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Chronic exposure to environmental concentrations of benzo[a]pyrene causes multifaceted toxic effects of developmental compromise, redox imbalance, and modulated transcriptional profiles in the early life stages of marine medaka (Oryzias melastigma)
Aquatic Toxicology ( IF 4.1 ) Pub Date : 2024-06-29 , DOI: 10.1016/j.aquatox.2024.107016 Rabia Zeb 1 , Xiaohan Yin 1 , Fangyi Chen 2 , Ke-Jian Wang 2
Aquatic Toxicology ( IF 4.1 ) Pub Date : 2024-06-29 , DOI: 10.1016/j.aquatox.2024.107016 Rabia Zeb 1 , Xiaohan Yin 1 , Fangyi Chen 2 , Ke-Jian Wang 2
Affiliation
Polycyclic aromatic hydrocarbons (PAHs) accumulate and integrate into aquatic environments, raising concerns about the well-being and safety of aquatic ecosystems. Benzo[a]pyrene (BaP), a persistent PAH commonly detected in the environment, has been extensively studied. However, the broader multifaceted toxicity potential of BaP on the early life stages of marine fish during chronic exposure to environmentally relevant concentrations needs further exploration. To fill these knowledge gaps, this study assessed the in vivo biotoxicity of BaP (1, 4, and 8 μg/L) in marine medaka (Oryzias melastigma ) during early development over a 30-day exposure period. The investigation included morphological, biochemical, and molecular-level analyses to capture the broader potential of BaP toxicity. Morphological analyses showed that exposure to BaP resulted in skeletal curvatures, heart anomalies, growth retardation, elevated mortality, delayed and reduced hatching rates. Biochemical analyses revealed that BaP exposure not only created oxidative stress but also disrupted the activities of antioxidant enzymes. This disturbance in redox balance was further explored by molecular level investigation. The transcriptional profiles revealed impaired oxidative phosphorylation (OXPHOS) and tricarboxylic acid (TCA) cycle pathways, which potentially inhibited the oxidative respiratory chain in fish following exposure to BaP, and reduced the production of adenosine triphosphate (ATP) and succinate dehydrogenase (SDH). Furthermore, this investigation indicated a potential connection to apoptosis, as demonstrated by fluorescence microscopy and histological analyses, and supported by an increase in the expression levels of related genes via real-time quantitative PCR. This study enhances our understanding of the molecular-level impacts of BaP's multifaceted toxicity in the early life stages of marine medaka, and the associated risks.
中文翻译:
长期暴露于环境浓度的苯并[a]芘会导致海洋青鳉 (Oryzias melastigma) 早期生命阶段发育损害、氧化还原失衡和调节转录谱的多方面毒性作用
多环芳烃 (PAH) 积累并融入水生环境,引发了人们对水生生态系统福祉和安全的担忧。苯并[a]芘 (BaP) 是一种在环境中常见检测到的持久性 PAH,已被广泛研究。然而,在长期暴露于环境相关浓度期间,苯并芘对海鱼早期生命阶段更广泛的多方面毒性潜力需要进一步探索。为了填补这些知识空白,本研究评估了 BaP(1、4 和 8 μg/L)在海洋青鳉 (Oryzias melastigma) 早期发育期间 30 天的暴露期内的体内生物毒性。该研究包括形态学、生化和分子水平分析,以捕捉 BaP 毒性的更广泛潜力。形态学分析表明,暴露于 BaP 会导致骨骼弯曲、心脏异常、生长迟缓、死亡率升高、孵化率延迟和降低。生化分析表明,苯并芘暴露不仅会产生氧化应激,还会破坏抗氧化酶的活性。通过分子水平研究进一步探索了氧化还原平衡的这种干扰。转录谱显示氧化磷酸化受损 (OXPHOS) 和三羧酸 (TCA) 循环途径,这可能抑制了暴露于 BaP 后鱼类的氧化呼吸链,并减少了三磷酸腺苷 (ATP) 和琥珀酸脱氢酶 (SDH) 的产生。此外,这项研究表明与细胞凋亡有潜在联系,如荧光显微镜和组织学分析所证明的那样,并通过实时定量 PCR 增加相关基因的表达水平来支持。 这项研究增强了我们对 BaP 的多方面毒性对海洋青鳉早期生命阶段的分子水平影响以及相关风险的理解。
更新日期:2024-06-29
中文翻译:
长期暴露于环境浓度的苯并[a]芘会导致海洋青鳉 (Oryzias melastigma) 早期生命阶段发育损害、氧化还原失衡和调节转录谱的多方面毒性作用
多环芳烃 (PAH) 积累并融入水生环境,引发了人们对水生生态系统福祉和安全的担忧。苯并[a]芘 (BaP) 是一种在环境中常见检测到的持久性 PAH,已被广泛研究。然而,在长期暴露于环境相关浓度期间,苯并芘对海鱼早期生命阶段更广泛的多方面毒性潜力需要进一步探索。为了填补这些知识空白,本研究评估了 BaP(1、4 和 8 μg/L)在海洋青鳉 (Oryzias melastigma) 早期发育期间 30 天的暴露期内的体内生物毒性。该研究包括形态学、生化和分子水平分析,以捕捉 BaP 毒性的更广泛潜力。形态学分析表明,暴露于 BaP 会导致骨骼弯曲、心脏异常、生长迟缓、死亡率升高、孵化率延迟和降低。生化分析表明,苯并芘暴露不仅会产生氧化应激,还会破坏抗氧化酶的活性。通过分子水平研究进一步探索了氧化还原平衡的这种干扰。转录谱显示氧化磷酸化受损 (OXPHOS) 和三羧酸 (TCA) 循环途径,这可能抑制了暴露于 BaP 后鱼类的氧化呼吸链,并减少了三磷酸腺苷 (ATP) 和琥珀酸脱氢酶 (SDH) 的产生。此外,这项研究表明与细胞凋亡有潜在联系,如荧光显微镜和组织学分析所证明的那样,并通过实时定量 PCR 增加相关基因的表达水平来支持。 这项研究增强了我们对 BaP 的多方面毒性对海洋青鳉早期生命阶段的分子水平影响以及相关风险的理解。