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Behavioral dysregulation in Nile tilapia (Oreochromis niloticus, GIFT) post-Streptococcus agalactia infection: Role of the microbiota-gut-brain axis 尼罗罗非鱼(Oreochromis niloticus, GIFT)感染无乳链球菌后的行为失调:微生物群-肠-脑轴的作用。
IF 3.9 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-16 DOI: 10.1016/j.cbpc.2024.110006

In the aquatic farming industry, understanding the factors affecting fish behavior is crucial, particularly in response to infections that compromise welfare and productivity. Swimming performance is a key life history trait critical to their ecology. This study explores the swimming behavior imbalance in Nile tilapia (Oreochromis niloticus, GIFT) post-infection with Streptococcus agalactiae (GBS), a common pathogen responsible for significant losses in aquaculture. We focused on how the microbiota-gut-brain axis influences the behavioral response of tilapia to GBS infection. Behavioral changes were quantified by measuring collision times and swimming speeds, which decreased significantly following infection. This behavioral downturn is mediated by alterations in the microbiota-gut-brain axis, evidenced by increased levels of monoamine neurotransmitters (serotonin, norepinephrine, and dopamine) in the brain and intestinal tissues. The study utilized pharmacological agents, the 5-HT1A receptor agonist (8-OH-DPAT) and antagonist (WAY-100635), to investigate their efficacy in mitigating these behavioral and biochemical changes. Both agents partially restored normal behavior by adjusting neurotransmitter concentrations disrupted by GBS infection. Additionally, a notable increase in the relative abundance of Streptococcus within the gut microbiota of infected fish highlights the potential role of specific bacterial populations in influencing host behavior. This research provides novel insights into the complex interactions between pathogen-induced gut microbiota changes and Nile tilapia's behavioral outcomes, highlighting potential avenues for improving fish health management through microbiota-targeted interventions.

在水产养殖业中,了解影响鱼类行为的因素至关重要,尤其是在应对影响鱼类福利和生产力的感染时。游泳性能是对其生态至关重要的关键生活史特征。本研究探讨了尼罗罗非鱼(Oreochromis niloticus,GIFT)感染猪链球菌(GBS)后的游泳行为失衡,猪链球菌是一种常见的病原体,在水产养殖中造成了重大损失。我们重点研究了微生物群-肠-脑轴如何影响罗非鱼对 GBS 感染的行为反应。通过测量罗非鱼的碰撞时间和游泳速度来量化其行为变化。这种行为衰退是由微生物群-肠-脑轴的改变介导的,大脑和肠道组织中单胺神经递质(5-羟色胺、去甲肾上腺素和多巴胺)水平的升高证明了这一点。该研究利用 5-HT1A 受体激动剂(8-OH-DPAT)和拮抗剂(WAY-100635)这两种药剂来研究它们在缓解这些行为和生化变化方面的功效。这两种药物通过调整因 GBS 感染而紊乱的神经递质浓度,部分恢复了正常行为。此外,受感染鱼类肠道微生物群中链球菌的相对丰度明显增加,这突出表明特定细菌群在影响宿主行为方面的潜在作用。这项研究为病原体诱导的肠道微生物群变化与尼罗罗非鱼行为结果之间复杂的相互作用提供了新的见解,突出了通过微生物群靶向干预改善鱼类健康管理的潜在途径。
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引用次数: 0
Acute lipopolysaccharide (LPS)-induced cell membrane hyperpolarization is independent of voltage gated and calcium activated potassium channels 急性脂多糖(LPS)诱导的细胞膜超极化与电压门控和钙激活钾通道无关。
IF 3.9 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-16 DOI: 10.1016/j.cbpc.2024.110004

The gram-negative toxin lipopolysaccharides (LPS) are known to trigger inflammatory cytokines in mammals, which can result in pathological responses. Upon treatment of bacterial sepsis with antibiotics, the lysing bacteria can present a surge in LPS, inducing a cytokine storm. However, LPS can also have direct cellular effects, including transient rapid hyperpolarizing of the membrane potential, blocking glutamate receptors and even promoting release of glutamate. The detailed mechanism of action for these immediate responses is still unresolved. In addressing the membrane hyperpolarization, voltage gated K+ channel blockers 4-aminopyridine (4-AP, 3 mM), quinidine hydrochloride monohydrate (0.1 mM) and tetraethylammonium (TEA, 20 mM) were examined along with RNAi knockdowns of potential calcium activated K+ channels. The immediate responses of LPS were not blocked. Even in the presence of glutamate, the membrane still hyperpolarizes with LPS. When the driving gradient for the ionotropic glutamate receptors is enhanced during hyperpolarization, spontaneous quantal responses are dampened in amplitude. Thus, glutamate receptors are blocked, and the mechanism of hyperpolarization remains unresolved. The larval Drosophila glutamatergic neuromuscular junction is used as a model synaptic preparation to address the direct rapid actions by LPS.

众所周知,革兰氏阴性毒素脂多糖(LPS)会引发哺乳动物体内的炎症细胞因子,从而导致病理反应。用抗生素治疗细菌性败血症时,溶解的细菌会使 LPS 激增,诱发细胞因子风暴。不过,LPS 也能对细胞产生直接影响,包括一过性地迅速使膜电位超极化、阻断谷氨酸受体,甚至促进谷氨酸的释放。这些直接反应的详细作用机制仍未确定。为了解决膜超极化问题,研究人员研究了电压门控 K+ 通道阻断剂 4-氨基吡啶(4-AP,3 毫摩尔)、一水盐酸奎尼丁(0.1 毫摩尔)和四乙基铵(TEA,20 毫摩尔)以及潜在钙激活 K+ 通道的 RNAi 敲除。LPS 的直接反应没有被阻断。即使在谷氨酸存在的情况下,LPS 仍会使膜超极化。在超极化过程中,当离子型谷氨酸受体的驱动梯度增强时,自发量子反应的幅度会受到抑制。因此,谷氨酸受体被阻断,超极化的机制仍悬而未决。本研究以果蝇幼虫谷氨酸能神经肌肉接头为突触制备模型,探讨 LPS 的直接快速作用。
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引用次数: 0
Mechanisms of mitochondrial resilience in teleostean radial glia under hypoxic stress 缺氧胁迫下桡神经胶质细胞线粒体的恢复机制
IF 3.9 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-14 DOI: 10.1016/j.cbpc.2024.110001

Radial glial cells (RGCs) are remarkable cells, essential for normal development of the vertebrate central nervous system. In teleost fishes, RGCs play a pivotal role in neurogenesis and regeneration of injured neurons and glia. RGCs also exhibit resilience to environmental stressors like hypoxia via metabolic adaptations. In this study, we assessed the physiology of RGCs following varying degrees of hypoxia, with an emphasis on reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP), mitophagy, and energy metabolism. Our findings demonstrated that hypoxia significantly elevated ROS production and induced MMP depolarization in RGCs. The mitochondrial disturbances were closely associated with increased mitophagy, based on the co-localization of mitochondria and lysosomes. Key mitophagy-related genes were also up-regulated, including those of the BNIP3/NIX mediated pathway as well as the FUNDC1 mediated pathway. Such responses suggest robust cellular mechanisms are initiated to counteract mitochondrial damage due to increasing hypoxia. A significant metabolic shift from oxidative phosphorylation to glycolysis was also observed in RGCs, which may underlie an adaptive response to sustain cellular function and viability following a reduction in oxygen availability. Furthermore, hypoxia inhibited the synthesis of mitochondrial complexes subunits in RGCs, potentially related to elevated HIF-2α expression with 3 % O2. Taken together, RGCs appear to exhibit complex adaptive responses to hypoxic stress, characterized by metabolic reprogramming and the activation of mitophagy pathways to mitigate mitochondrial dysfunction.

放射状神经胶质细胞(RGC)是脊椎动物中枢神经系统正常发育必不可少的重要细胞。在远洋鱼类中,RGCs 在神经发生以及受伤神经元和神经胶质的再生过程中发挥着关键作用。RGCs 还能通过新陈代谢适应缺氧等环境压力而表现出恢复能力。在这项研究中,我们评估了不同程度缺氧后 RGCs 的生理状况,重点是活性氧(ROS)生成、线粒体膜电位(MMP)、有丝分裂和能量代谢。我们的研究结果表明,缺氧会显著增加 ROS 的产生,并诱导 RGC 的线粒体膜电位去极化。根据线粒体和溶酶体的共定位,线粒体紊乱与有丝分裂的增加密切相关。与有丝分裂相关的关键基因也被上调,包括 BNIP3/NIX 介导的途径和 FUNDC1 介导的途径。这些反应表明,细胞启动了强大的机制来抵消因缺氧加剧而造成的线粒体损伤。在 RGCs 中还观察到从氧化磷酸化到糖酵解的重大代谢转变,这可能是氧气供应减少后维持细胞功能和活力的适应性反应的基础。此外,缺氧抑制了 RGC 中线粒体复合物亚基的合成,这可能与 3%O2 时 HIF-2α 表达的升高有关。总之,RGCs 似乎对缺氧压力表现出复杂的适应性反应,其特点是代谢重编程和激活有丝分裂途径以缓解线粒体功能障碍。
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引用次数: 0
Hexavalent chromium damages intestinal cells and coelomocytes and impairs immune function in the echiuran worm Urechis unicinctus by causing oxidative stress and apoptosis 六价铬通过导致氧化应激和细胞凋亡,损害肠道细胞和腔室细胞,并损害棘尾蚯蚓(Urechis unicinctus)的免疫功能。
IF 3.9 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-14 DOI: 10.1016/j.cbpc.2024.110002

Hexavalent chromium (Cr(VI)) is a common pollutant in the marine environment, which impairs immunity and causes reproductive and heredity disorders in organisms. To clarify the immunotoxic effects of Cr (VI) on the marine worm Urechis unicinctus, we analyzed tissue damage and immune dysfunction caused by Cr (VI) in this organism at histopathologic, zymologic, apoptotic and molecular levels. The results indicated that the bioaccumulation of Cr (VI) bioaccumulation levels in coelomocytes was significantly higher than in the intestines and muscles. Pathological observation showed that Cr (VI) caused damage to the respiratory intestine, stomach and midgut. Cr (VI) also increased the replication of goblet cells and a reduction in the replication of epithelial cells. Meanwhile, Cr (VI) induced apoptosis of intestinal cells and coelomocytes, accompanied by an increase in the expression of Caspase-3, COX-2, and MyD88 in the intestine and coelomocytes. At the same time, Cr (VI) significantly affected the activities of antioxidant enzymes such as SOD, ACP, CAT, CAT, and GST, and increased H2O2 and MDA contents in U. unicinctus. Moreover, Cr (VI) exposure also up-regulated the transcription of hsc70, mt and jnk genes but decreased that of sod in the intestines. In contrast, Cr (VI) down-regulated the expression of sod, hsc70, mt, and jnk genes in coelomocytes. Collectively, Cr (VI) bioaccumulated in U. unicinctus cells and tissues, causing several histopathological changes, oxidative stress, and apoptosis of several cells in the organism, resulting in intestinal and coelomocyte damage and immune dysfunctioning.

六价铬(Cr(VI))是海洋环境中常见的污染物,会损害生物的免疫力,导致生物的生殖和遗传紊乱。为了弄清铬(VI)对海洋蠕虫 Urechis unicinctus 的免疫毒性影响,我们从组织病理学、酶学、细胞凋亡和分子水平分析了铬(VI)对该生物造成的组织损伤和免疫功能障碍。结果表明,Cr(VI)在腹腔细胞中的生物累积水平明显高于肠道和肌肉。病理学观察表明,铬(Ⅵ)对呼吸肠、胃和中肠造成了损害。铬(Ⅵ)还会增加鹅口疮细胞的复制,减少上皮细胞的复制。同时,铬(Ⅵ)会诱导肠道细胞和辅膜细胞凋亡,并伴随着肠道和辅膜细胞中 Caspase-3、COX-2 和 MyD88 表达的增加。同时,铬(Ⅵ)会明显影响鳗鲡体内 SOD、ACP、CAT、CAT 和 GST 等抗氧化酶的活性,并增加 H2O2 和 MDA 的含量。此外,接触铬(Ⅵ)还会上调肠道中 hsc70、mt 和 jnk 基因的转录,但会降低 sod 基因的转录。相反,铬(Ⅵ)会降低 sod、hsc70、mt 和 jnk 基因在腹腔细胞中的表达。总之,铬(六价铬)在乌鳢细胞和组织中的生物蓄积会引起多种组织病理学变化、氧化应激和多种细胞凋亡,导致肠道和腹腔细胞损伤和免疫功能失调。
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引用次数: 0
Lactobacillus delbrueckii ameliorates Aeromonas hydrophila-induced oxidative stress, inflammation, and immunosuppression of Cyprinus carpio huanghe var NF-κB/Nrf2 signaling pathway 德尔布鲁贝克乳杆菌可改善嗜水气单胞菌诱导的氧化应激、炎症和鲤鱼黄鹤楼变种NF-κB/Nrf2信号通路的免疫抑制。
IF 3.9 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-13 DOI: 10.1016/j.cbpc.2024.110000

Aeromonas hydrophila (A. hydrophila) is one of the most pathogenic disease-causing bacteria, and causes massive death of animals including fish. Thus, strategies are being sought to ameliorate the impact of A. hydrophila. In this study, we have evaluated the ameliorative potential of dietary Lactobacillus delbrueckii (L. delbrueckii). The fishes were divided into the control group, an A. hydrophila group (A. hydrophila), and an L. delbrueckii group (A. hydrophila + 1*107 CFU/g L. delbrueckii). The results showed that A. hydrophila increased reactive oxygen species (ROS) content. However, dietary supplementation with L. delbrueckii prevented oxidative damage caused by elevated levels of ROS. The toxic effects of A. hydrophila on superoxide dismutase (SOD) activity, glutathione-S-transferase (GST), glutathione peroxidase (GPx), and glutathione reductase (GR), along with the levels of glutathione (GSH), were mitigated by dietary L. delbrueckii (P < 0.05). Also, Dietary L. delbrueckii induced the expression of antioxidant-related genes (sod, cat, gpx, gst, NF-E2-related factor 2 (nrf2), Kelch-like-ECH-and associated protein 1a (keap1a)) in the intestine of fish (P < 0.05). Furthermore, L. delbrueckii increased A. hydrophila-induced lysozyme, ACP, C3, and C4 decline. The mRNA expression levels of interleukin 1β (il-1β), interleukin 8 (il-8), tumour necrosis factor α (tnf-α), and nuclear transcription factor-κB p65 (nf-κb p65) were significantly elevated by A. hydrophila. In contrast, the relative mRNA expression levels of inhibitor factor κBα (iκbα) in the intestine were decreased by A. hydrophila (P < 0.05). However, L. delbrueckii prevented A. hydrophila-induced the relative mRNA expression changes. These present results demonstrate that dietary L. delbrueckii alleviated A. hydrophila-induced oxidative stress, immunosuppression, inflammation, and apoptosis in common Cyprinus carpio.

嗜水气单胞菌(A. hydrophila)是致病性最强的细菌之一,会导致包括鱼类在内的大量动物死亡。因此,人们一直在寻求改善嗜水气单胞菌影响的策略。在这项研究中,我们评估了饮食中的德尔布鲁贝克乳杆菌(L. delbrueckii)的改善潜力。鱼类被分为对照组、蚜茧蜂毒素组(蚜茧蜂毒素)和 delbrueckii 乳杆菌组(蚜茧蜂毒素 + 1*107 CFU/g delbrueckii 乳杆菌)。结果表明,嗜水蝇增加了活性氧(ROS)的含量。然而,膳食中补充 L. delbrueckii 可以防止 ROS 水平升高造成的氧化损伤。膳食中添加 L. delbrueckii(P<0.05)可减轻纤毛虫对超氧化物歧化酶(SOD)活性、谷胱甘肽-S-转移酶(GST)、谷胱甘肽过氧化物酶(GPx)和谷胱甘肽还原酶(GR)以及谷胱甘肽(GSH)水平的毒性影响。
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引用次数: 0
Basal release and relaxation responses to 6-nitrodopamine in swine carotid, coronary, femoral, and renal arteries 猪颈动脉、冠状动脉、股动脉和肾动脉对 6-硝基多巴胺的基础释放和松弛反应。
IF 3.9 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-13 DOI: 10.1016/j.cbpc.2024.110003

Mammalian and reptilian vascular tissues present basal release of 6-nitrodopamine, which is reduced when the tissues are pre-incubated with the NO synthase inhibitor L-NG-Nitro arginine methyl ester (L-NAME), or when the endothelium is mechanically removed. 6-Nitrodopamine induces vasorelaxation in pre-contracted vascular rings by antagonizing the dopaminergic D2-like receptor. Here it was investigated whether male swine vessels (including carotid, left descendent coronary, renal, and femoral arteries) release 6-nitrodopamine, dopamine, noradrenaline, and adrenaline, as measured by liquid chromatography coupled to tandem mass spectrometry. The in vitro vasorelaxant action of 6-nitrodopamine was evaluated in carotid, coronary, renal, and femoral arteries precontracted by U-46619 (3 nM), and compared to that induced by the dopamine D2-receptor antagonist L-741,626. Expression of tyrosine hydroxylase and the neuromaker calretinin was investigated by immunohistochemistry. All vascular tissues presented basal release of endothelium-derived catecholamines. The relaxation induced by 6-nitrodopamine was not affected by preincubation of the tissues with either L-NAME (100 μM, 30-min preincubation) or the heme-site inhibitor of soluble guanylyl cyclase ODQ (100 μM, 30-min preincubation). Electrical field stimulation (EFS)-induced contractions were significantly potentiated by previous incubation with L-NAME, but unaffected by ODQ preincubation. The contractions induced by EFS were reduced by preincubation with either 6-nitrodopamine or L-741,626. Immunohistochemistry in all arteries revealed the presence of tyrosine hydroxylase in the endothelium, whereas immunoreactivity for calretinin was negative. Swine vessels present basal release of endothelium-derived catecholamines and expression of tyrosine hydroxylase in the endothelium. The vasodilation induced by 6-nitrodopamine is due to blockade of dopaminergic D2-like receptors.

哺乳动物和爬行动物的血管组织存在 6-硝基多巴胺的基础释放,当预先用氮氧化物合成酶抑制剂 L-NG-硝基精氨酸甲酯(L-NAME)孵育这些组织或机械去除内皮时,这种释放会减少。6-硝基多巴胺通过拮抗 D2 样多巴胺能受体诱导预收缩血管环的血管舒张。本文研究了雄性猪血管(包括颈动脉、左冠状动脉降支、肾动脉和股动脉)是否释放 6-硝基多巴胺、多巴胺、去甲肾上腺素和肾上腺素。评估了 6-硝基多巴胺对颈动脉、冠状动脉、肾动脉和股动脉在 U-46619 (3 nM)作用下的体外血管舒张作用,并与多巴胺 D2 受体拮抗剂 L-741,626 诱导的作用进行了比较。免疫组化法检测了酪氨酸羟化酶和神经元钙调蛋白的表达。所有血管组织都有内皮衍生儿茶酚胺的基础释放。用 L-NAME(100 μM,预孵育 30 分钟)或可溶性鸟苷酸环化酶血红素位点抑制剂 ODQ(100 μM,预孵育 30 分钟)预孵育组织不会影响 6-硝基多巴胺诱导的松弛。电场刺激(EFS)诱导的收缩会因先前与 L-NAME 的预孵育而明显增强,但 ODQ 的预孵育不会对其产生影响。预孵育 6-硝基多巴胺或 L-741,626 可减少 EFS 诱导的收缩。所有动脉的免疫组化都显示内皮中存在酪氨酸羟化酶,而钙网蛋白的免疫反应呈阴性。猪血管的内皮源性儿茶酚胺的基础释放和内皮中酪氨酸羟化酶的表达。6-硝基多巴胺诱导的血管扩张是由于阻断了多巴胺能 D2 样受体。
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引用次数: 0
Dopaminergic and anti-estrogenic responses in juvenile steelhead (Oncorhynchus mykiss) exposed to bifenthrin 暴露于联苯菊酯的钢鳟鱼幼鱼的多巴胺能和抗雌激素反应。
IF 3.9 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-05 DOI: 10.1016/j.cbpc.2024.109995

The frequency of detection and concentrations of bifenthrin, a pyrethroid insecticide, in the waterways inhabited by the endangered species, steelhead trout (Oncorhynchus mykiss), has become a significant concern for regulatory agencies. Endocrine disruption has been observed with estrogenic and anti-estrogenic responses in fish species at different life stages. Since several studies have indicated alterations in dopaminergic signaling associated with endocrine responses, juvenile steelhead were exposed to environmentally relevant concentrations of 60 or 120 ng/L bifenthrin for two weeks. Fish brains were assessed for dopamine levels and the expression of genes involved in dopaminergic and estrogenic processes, such as catechol-o-methyltransferase (comt) and monoamine oxidase (mao). Vitellogenin (vtg) and estrogenic receptors (ERα1, ERβ1, and ERβ2) were also evaluated in livers of the animals. Dopamine concentrations were significantly higher in fish brains following bifenthrin exposure. Consistent with a reduction in dopamine clearance, there was a significant decrease in the mRNA expression of comt with increased bifenthrin concentration. Hepatic expression of ERα1 and ERβ2 mRNA was significantly decreased with increased bifenthrin concentration. These data support the possible mechanism of bifenthrin altering the dopaminergic pathway at low ng/L concentrations, in juvenile steelhead, which could interfere with endocrine feedback loops. These findings support the need for and importance of identifying species and life stage differences in pesticide modes of action to reduce uncertainties in risk assessments.

在濒危物种钢鳟鱼(Oncorhynchus mykiss)栖息的水道中,联苯菊酯(一种拟除虫菊酯杀虫剂)的检测频率和浓度已成为监管机构关注的一个重要问题。在不同生命阶段的鱼类物种中,已观察到雌激素和抗雌激素反应对内分泌的干扰。由于多项研究表明多巴胺能信号的改变与内分泌反应有关,因此将幼年钢鲤暴露于环境相关浓度为 60 或 120 纳克/升的联苯菊酯中两周。对鱼脑中的多巴胺水平以及参与多巴胺能和雌激素过程的基因(如儿茶酚-邻甲基转移酶(comt)和单胺氧化酶(mao))的表达进行了评估。还对动物肝脏中的卵黄素(vtg)和雌激素受体(ERα1、ERβ1 和 ERβ2)进行了评估。接触联苯菊酯后,鱼脑中的多巴胺浓度明显升高。与多巴胺清除率降低相一致,随着联苯菊酯浓度的增加,comt的mRNA表达量也显著下降。肝脏中 ERα1 和 ERβ2 mRNA 的表达量随着联苯菊酯浓度的增加而显著下降。这些数据支持联苯菊酯在低浓度(ng/L)时改变钢鲤幼鱼多巴胺能通路的可能机制,这可能会干扰内分泌反馈回路。这些发现支持了确定农药作用模式中物种和生命阶段差异的必要性和重要性,以减少风险评估中的不确定性。
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引用次数: 0
Effect of tributyltin exposure on the embryonic development and behavior of a molluscan model species, Lymnaea stagnalis 三丁基锡暴露对软体动物模型物种 Lymnaea stagnalis 的胚胎发育和行为的影响。
IF 3.9 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-05 DOI: 10.1016/j.cbpc.2024.109996

The presence of the organotin compound tributyltin (TBT) in aquatic ecosystems has been a serious environmental problem for decades. Although a number of studies described the negative impact of TBT on mollusks at different levels, investigations connected to its potential effects during embryogenesis have been neglected. For a better understanding of the impact of TBT on mollusks, in the present study, embryos of previously TBT-treated or not treated specimens of the great pond snail (Lymnaea stagnalis) were exposed to 100 ng L−1 TBT from egg-laying (single-cell stage) until hatching. According to our results, TBT significantly delayed hatching and caused shell malformation. TBT transiently decreased the locomotion (gliding) and also reduced the feeding activity, demonstrating for the first time that this compound can alter the behavioral patterns of molluscan embryos. The heart rate was also significantly reduced, providing further support that cardiac activity is an excellent indicator of metal pollution in molluscan species. At the histochemical level, tin was demonstrated for the first time in TBT-treated hatchlings with intensive reaction in the central nervous system, kidney, and hepatopancreas. Overall, the most notable effects were observed in treated embryos derived from TBT treated snails. Our findings indicate that TBT has detrimental effects on the development and physiological functions of Lymnaea embryos even at a sub-lethal concentration, potentially influencing their survival and fitness. Highlighting our observations, we have demonstrated previously unknown physiological changes (altered heart rate, locomotion, and feeding activity) caused by TBT, as well as visualized tin at the histochemical level in a molluscan species for the first time following TBT exposure. Further studies are in progress to reveal the cellular and molecular mechanisms underlying the physiological and behavioral changes described in the present study.

几十年来,有机锡化合物三丁基锡(TBT)在水生生态系统中的存在一直是一个严重的环境问题。尽管许多研究都描述了三丁基锡化合物在不同水平上对软体动物的负面影响,但有关其在胚胎发育过程中的潜在影响的研究却被忽视了。为了更好地了解三丁基锡化合物对软体动物的影响,本研究将大塘螺(Lymnaea stagnalis)胚胎暴露于 100 ng L-1 的三丁基锡化合物中,从产卵(单细胞阶段)一直到孵化。结果表明,三丁基锡化合物会明显延迟孵化,并导致贝壳畸形。三丁基锡化合物可短暂降低胚胎的运动(滑行)能力,并减少摄食活动,首次证明了该化合物可改变软体动物胚胎的行为模式。心率也明显降低,进一步证明心脏活动是软体动物体内金属污染的极佳指标。在组织化学水平上,经三丁基锡化合物处理的幼体首次出现锡中毒现象,中枢神经系统、肾脏和肝胰脏都出现了强烈反应。总之,在经三丁基锡化合物处理的蜗牛胚胎中观察到了最显著的影响。我们的研究结果表明,即使在亚致死浓度下,三丁基锡化合物也会对莱姆蜗牛胚胎的发育和生理功能产生有害影响,从而可能影响其存活率和适应能力。为了突出我们的观察结果,我们展示了三丁基锡化合物引起的之前未知的生理变化(心率、运动和摄食活动的改变),并首次在软体动物中暴露于三丁基锡化合物后在组织化学水平上观察到锡的变化。目前正在开展进一步研究,以揭示本研究中描述的生理和行为变化的细胞和分子机制。
{"title":"Effect of tributyltin exposure on the embryonic development and behavior of a molluscan model species, Lymnaea stagnalis","authors":"","doi":"10.1016/j.cbpc.2024.109996","DOIUrl":"10.1016/j.cbpc.2024.109996","url":null,"abstract":"<div><p>The presence of the organotin compound tributyltin (TBT) in aquatic ecosystems has been a serious environmental problem for decades. Although a number of studies described the negative impact of TBT on mollusks at different levels, investigations connected to its potential effects during embryogenesis have been neglected. For a better understanding of the impact of TBT on mollusks, in the present study, embryos of previously TBT-treated or not treated specimens of the great pond snail (<em>Lymnaea stagnalis</em>) were exposed to 100 ng L<sup>−1</sup> TBT from egg-laying (single-cell stage) until hatching. According to our results, TBT significantly delayed hatching and caused shell malformation. TBT transiently decreased the locomotion (gliding) and also reduced the feeding activity, demonstrating for the first time that this compound can alter the behavioral patterns of molluscan embryos. The heart rate was also significantly reduced, providing further support that cardiac activity is an excellent indicator of metal pollution in molluscan species. At the histochemical level, tin was demonstrated for the first time in TBT-treated hatchlings with intensive reaction in the central nervous system, kidney, and hepatopancreas. Overall, the most notable effects were observed in treated embryos derived from TBT treated snails. Our findings indicate that TBT has detrimental effects on the development and physiological functions of <em>Lymnaea</em> embryos even at a sub-lethal concentration, potentially influencing their survival and fitness. Highlighting our observations, we have demonstrated previously unknown physiological changes (altered heart rate, locomotion, and feeding activity) caused by TBT, as well as visualized tin at the histochemical level in a molluscan species for the first time following TBT exposure. Further studies are in progress to reveal the cellular and molecular mechanisms underlying the physiological and behavioral changes described in the present study.</p></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1532045624001649/pdfft?md5=0141f6a19ec0cf187d02beaa9bc35580&pid=1-s2.0-S1532045624001649-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141901169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The effects of Cl− channel inhibitors and pyrethroid insecticides on calcium-activated chloride channels in neurons of Helicoverpa armigera Cl- 通道抑制剂和拟除虫菊酯杀虫剂对 Helicoverpa armigera 神经元中钙激活氯通道的影响。
IF 3.9 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-05 DOI: 10.1016/j.cbpc.2024.109999

TMEM16A, a member of the Transmembrane protein 16 family, serves as the molecular basis for calcium activated chloride channels (CaCCs). We use RT-PCR to demonstrate the expression of TMEM16A in the neurons of Helicoverpa armigera, and record the CaCCs current of acute isolated neurons of H. armigera for the first time using patch clamp technology. In order to screen effective inhibitors of calcium-activated chloride channels, the inhibitory effects of four chloride channel inhibitors, CaCCinh-A01, NPPB, DIDS, and SITS, on CaCCs were compared. The inhibitory effects of the four inhibitors on the outward current of CaCCs were CaCCinh-A01 (10 μM, 56.31 %), NPPB (200 μM, 43.69 %), SITS (1 mM, 12.41 %) and DIDS (1 mM, 13.29 %). Among these inhibitors, CaCCinh-A01 demonstrated the highest efficacy as a blocker. To further explore whether calcium channel proteins can serve as potential targets of pyrethroids, we compared the effects of (type I) tefluthrin and (type II) deltamethrin on CaCCs. 10 μM and 100 μM tefluthrin can stimulate a large tail current in CaCCs, prolonging their deactivation time by 10.44 ms and 31.49 ms, and the V0.5 shifted in the hyperpolarization by 2–8 mV. Then, deltamethrin had no obvious effect on the deactivation and activation of CaCCs. Therefore, CaCCs of H. armigera can be used as a potential target of pyrethroids, but type I and type II pyrethroids have different effects on CaCCs.

TMEM16A是跨膜蛋白16家族的成员,是钙激活氯通道(CaCCs)的分子基础。我们利用 RT-PCR 技术证明了 TMEM16A 在蓟马神经元中的表达,并首次利用膜片钳技术记录了蓟马急性分离神经元的钙激活氯通道电流。为了筛选有效的钙激活氯离子通道抑制剂,比较了 CaCCinh-A01、NPPB、DIDS 和 SITS 四种氯离子通道抑制剂对 CaCCs 的抑制作用。四种抑制剂对 CaCCs 外向电流的抑制作用分别为 CaCCinh-A01 (10 μM,56.31%)、NPPB (200 μM,43.69%)、SITS (1 mM,12.41%)和 DIDS (1 mM,13.29%)。在这些抑制剂中,CaCCinh-A01 的阻断效力最高。为了进一步探讨钙通道蛋白是否可以作为拟除虫菊酯的潜在靶标,我们比较了(I 型)四氟菊酯和(II 型)溴氰菊酯对 CaCC 的影响。10 μM和100 μM的氟氯氰菊酯能刺激CaCCs产生较大的尾电流,使其失活时间分别延长10.44 ms和31.49 ms,超极化时V0.5偏移2-8 mV。而溴氰菊酯对CaCCs的失活和激活无明显影响。因此,拟除虫菊酯可作为除虫菊酯的潜在靶标,但Ⅰ型和Ⅱ型除虫菊酯对CaCCs的影响不同。
{"title":"The effects of Cl− channel inhibitors and pyrethroid insecticides on calcium-activated chloride channels in neurons of Helicoverpa armigera","authors":"","doi":"10.1016/j.cbpc.2024.109999","DOIUrl":"10.1016/j.cbpc.2024.109999","url":null,"abstract":"<div><p>TMEM16A, a member of the Transmembrane protein 16 family, serves as the molecular basis for calcium activated chloride channels (CaCCs). We use RT-PCR to demonstrate the expression of TMEM16A in the neurons of <em>Helicoverpa armigera</em>, and record the CaCCs current of acute isolated neurons of <em>H. armigera</em> for the first time using patch clamp technology. In order to screen effective inhibitors of calcium-activated chloride channels, the inhibitory effects of four chloride channel inhibitors, CaCCinh-A01, NPPB, DIDS, and SITS, on CaCCs were compared. The inhibitory effects of the four inhibitors on the outward current of CaCCs were CaCCinh-A01 (10 μM, 56.31 %), NPPB (200 μM, 43.69 %), SITS (1 mM, 12.41 %) and DIDS (1 mM, 13.29 %). Among these inhibitors, CaCCinh-A01 demonstrated the highest efficacy as a blocker. To further explore whether calcium channel proteins can serve as potential targets of pyrethroids, we compared the effects of (type I) tefluthrin and (type II) deltamethrin on CaCCs. 10 μM and 100 μM tefluthrin can stimulate a large tail current in CaCCs, prolonging their deactivation time by 10.44 ms and 31.49 ms, and the V<sub>0.5</sub> shifted in the hyperpolarization by 2–8 mV. Then, deltamethrin had no obvious effect on the deactivation and activation of CaCCs. Therefore, CaCCs of <em>H. armigera</em> can be used as a potential target of pyrethroids, but type I and type II pyrethroids have different effects on CaCCs.</p></div>","PeriodicalId":10602,"journal":{"name":"Comparative Biochemistry and Physiology C-toxicology & Pharmacology","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141901170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Acute and chronic effects of the antifouling booster biocide Irgarol 1051 on the water flea Moina macrocopa revealed by multi-biomarker determination 通过多生物标记测定揭示防污增效杀菌剂 Irgarol 1051 对水蚤 Moina macrocopa 的急性和慢性影响。
IF 3.9 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-05 DOI: 10.1016/j.cbpc.2024.109994

Irgarol 1051 is an herbicide extensively utilized in antifouling paint due to its ability to inhibit photosynthesis. Irgarol and its photodegradation products are highly persistent in waters and sediments, although they are present in low concentrations. However, our understanding of the harmful effects of Irgarol on non-target organisms remains limited. In this study, we assessed the effects of acute (24 h) and chronic (14 days across three generations) exposure to different concentrations (including the 1/10 NOEC, NOEC, and 1/10 LC50 calculated from the 24-h acute toxicity test) of Irgarol using the water flea Moina macrocopa. Acute exposure to 1/10 LC50 significantly decreased survival, feeding rate, thoracic limb activity, heart rate, and acetylcholinesterase activity. Elevated levels of intracellular reactive oxygen species and malondialdehyde, along with a significant increase in catalase and superoxide dismutase activity, suggested the induction of oxidative stress in response to 1/10 LC50. An initial boost in glutathione level and the enzymatic activities of glutathione peroxidase and glutathione reductase, followed by a plunge, implies some compromise in the antioxidant defense system. Upon chronic exposure to the NOEC value, both generations F1 and F2 displayed a significant decrease in survival rate, body length, number of neonates per brood, and delayed sexual maturation, suggesting maternal transfer of potential damage through generations. Taken together, Irgarol induced acute toxicity through physiological and cholinergic damage, accompanied by the induction of oxidative stress, in the water flea. Even its sub-lethal concentrations can induce detrimental effects across generations when consistently exposed.

Irgarol 1051 是一种除草剂,因其能够抑制光合作用而被广泛用于防污漆中。Irgarol及其光降解产物在水体和沉积物中具有很强的持久性,尽管它们的浓度很低。然而,我们对Irgarol对非目标生物有害影响的了解仍然有限。在本研究中,我们利用水蚤 Moina macrocopa 评估了急性(24 小时)和慢性(14 天,共三代)接触不同浓度(包括 24 小时急性毒性试验计算出的 1/10 NOEC、NOEC 和 1/10 LC50)的醚菌醇的影响。急性接触 1/10 LC50 会显著降低存活率、摄食率、胸肢活动、心率和乙酰胆碱酯酶活性。细胞内活性氧和丙二醛水平的升高,以及过氧化氢酶和超氧化物歧化酶活性的显著增加,表明 1/10 LC50 诱导了氧化应激反应。谷胱甘肽水平以及谷胱甘肽过氧化物酶和谷胱甘肽还原酶的酶活性最初有所提高,随后出现下降,这意味着抗氧化防御系统受到了一定程度的损害。当长期暴露于无观测效应浓度值时,F1 和 F2 代的存活率、体长、每窝产仔数和性成熟延迟均显著下降,这表明潜在的母体损伤会通过代际传递。总之,Irgarol 通过生理和胆碱能损伤以及氧化应激诱导水蚤产生急性毒性。即使是亚致死浓度的雌二醇,如果持续接触也会诱发跨代的有害影响。
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引用次数: 0
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Comparative Biochemistry and Physiology C-toxicology & Pharmacology
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