Microscopical analysis of the chromium content in the bronchial and lung tissues of chromate workers and genomic changes of the premalignant lesions.

它是已知的，铬是一种吸入性致癌物和一个重要的危险因素，在肺癌的发展。方法1和2：作者使用了显微镜X射线荧光分析仪与透射X射线映射成像（堀场，京都，日本），以测量铬的积累，在10个切除的肺组织标本和90个活检标本铬酸盐工人。结果1和2：在10个切除的肺组织样本中的最大铬积累（平均值±标准差）为197 ± 238计数每秒（cps）/毫安（mA）（范围，4-649 cps/mA）。铬蓄积在6个组织标本中分散，在1个标本中弥漫。近端支气管中的铬蓄积少于肺的细支气管或胸膜下区域。90份活检标本中有63份（70%）可检测到铬蓄积，平均蓄积为6.5 ± 9.2 cps/mA（范围：0-46.5 cps/mA）。在支气管组织标本中检测到的铬沉积在支气管中 关于我们 间质中，而不是在上皮中。铬酸盐工人的发育异常（n=3）、鳞状化生（n=10）和正常支气管上皮（n=9）以及非铬酸盐工人的正常支气管上皮（n=3）中的最大铬蓄积量分别为20.2 ± 5.4、18.3 ± 12.2、13.2 ± 13.4和3.0 ± 1.8 cps/mA。随着支气管上皮恶变的进展，铬的蓄积量明显增加方法3：应用6个微卫星标记检测了3例异型增生和10例鳞状化生组织中的复制错误（RER）和杂合性丢失（洛）。D3 S647（3 p23）、D3 S966（3p21.3）、D3 S1289（3p21.1）、D5 S346（5 q21-q22）、D9 S161（9 p21）和TP 53（17p13.1）。RER表型定义为在两个或多个位点存在微卫星不稳定性（MSI）。结果3：结论：考虑这些癌前病变中的遗传畸变和铬积累是有用的，以阐明铬诱发肺癌的致癌过程。少

It is known that chromium is an inhaled carcinogen and an important risk factor in the development of lung carcinoma.METHODS 1 and 2 : The authors used a microscopic X-ray fuorescence analyzer with transmitted X-ray mapping imaging (Horiba, Kyoto, Japan) to measure the accumulation of chromium in 10 resected lung tissue specimens and 90 biopsy specimens from chromate workers. RESULTS 1 and 2 : The maximum chromium accumulation (mean ± standard deviation) in 10 resected lung tissue specimens was 197 ± 238 counts per second (cps)/mili ampere (mA) (range, 4-649 cps/mA). Chromium accumulation was scattered in six tissue specimens and diffuse in one specimen. Chromium accumulation in the proximal bronchi was less than in the bronchioles or subpleural regions of the lung. Chromium accumulation was detectable in 63 (70%) of 90 biopsy specimens, and the mean accumulation was 6.5 ± 9.2 cps/mA (range, 0-46.5 cps/mA). Chromium detected in bronchial tissue specimens was deposited in the bronchial … More stroma but not in the epithelium. The maximum chromium accumulations in dysplastic (n=3), squamous metaplastic (n=10), and normal bronchial epithelia (n=9) in chromate workers and in normal bronchial epithelia (n=3) in non-chromate workers were 20.2 ± 5.4, 18.3 ± 12.2, 13.2 ± 13.4, and 3.0 ± 1.8 cps/mA, respectively. The amount of chromium accumulation significantly increased according to the progression of malignant change of the bronchial epithelium (P=0.003).METHODS 3 : We examined the replication error (RER) and loss of heterozygosity (LOH) in DNA of dysplastic (n=3), squamous metaplastic (n=10) tissues, using six microsatellite markers containing CA repeats : D3S647 (3p23), D3S966 (3p21.3), D3S1289 (3p21.1), D5S346 (5q21-q22), D9S161 (9p21), and TP53 (17p13.1). The RER phenotype was defined as the presence of microsatellite instability (MSI) at two or more loci. RESULTS 3 : Five (78.9%) of 9 premalignant lesions exhibited RER.CONCLUSIONS : Considering genetic aberrations and chromium accumulation in these premalignant lesions is useful for elucidating the process of carcinogenesis in chromium-induced lung carcinoma. Less