronidase and cathepsin D. Enhanced lipid peroxidation and activity of beta-glucuronidase may contribute to the delayed, carcinogenic effects of crocidolite asbestos.     

Enhanced lipid peroxidation and lysosomal enzyme activity in the lungs of rats with prolonged pulmonary deposition of crocidolite asbestos

The interaction of UICC crocidolite asbestos with biological membranes in vivo was studied in rats after a single intratracheal dose of a suspension of 20 mg of fibres per rat. Development of lung fibrosis (increased level of hydroxyproline, a collagen index together with corresponding pathomorphological alteration) confirmed the penetration of crocidolite fibres into the lungs in the course of seven months exposure. The pulmonary deposition of crocidolite affected the lysosomal membranes of lung cells as manifested by (1) enhanced lipid peroxidation with (2) stimulation (release) of activity of beta-glucuronidase and cathepsin D. Enhanced lipid peroxidation and activity of beta-glucuronidase may contribute to the delayed, carcinogenic effects of crocidolite asbestos.     

Fibrogenic effect of wollastonite compared with asbestos dust and dusts containing quartz.

The distribution of length and diameter and the aspect ratio of crocidolite asbestos, a mineral substitute for asbestos (wollastonite), a manmade mineral fibre (glass wool), and synthetic fibres (polypropylene and polyacrylonitrite) were determined by light microscopy with phase contrast and, for crocidolite, also with transmission electron microscopy. The synthetic organic fibres and manmade mineral fibre used were of a size exceeding that considered respirable. Respirable materials were given to rats by the intratracheal method and after exposure for a standard time interval the main indices of fibrogenic effects--the total hydroxyproline content, the wet weight of the lung, and the total lipid content in the lung--were estimated. For wollastonite there was a significant increase in these variables in comparison with the controls. The fibrogenicity was considerably less than that of crocidolite and quartz.     

青石棉诱导AL细胞CD59基因突变和DNA氧化损伤的研究

目的　研究谷胱甘肽合成酶抑制剂buthioninesulfoximine(BSO)和自由基清除剂二甲亚砜 (DMSO)对青石棉诱导人鼠杂交瘤 (AL)细胞CD59基因突变率的影响以及青石棉引发细胞内 8 羟基脱氧鸟苷 (8 OHdG)产生的规律。方法　细胞毒性、遗传毒性检测分别采用克隆法 ;8 OHdG检测采用ABC酶免疫染色法 ;非蛋白巯基化合物 (NPSH)检测采用改进后的Tietze法。结果　 2 5μmol/LBSO预处理AL 细胞 2 4h后的细胞内NPSH含量降为 2nmol/ 10 7细胞 ,仅为对照组的 5%。青石棉单独处理组AL 细胞CD59基因突变率为 2 0 8± 18。BSO预处理 2 4h后与青石棉继续共同孵育组细胞突变率可达到 3 97± 55,是青石棉单独处理组的 2倍左右 ,差异有显著性 (P <0 .0 5) ;而DMSO存在时 ,青石棉诱导的CD59基因突变率仅为 57± 8,比青石棉单独处理组降低 72 .6%。细胞内 8 OHdG的产生随着青石棉处理剂量的增加而线性增加 (y =150 2 0x ,r =0 .962 1)。当青石棉处理剂量为 6μg/cm2 时 ,细胞内 8 OHdG含量由对照组的 13 7± 9提高到 2 89± 6,是对照组的 2倍以上。DMSO存在时 ,可使 6μg/cm2 石棉诱导的细胞内 8 OHdG含量由 2 89± 6降低到 170± 3。结论　自由基是青石棉诱导基因突变和DNA损伤过程中重要的调节物 ,具有剂量 -效应关系     

Pleural mesotheliomas in Sprague-Dawley rats by erionite: first experimental evidence

Erionite and crocidolite fibers were tested for carcinogenicity by intrapleural and intraperitoneal injection (una tantum) in 40 Sprague-Dawley rats per route for each fiber type. Pleural mesotheliomas were found in nine of ten animals that died within a year after intrapleural injection with erionite fibers. No pleural tumors were found among the animals treated at the same time and in the same way with crocidolite. Intraperitoneal injection of erionite did not produce mesotheliomas of the peritoneum, while a high incidence of these tumors was found among the animals treated by intraperitoneal injection of crocidolite. The studies are still in progress.     

青石棉污染区农民恶性肿瘤死亡率的回顾队列调查

目的：了解在生活环境中接触低浓度青石棉、农民患恶性肿瘤,特别是间皮瘤和肺癌之间的关系。方法：采用回顾队列调查方法对青石棉污染区的农民进行恶性肿瘤死亡率的调查,以该县无石棉污染的农民为对照,结果：观察组有5人死于间皮瘤死亡率为36．46／10万人年,而对照组无1例发生;肺癌死亡率为43．75／10万人年,与对照组比较,差别有非常显著性意义（P＜0．001）,结论：间皮瘤死亡率在青石棉污染区很高,青石棉与间皮瘤,肺癌之间存在很强的病因学联系。     

Induction of mesothelioma after intrapleural inoculation of F344 rats with silicon carbide whiskers or continuous ceramic filaments.

OBJECTIVE: To find whether continuous ceramic filaments (CCFs) and silicon carbide whiskers (SiCWs), which are used in many industries as reinforcing materials in advanced ceramic composites, are carcinogenic in the intrapleural inoculation assay. METHODS: Samples of SiCWs, CCF, International Union Against Cancer crocidolite, or saline were injected into the pleural cavities of female F344/N rats to find whether the samples of SiCW and CCF had the potential to induce mesotheliomas after the direct application of the materials to the surface of the pleural mesothelium. RESULTS: Rats injected with two of the three individual samples of SiCW or the crocidolite had significantly reduced life spans compared with the rats treated with saline, CCFs, or the third SiCW sample. Rats treated with either of the two SiCW samples or crocidolite developed mesotheliomas. By contrast, rats treated with saline or CCF did not. The two SiCW samples that induced shortened life spans also induced a higher rate of mesothelioma (87%-90%), than the crocidolite (57%) and the third SiCW sample (23%). CONCLUSION: SiCWs but not CCFs could induce mesotheliomas after intrapleural injection in rats. The difference in biological activity between the SiCW samples could not be explained on the basis of their physical dimensions or biological activity toward cultured cells. Results from this study indicated that SiCWs should be handled with care as they might be carcinogenic if inhaled. However, there is controversy as to whether results of intrapleural injection assays are sufficient to determine a fibre's carcinogenic activity. The results also showed that a collection of fibrous materials such as SiCWs could have considerably different biological activities despite similar physical dimensions.