白脊管藤壶对苯并[α]芘的生理响应研究

Response of Fistulobalanus albicostatus under Benzo[α]pyrene stress

中文关键词:  苯并[α]芘  白脊管藤壶  毒理效应  转录组学

英文关键词:Benzo[α]pyrene  Fistulobalanus albicostatus  response  transcriptome

中文摘要:

      苯并[α]芘（Benzo[α]pyrene，BaP）是Ⅰ类致癌物，被世界卫生组织纳入重点监控的环境污染物之列。为了揭示BaP对蔓足类的毒性效应，本研究以海州湾广布种白脊管藤壶（Fistulobalanus albicostatus）为研究对象，将其暴露于0.1 μg/L、1 μg/L和10 μg/L BaP溶液中，分别于0 d、1 d、3 d、6 d、10 d、15 d取白脊管藤壶软组织，从生理生化水平和转录水平全面评估BaP暴露对白脊管藤壶的毒性效应。结果显示：BaP暴露显著影响了白脊管藤壶体内外源物质代谢通路和抗氧化防御系统，引发了关键酶活性的改变以及相关基因转录水平的显著波动。生理生化水平上，BaP暴露引起了白脊管藤壶体内Ⅰ相代谢酶EROD、Ⅱ相代谢酶GST、UGT和SULT活性的变化，其中GST活性在暴露后期被显著抑制；BaP暴露诱导了白脊管藤壶体内抗氧化防御体系，其中SOD、CAT和GPx活性均出现被诱导升高现象；在BaP暴露初期，白脊管藤壶体内MDA含量显著上升，且存在明显的时间-剂量效应，第3 d时出现峰值，其后诱导作用呈下降趋势，但仍显著高于对照组水平；10 μg/L的BaP暴露，可引起白脊管藤壶体内8-OHdG含量显著上升。在转录水平上，BaP暴露初期白脊管藤壶体内外源物质代谢和氧化应激反应更强烈，部分基因的转录表达存在一定的时间效应。其中，Ⅰ相代谢相关的CYP450基因家族的cyp3a被显著诱导表达，cyp2b2基因的转录表达先被抑制后诱导，cyp12基因则逐渐被抑制转录表达；Ⅱ相物质转化相关的ugt、gst和sult基因均被不同程度的抑制转录表达；Ⅲ相物质转运蛋白相关的abca、abcc和abcg基因的转录表达水平在暴露初期被诱导或抑制，至暴露后期仅abca基因被显著诱导表达。因此，BaP暴露会使白脊管藤壶发生氧化应激，对生物大分子造成氧化损伤，并影响外源物质代谢、抗氧化防御等过程。本实验为研究BaP对蔓足类的潜在毒性效应提供了新的数据支撑，对揭示外源污染物对海洋生物的毒性作用机制具有重要意义。

英文摘要:

      Benzo[α]pyrene (BaP) is a Class I carcinogen and has been designated as a key environmental pollutant for monitoring by the World Health Organization. In order to elucidate the toxic effects of BaP on Cirripedia, this study used the widely distributed species of Fistuolanus albicostatus in China as the research object, exposing them to 0.1 μg/L, 1 μg/L, and 10 μg/L BaP solutions. Whole organism of F. albicostatus were collected at 0 d, 1 d, 3 d, 6 d, 10 d, and 15 d, and the toxic effects of BaP stress on F. albicostatus were comprehensively evaluated at physiological, biochemical, and transcriptomic levels. The results showed that BaP exposure significantly affected the xenobiotic metabolism pathways and the antioxidant defense system in F. albicostatus, leading to alterations in key enzyme activities and pronounced fluctuations in the transcriptional levels of associated genes. At the physiological and biochemical levels, BaP exposure can cause changes in the activities of phase I metabolic enzymes EROD, phase II metabolic enzymes GST, UGT and SULT in the F. albicostatus, Among them, the activity of GST was significantly inhibited in the later stage of exposure; BaP exposure induced the antioxidant defense system in the F. albicostatus, with the activities of SOD, CAT and GPx all being induced to increase; In the early stage of BaP exposure, the MDA content in the F. albicostatus significantly increased, and there was a clear time-dose effect, the peak value appeared on the 3rd day, and the induction effect showed a downward trend thereafter, but it was still significantly higher than the control group level; Exposure to 10 μg/L BaP can cause a significant increase in the content of 8-OHdG in the F. albicostatus. At the transcriptome level, in the early stage of BaP exposure, the metabolism of exogenous substances and oxidative stress responses in F. albicostatus are more intense, and there is a certain time effect in the transcriptional expression of some genes. Among them, cyp3a of the CYP450 gene family related to phase I metabolism was significantly induced to express, the transcriptional expression of the cyp2b2 gene was first inhibited and then induced, and the transcriptional expression of the cyp12 gene was gradually inhibited. The ugt, gst and sult genes related to phase II substance transformation were all inhibited in transcriptional expression to varying degrees. The transcriptional expression levels of abca, abcc and abcg genes related to phase III substance transporters were induced or inhibited in the early stage of exposure, and only the abca gene was significantly induced to be expressed in the late stage of exposure. Therefore, BaP exposure can cause oxidative stress in F. albicostatus, leading to oxidative damage to biomolecules and affecting metabolic and antioxidant processes. This study provides new data supporting the potential toxic effects of BaP on Cirripedia, and is of significant importance in elucidating the mechanisms of toxicity of xenobiotics on marine organisms.