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首页> 外文期刊>RSC Advances >Ketamine-induced oxidative stress at different developmental stages of zebrafish (Danio rerio) embryos
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Ketamine-induced oxidative stress at different developmental stages of zebrafish (Danio rerio) embryos

机译：在斑马鱼（Danio Rerio）胚胎的不同发育阶段的氯胺酮诱导的氧化应激

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Ketamine, a widely used anesthetic in a variety of species, has been shown to exert a potential teratogenic effect during the early life stages of zebrafish. A number of mechanisms have been suggested for the etiology of teratogens. One of the most studied involves reactive oxygen species (ROS) formation and oxidative damage. In this study, zebrafish embryos were used to analyze oxidative stress as a potential mechanism of ketamine-induced toxicity. The changes in the accumulation and in vivo patterns of ROS, enzymatic activities (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), lactate dehydrogenase (LDH) and acetylcholinesterase (AChE)), glutathione levels (oxidized (GSSG) and reduced (GSH)), oxidative damage (lipid peroxidation (LPO) and protein carbonyls (CO)) and gene expression ( gclc , gstp1 , sod1 and cat ) were evaluated at 8 and 24 hours post fertilization (hpf) in zebrafish embryos exposed during 20 minutes to 0.2, 0.4 and 0.8 mg mL ~(?1) ketamine in the course of blastula (2.5 hours post fertilization-hpf), gastrula (5.5 hpf) and segmentation (10.5 hpf). Although no changes in ROS patterns were visible after all ketamine exposures, an increase in GSH levels was observed after exposure during blastula, indicating possible alterations in cell oxidative capacity. After exposure in gastrula, an increase in SOD and CAT enzymatic activities along with an increase in GSSG levels were observed at 8 hpf. At 24 hpf, CAT activity remained higher in ketamine exposed groups. The expression of the cat gene was also augmented at this time point. The changes were related with the ability of the embryo to handle oxidative stress and to a turning point during development of the oxidative defense system. At segmentation, the exposure to ketamine induced changes in the accumulation of ROS and sod gene expression which were related to protective mechanisms against ketamine-induced oxidative stress. Changes in acetylcholinesterase were also observed which may be related to changes in ROS. The overall results show that ketamine induces phase-dependent oxidative stress misregulation that could be the key factor for ketamine toxicity and could help to elucidate and provide more information on the mechanism of embryotoxicity of ketamine.
机译：氯胺酮是各种物种中广泛使用的麻醉剂，已被证明在斑马鱼的早期寿命期间发挥潜在的致畸作用。已经提出了许多机制对于畸胎孔的病因。其中最受研究的一种涉及反应性氧（ROS）形成和氧化损伤。在该研究中，斑马鱼胚胎用于分析氧化胁迫作为氯胺诱导的毒性的潜在机制。 ROS的积累和体内模式的变化，酶活性（超氧化物歧化酶（SOD），过氧化氢酶（CAT），谷胱甘肽过氧化物酶（GPX），乳酸脱氢酶（LDH）和乙酰胆碱酯酶（ACHE），谷胱甘肽水平（氧化（GSSG） ）在斑马鱼胚胎中的8和24小时评估氧化损伤（GSH）），氧化损伤（脂质过氧化（LPO）和蛋白质羰基（CO））和基因表达（GCLC，GSTP1，SOD1和猫）在Blastula的过程中20分钟至0.2,0.4和0.8mg ml〜（α1）氯胺酮在囊肿（后施肥后2.5小时），胃肠杆菌（5.5 HPF）和细分（10.5 HPF）。虽然在所有氯胺酮暴露后没有可见ROS模式的变化，但在Blastula期间暴露后观察到GSH水平的增加，表明细胞氧化能力的可能改变。在胃肠暴露后，在8 hPF下观察到SOD和CAT酶活性的增加以及GSSG水平的增加。在24 HPF，氯胺曝光组猫活性仍然较高。在这个时间点也增添了猫基因的表达。该变化与胚胎处理氧化应激和在氧化防御系统的开发过程中的转折点有关。在分割时，暴露于氯胺酮诱导的ROS和SOD基因表达积累的变化，其与氯胺酮诱导的氧化应激的保护机制有关。还观察到乙酰胆碱酯酶的变化可能与ROS的变化有关。总体结果表明，氯胺酮诱导相依赖性氧化应激误导，这可能是氯胺酮毒性的关键因素，并且可以帮助阐明并提供更多关于氯胺酮胚胎毒性机制的更多信息。

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