Nour Ola Mohamed, El-Saidy Salwa A, Ghoneim Aml Z
Department of Biology and Geology, Faculty of Education, Alexandria University, Alexandria, 21526, Egypt.
Zoology Department, Faculty of Science, Damanhour University, Damanhour, Egypt.
BMC Zool. 2024 Aug 12;9(1):19. doi: 10.1186/s40850-024-00211-1.
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.
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.
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.
双酚A（BPA）是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、奶瓶及纸制品。先前的研究表明，BPA对水生生物具有潜在毒性，会导致内分泌紊乱和行为失调。当前研究旨在采用多生物标志物方法（死亡率、生化研究、彗星试验检测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），确定BPA对可食用海洋蛤蜊波纹巴非蛤的毒性影响。蛤蜊在实验室条件下暴露于三种浓度的BPA（0 “对照”、1和5 μg/L）中，持续21天。暴露期结束后，在消化腺中评估BPA的影响，消化腺是生态毒理学研究中一个通用且与环境相关的器官。
在经BPA处理的蛤蜊中，仅在最高BPA浓度（5 μg/L）下出现了死亡率（10%）。由于BPA暴露，生化损伤呈浓度依赖性被检测到。丙二醛（MDA）和谷胱甘肽（GSH）水平显著升高，而过氧化氢酶（CAT）活性显著降低。我们的结果表明，BPA在波纹巴非蛤中诱导了神经毒性，这表现为乙酰胆碱酯酶（AChE）活性呈剂量依赖性受到抑制。此外，随着BPA水平升高，DNA损伤被强烈诱导。此外，我们的结果在BPA处理后的消化腺组织变化中得到了证实，这些变化可能会损害蛤蜊的食物吸收能力；这些变化主要包括萎缩和坏死的消化小管、上皮细胞空泡化、血细胞浸润以及管间纤维化。基于从半定量和定量组织病理学分析获得的数据，与对照蛤蜊相比，蛤蜊消化腺暴露于浓度为1和5 μg/L的BPA中21天显示出显著的组织病理学改变。
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（如BPA）影响的有用工具。水中的BPA会导致氧化应激、神经毒性、基因毒性以及对蛤蜊消化腺产生有害影响；所有这些都可能使蛤蜊的性能和健康恶化，导致组织功能障碍。
