双酚A致文蛤鳃组织氧化损伤
Oxidative Damage of Bisphenol A to Meretrix petechialis Gill Tissues
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摘要: 双酚A(bisphenol A, BPA)是全球产量最大的化工产品之一，在塑料制品生产中得到广泛应用。然而，BPA的大量应用导致其在水环境中被频繁检出，对水生生物健康构成潜在威胁。相关研究证实BPA对水生生物的生殖和发育具有一定的毒性效应，但对双壳贝类毒性效应研究却十分有限。本研究将文蛤(Meretrix petechialis)分别暴露于1、10、100 μg·L-1 BPA中14 d，检测了文蛤鳃滤水率以及组织病理学变化，同时测定鳃组织过氧化氢(hydrogen peroxide, H2O2)和丙二醛(malondialdehyde, MDA)含量，以及过氧化氢酶(catalase, CAT)、谷胱甘肽-S-转移酶(glutathione-S-transferase, GST)、超氧化物歧化酶(superoxide dismutase, SOD)的活性，并对Nrf2/Keap1信号通路相关基因的表达水平进行分析。结果表明，BPA暴露干扰了文蛤鳃滤水率，导致文蛤鳃组织上皮细胞损伤和增生，并观察有纤毛和鳃丝减少的现象，且BPA浓度越高对文蛤鳃组织的影响越明显。BPA暴露导致文蛤鳃组织H2O2和MDA水平显著升高，1 μg·L-1 BPA处理组鳃组织氧化应激水平最为明显；BPA暴露引起鳃组织CAT活性显著降低，但对SOD活性无显著影响；1 μg·L-1 BPA暴露导致GST活性显著升高。此外，1 μg·L-1 BPA暴露下，文蛤鳃组织中Nrf2、Keap1、cat和tnf-α的基因表达水平均受到抑制。10 μg·L-1 BPA暴露显著上调了cat基因表达。总之，本研究发现BPA暴露能诱发文蛤鳃组织出现氧化应激反应并引起组织损伤。
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关键词:
- 双酚A /
- 文蛤 /
- 氧化应激 /
- Nrf2/Keap1信号通路
Abstract: Bisphenol A (BPA) is one of the highly produced chemicals globally and extensively utilized in the manufacturing of plastic products. However, the widespread application of BPA has led to its frequent detection in aquatic environments, posing potential threats to the health of aquatic organisms. Previous studies have confirmed the reproductive and developmental toxic effects of BPA on various aquatic organisms; however, limited research exists regarding its impact on bivalve shellfish. In this study, clams (Meretrix petechialis) were exposed to concentrations of 1, 10, and 100 μg·L-1 BPA for 14 d. The filtration rate of gill water and histopathological changes were examined while expression levels of genes in the Nrf2/Keap1 signaling pathway and the enzymatic activity, including the hydrogen peroxide (H2O2) and malondialdehyde (MDA), activities of catalase (CAT), glutathione-S-transferase (GST) and superoxide dismutase (SOD) were analyzed. The results showed that BPA exposure significantly influenced the filtration rate of the clam. BPA induced epithelial cell damage and hyperplasia in the gill tissues of the clam, accompanied by a reduction in cilia and gill filaments. Notably, the gill damage became more pronounced with increasing concentrations of BPA. BPA exposure significantly increased the levels of H2O2 and MDA, and the oxidative stress level was the most obvious under 1 μg·L-1 BPA exposure group. BPA exposure significantly decreased CAT activity in gill tissue, but had no significant effect on SOD activity. 1 μg·L-1 BPA exposure resulted in a significant increase in GST activity. In addition, the gene expression levels of Nrf2, Keap1, cat, and tnf-α in the gill tissue of clams were inhibited by 1 μg·L-1 BPA exposure. However, it is worth noting that cat gene expression was upregulated specifically under 10 μg·L-1 BPA exposure. This study reveals that BPA exposure induces oxidative stress and tissue damage in clam gill tissues.-
Key words:
- bisphenol A /
- Meretrix petechialis /
- oxidative stress /
- Nrf2/Keap1 signaling pathway
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