PDF(Pubmed)
Abstract：
BACKGROUND: Bisphenol A (BPA), a plastic additive monomer, is among the most highly produced chemicals worldwide, and is broadly used in many industries, such as food and beverage containers, milk bottles, and paper products. Previous studies demonstrated that BPA has potential toxicity to aquatic organisms, causing endocrine disturbance and behavioural disorders. The current work aimed to determine the toxic impacts of BPA on the edible marine clam Ruditapes decussatus considering a multi-biomarker approach (mortality, biochemical studies, DNA strand breaks using comet assay, and histopathological examinations with semi-quantitative and quantitative histopathological analyses). The clams were exposed under laboratory conditions to three concentrations of BPA (0 \"control\", 1, and 5 µg/L) for a period of 21 days. After the exposure period, BPA impacts were assessed in the digestive gland as a versatile and environmentally relevant organ for ecotoxicological studies.
RESULTS: In BPA-treated clams, mortality (10%) occurred only at the highest BPA concentration (5 µg/L). Biochemical impairments were detected in a concentration-dependent manner as a consequence of BPA exposure. There were significant increases in malondialdehyde (MDA) and glutathione (GSH) levels, while catalase (CAT) activity was significantly reduced. Our results revealed that BPA induced neurotoxicity in R. decussatus, as evidenced by the inhibition of acetylcholinesterase (AChE) activity in a dose-dependent manner. Furthermore, DNA damage was strongly induced as BPA levels increased. Additionally, our results have been affirmed by alterations in digestive gland tissues at BPA treatments, which consequently can impair the clam\'s ability for food absorption; these alterations included mainly atrophic and necrotic digestive tubules, epithelial cell vacuolization, hemocyte infiltration, and intertubular fibrosis. Based on the data obtained from the semi-quantitative and quantitative histopathological analyses, the exposure of the clam\'s digestive gland to BPA with concentrations of 1 and 5 µg/L for 21 days showed significant histopathological alterations compared with the control clams.
CONCLUSIONS: The multi-biomarker approach used in the current study proved to be a useful tool for assessing the impact of diphenylmethane compounds, such as BPA. Water-borne BPA causes oxidative stress, neurotoxicity, genotoxicity, and deleterious effects on the clam digestive gland; all of these could deteriorate clam performance and health, causing tissue dysfunction.
RESULTS: In BPA-treated clams, mortality (10%) occurred only at the highest BPA concentration (5 µg/L). Biochemical impairments were detected in a concentration-dependent manner as a consequence of BPA exposure. There were significant increases in malondialdehyde (MDA) and glutathione (GSH) levels, while catalase (CAT) activity was significantly reduced. Our results revealed that BPA induced neurotoxicity in R. decussatus, as evidenced by the inhibition of acetylcholinesterase (AChE) activity in a dose-dependent manner. Furthermore, DNA damage was strongly induced as BPA levels increased. Additionally, our results have been affirmed by alterations in digestive gland tissues at BPA treatments, which consequently can impair the clam\'s ability for food absorption; these alterations included mainly atrophic and necrotic digestive tubules, epithelial cell vacuolization, hemocyte infiltration, and intertubular fibrosis. Based on the data obtained from the semi-quantitative and quantitative histopathological analyses, the exposure of the clam\'s digestive gland to BPA with concentrations of 1 and 5 µg/L for 21 days showed significant histopathological alterations compared with the control clams.
CONCLUSIONS: The multi-biomarker approach used in the current study proved to be a useful tool for assessing the impact of diphenylmethane compounds, such as BPA. Water-borne BPA causes oxidative stress, neurotoxicity, genotoxicity, and deleterious effects on the clam digestive gland; all of these could deteriorate clam performance and health, causing tissue dysfunction.
摘要：
背景：双酚A（BPA），一种塑料添加剂单体，是全球产量最高的化学品之一，广泛应用于许多行业，如食品和饮料容器，牛奶瓶,和纸制品。以前的研究表明，双酚A对水生生物具有潜在的毒性，引起内分泌紊乱和行为障碍。当前的工作旨在确定BPA对可食用海洋蛤仔的毒性影响，考虑采用多生物标志物方法（死亡率，生化研究,使用彗星试验的DNA链断裂，以及半定量和定量组织病理学分析的组织病理学检查）。在实验室条件下将蛤仔暴露于三种浓度的BPA（0“对照”，1和5µg/L），为期21天。在暴露期之后,在消化腺中评估了BPA的影响，作为一种多功能且与环境相关的器官，用于生态毒理学研究。
结果：在双酚A处理的蛤类中，死亡率（10％）仅在最高的BPA浓度（5µg/L）下发生。由于BPA暴露，以浓度依赖性方式检测到生化损伤。丙二醛（MDA）和谷胱甘肽（GSH）水平显着增加，而过氧化氢酶(CAT)活性显著降低。我们的结果表明，双酚A在杜松子鱼中引起神经毒性，如通过以剂量依赖性方式抑制乙酰胆碱酯酶（AChE）活性所证明的。此外，随着BPA水平的增加，DNA损伤被强烈诱导。此外,我们的结果得到了BPA治疗消化腺组织变化的证实，因此，这可能会削弱蛤仔对食物的吸收能力；这些改变主要包括萎缩和坏死的消化管，上皮细胞空泡化，血细胞浸润,和管间纤维化。根据半定量和定量组织病理学分析获得的数据，与对照蛤类相比，蛤类消化腺暴露于浓度为1和5µg/L的BPA21天显示出显著的组织病理学改变。
结论：当前研究中使用的多生物标志物方法被证明是评估二苯基甲烷化合物影响的有用工具，比如BPA。水性BPA引起氧化应激，神经毒性，遗传毒性，以及对蛤类消化腺的有害影响；所有这些都会恶化蛤类的性能和健康，导致组织功能障碍。
结果：在双酚A处理的蛤类中，死亡率（10％）仅在最高的BPA浓度（5µg/L）下发生。由于BPA暴露，以浓度依赖性方式检测到生化损伤。丙二醛（MDA）和谷胱甘肽（GSH）水平显着增加，而过氧化氢酶(CAT)活性显著降低。我们的结果表明，双酚A在杜松子鱼中引起神经毒性，如通过以剂量依赖性方式抑制乙酰胆碱酯酶（AChE）活性所证明的。此外，随着BPA水平的增加，DNA损伤被强烈诱导。此外,我们的结果得到了BPA治疗消化腺组织变化的证实，因此，这可能会削弱蛤仔对食物的吸收能力；这些改变主要包括萎缩和坏死的消化管，上皮细胞空泡化，血细胞浸润,和管间纤维化。根据半定量和定量组织病理学分析获得的数据，与对照蛤类相比，蛤类消化腺暴露于浓度为1和5µg/L的BPA21天显示出显著的组织病理学改变。
结论：当前研究中使用的多生物标志物方法被证明是评估二苯基甲烷化合物影响的有用工具，比如BPA。水性BPA引起氧化应激，神经毒性，遗传毒性，以及对蛤类消化腺的有害影响；所有这些都会恶化蛤类的性能和健康，导致组织功能障碍。
