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首页> 外文期刊>Human and Experimental Toxicology >An approach to evaluating the potential teratogenic and neurotoxic mechanism of BHA based on apoptosis induced by oxidative stress in zebrafish embryo ( Danio rerio )
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An approach to evaluating the potential teratogenic and neurotoxic mechanism of BHA based on apoptosis induced by oxidative stress in zebrafish embryo ( Danio rerio )

机译：基于斑马鱼胚胎氧化胁迫诱导的凋亡评价BHA潜在致畸和神经毒理机制的方法（Danio Rerio）

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Butylated hydroxyanisole (BHA) has been widely used in the cosmetics, pharmaceutical, and food industries due to its antioxidant activity. Despite the antioxidant effects, reported adverse effects of BHA at the cellular level have made its use controversial. In this regard, this study was performed to elucidate the potential toxicity mechanism caused by BHA at the molecular level in zebrafish embryos. For this purpose, zebrafish embryos were exposed to BHA at levels of 0.5, 1, 5, 7.5 and 10 ppm and monitored at 24, 48, 72 and 96 hours. Survival rate, hatching rate and malformations were evaluated. We examined the potential for reactive oxygen species (ROS) production and apoptosis signalling accumulation in the whole body. Moreover, we evaluated histopathological and immunohistochemical (8-OHDG) characterization of the brain in zebrafish embryos at the 96th hour. We also examined apoptosis, histopathological and immunohistochemical (8-OHDG) characteristics in 96 hpf zebrafish larvae exposed to tertiary butylhydroquinone (TBHQ), one of the major metabolites of BHA, at doses of 0.5, 2.5, 3.75 and 5 ppm. Consequently, it has been considered that increased embryonic and larval malformations in this study may have been caused by ROS-induced apoptosis. After 96 h of exposure, positive 8-OHdG immunofluorescence, degenerative changes, and necrosis were observed in the brain of BHA and TBHQ-treated zebrafish larvae in a dose-dependent manner. BHA and TBHQ exposure could lead to an increase in 8-OHdG activities by resulting oxidative DNA damage. In particular, the obtained data indicate that the induction of ROS formation, occurring during exposure to BHA and/or multiple hydroxyl groups, could be responsible for apoptosis.
机译：丁基羟基茴香醚（BHA）具有抗氧化活性，已广泛应用于化妆品、制药和食品工业。尽管有抗氧化作用，但据报道，BHA在细胞水平上的不良反应使其使用备受争议。在这方面，本研究旨在阐明BHA在分子水平上对斑马鱼胚胎造成的潜在毒性机制。为此，斑马鱼胚胎暴露于浓度为0.5、1、5、7.5和10 ppm的BHA中，并在24、48、72和96小时进行监测。评估存活率、孵化率和畸形率。我们检测了活性氧（ROS）产生和凋亡信号在全身积累的可能性。此外，我们评估了斑马鱼胚胎在96小时时大脑的组织病理学和免疫组织化学（8-OHDG）特征。我们还检测了96 hpf斑马鱼幼虫在0.5、2.5、3.75和5 ppm剂量下暴露于叔丁基对苯二酚（TBHQ）的细胞凋亡、组织病理学和免疫组织化学（8-OHDG）特征。叔丁基对苯二酚是BHA的主要代谢物之一。因此，本研究认为，胚胎和幼虫畸形的增加可能是由ROS诱导的细胞凋亡引起的。暴露96h后，在BHA和TBHQ处理的斑马鱼幼虫的大脑中观察到8-OHdG免疫荧光阳性、变性改变和坏死，呈剂量依赖性。BHA和TBHQ暴露可导致氧化DNA损伤，从而导致8-OHdG活性增加。尤其是，获得的数据表明，在暴露于BHA和/或多个羟基期间发生的ROS形成诱导可能是细胞凋亡的原因。

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