硫化氢对人肠上皮细胞 FH74Int 的 DNA 损伤和毒理基因组学分析。

DNA damage and toxicogenomic analyses of hydrogen sulfide in human intestinal epithelial FHs 74 Int cells.

机构信息

Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA.

出版信息

Environ Mol Mutagen. 2010 May;51(4):304-14. doi: 10.1002/em.20546.

Abstract

Hydrogen sulfide (H(2)S), a metabolic end product of sulfate-reducing bacteria, represents a genotoxic insult to the colonic epithelium, which may also be linked with chronic disorders such as ulcerative colitis and colorectal cancer. This study defined the early (30 min) and late (4 hr) response of nontransformed human intestinal epithelial cells (FHs 74 Int) to H(2)S. The genotoxicity of H(2)S was measured using the single-cell gel electrophoresis (comet) assay. Changes in gene expression were analyzed after exposure to a genotoxic, but not cytotoxic, concentration of H(2)S (500 muM H(2)S) using pathway-specific quantitative RT-PCR gene arrays. H(2)S was genotoxic in a concentration range from 250 to 2,000 microM, which is similar to concentrations found in the large intestine. Significant changes in gene expression were predominantly observed at 4 hr, with the greatest responses by PTGS2 (COX-2; 7.92-fold upregulated) and WNT2 (7.08-fold downregulated). COX-2 was the only gene upregulated at both 30 min and 4 hr. Overall, the study demonstrates that H(2)S modulates the expression of genes involved in cell-cycle progression and triggers both inflammatory and DNA repair responses. This study confirms the genotoxic properties of H(2)S in nontransformed human intestinal epithelial cells and identifies functional pathways by which this bacterial metabolite may perturb cellular homeostasis and contribute to the onset of chronic intestinal disorders.

摘要

硫化氢(H2S)是硫酸盐还原菌的代谢终产物,代表了对结肠上皮的遗传毒性损伤,这可能与溃疡性结肠炎和结直肠癌等慢性疾病有关。本研究定义了非转化人肠上皮细胞(FHs 74 Int)对 H2S 的早期(30 分钟)和晚期(4 小时)反应。使用单细胞凝胶电泳(彗星)分析测定 H2S 的遗传毒性。在用遗传毒性但非细胞毒性浓度的 H2S(500 μM H2S)暴露后,使用通路特异性定量 RT-PCR 基因芯片分析基因表达的变化。H2S 在 250 至 2000 μM 的浓度范围内具有遗传毒性,这与大肠中发现的浓度相似。基因表达的显著变化主要发生在 4 小时,PTGS2(COX-2;上调 7.92 倍)和 WNT2(下调 7.08 倍)的反应最大。COX-2 是在 30 分钟和 4 小时均上调的唯一基因。总的来说,该研究表明 H2S 调节参与细胞周期进程的基因表达,并引发炎症和 DNA 修复反应。本研究证实了 H2S 在非转化人肠上皮细胞中的遗传毒性,并确定了这种细菌代谢物可能破坏细胞内稳态并导致慢性肠道疾病发作的功能途径。

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