School of Environmental Science and Engineering, Shandong University, China-America CRC for Environment & Health, 72# Jimo Binhai Road, Qingdao, Shandong 266237, PR China.
School of Environmental Science and Engineering, Shandong University, China-America CRC for Environment & Health, 72# Jimo Binhai Road, Qingdao, Shandong 266237, PR China.
Sci Total Environ. 2023 May 1;871:162014. doi: 10.1016/j.scitotenv.2023.162014. Epub 2023 Feb 3.
Fluorene is a commonly identified PAH pollutant in soil and exhibits various worrisome hazardous effects to soil organisms. Currently, the toxicity profiles of fluorene on earthworm brain are rare, and the mechanisms and their corresponding pathways involved in fluorene-triggered neurotoxicity, genotoxicity, and behavior changes have not been reported hitherto. Herein, earthworm (Eisenia fetida) brain was chosen as targeted receptor to explore the neurotoxic effects, genetic toxicity, behavioral disorders, and related mechanisms caused by fluorene-induced oxidative stress pathways. The results showed excess fluorene initiated the release of excessive quantities of ROS in earthworm brain, which have caused oxidative stress and accompanied by serious oxidative effects, including LPO (lipid peroxidation) and DNA injury. To minimize the damage effects, the antioxidant defense mechanisms (antioxidant enzymes and non-enzymatic antioxidants) were activated, and entailed a decrease of the antioxidant capacity in E. fetida brain, which, in turn, causes further ROS-induced ROS release. Exposure of fluorene induced the abnormal mRNA expression of genes relevant to oxidative stress (e.g., GST, SOD, CAT, GPx, MT, and Hsp70) and neurotoxicity (e.g., H02, C04, D06, and E08) in E. fetida brain. Specifically, fluorene can bind directly to AChE, destroying the conformation of this protein, and even affecting its physiological functions. This occurrence caused the inhibition of AChE activity and excess ACh accumulation at the nicotinic post-synaptic membrane, finally triggering neurotoxicity by activation of pathways related to oxidative stress. Moreover, the avoidance responses and burrowing behavior were obviously disturbed by oxidative stress-induced neurotoxicity after exposure to fluorene. The results form IBR suggested more severe poisoning effects to E. fetida brain initiated by high-dose and long-term exposure of fluorene. Among, oxidative stress injury and genotoxic potential are more sensitive endpoint than others. Collectively, fluorene stress can provoke potential neurotoxicity, genotoxicity, and behavioral disturbances targeted to E. fetida brain through the ROS-mediated pathways involving oxidative stress. These findings are of great significance to estimate the detrimental effects of fluorene and the corresponding mechanisms on soil eco-safety.
荧蒽是土壤中常见的多环芳烃污染物,对土壤生物表现出各种令人担忧的有害影响。目前,荧蒽对蚯蚓大脑的毒性特征很少见,也没有报道荧蒽引发的神经毒性、遗传毒性和行为变化的机制及其相应途径。本文选择蚯蚓(Eisenia fetida)大脑作为靶向受体,探讨荧蒽诱导的氧化应激途径引起的神经毒性、遗传毒性、行为障碍及相关机制。结果表明,过量的荧蒽在蚯蚓脑中引发了过量的 ROS 释放,导致了氧化应激,并伴有严重的氧化效应,包括 LPO(脂质过氧化)和 DNA 损伤。为了最小化损伤效应,抗氧化防御机制(抗氧化酶和非酶抗氧化剂)被激活,导致 E. fetida 大脑中的抗氧化能力下降,进而导致进一步的 ROS 诱导的 ROS 释放。荧蒽暴露导致与氧化应激(如 GST、SOD、CAT、GPx、MT 和 Hsp70)和神经毒性(如 H02、C04、D06 和 E08)相关的基因的异常 mRNA 表达在 E. fetida 脑中。具体来说,荧蒽可以直接与 AChE 结合,破坏该蛋白的构象,甚至影响其生理功能。这种情况导致 AChE 活性抑制和烟碱型突触后膜中 ACh 积累过量,最终通过激活与氧化应激相关的途径引发神经毒性。此外,暴露于荧蒽后,氧化应激诱导的神经毒性明显干扰了蚯蚓的回避反应和掘洞行为。IBR 的结果表明,高剂量和长期暴露于荧蒽对 E. fetida 大脑的毒性作用更严重。其中,氧化应激损伤和遗传毒性潜力比其他指标更敏感。总的来说,荧蒽胁迫通过 ROS 介导的氧化应激途径,引发 E. fetida 大脑潜在的神经毒性、遗传毒性和行为障碍。这些发现对于评估荧蒽对土壤生态安全的有害影响及其相应机制具有重要意义。