UNESP - Sao Paulo State University, Department of Chemistry and Environmental Sciences, São Paulo, Brazil.
UFSC - Federal University of Santa Catarina, Department of Biochemistry, Florianópolis, SP, Brazil.
Ecotoxicol Environ Saf. 2020 Mar 1;190:110107. doi: 10.1016/j.ecoenv.2019.110107. Epub 2020 Jan 2.
Increased malondialdehyde (MDA) levels are commonly considered an indicator of lipid peroxidation derived from oxidative stress insults promoted by exposure of fish to pollutants. However, a decrease in MDA levels after xenobiotic exposure has been also reported, an effect that is mostly attributed to enhanced antioxidant defenses. In this study, we assessed whether pollutant-mediated MDA decrease would be associated with antioxidant enhancement or with its metabolism by aldehyde dehydrogenase (ALDH) in the liver and gills of lambari (Astyanax altiparanae) exposed to diesel oil (0.001, 0.01, and 0.1 mL/L). MDA levels were decreased in the liver of lambari exposed to diesel. The activities of the antioxidant enzymes, catalase (CAT) and glutathione peroxidase (GPx), were unchanged in the liver, while that of glucose-6-phosphate dehydrogenase (G6PDH) was decreased. In contrast, levels of total glutathione (tGSH) and the activity of glutathione S-transferase (GST) were increased in the liver, which partly support antioxidant protection against lipid peroxidation. More importantly, ALDH activity increased in a concentration-dependent manner, being negatively correlated with MDA levels, indicating MDA metabolism by ALDH. In the gills, diesel exposure increased MDA and lipid hydroperoxide levels, and promoted increases in antioxidant defenses, indicating oxidative stress. Curiously, ALDH activity was undetectable in the gills, supporting the possibility of direct MDA excretion in the water by the gills. Analyses of MDA in the water revealed increased levels of MDA in the aquaria in which the fish were exposed to diesel, compared to control aquaria. A second experiment was carried out in which the fish were intraperitoneally injected with MDA (10 mg/kg) and analyzed after 1, 6, and 12 h. MDA injection caused a time-dependent decrease in hepatic MDA levels, did not alter ALDH, CAT, GPx, and GST activities, and decreased G6PDH activity and tGSH levels. In the gills, MDA injection caused a slight increase in MDA levels after 1 h, but did not alter GPx, G6PDH, and GST activities. MDA injection also enhanced CAT activity and tGSH levels in the gills. MDA concentration in water increased progressively after 1, 6, and 12 h, supporting the hypothesis of direct MDA excretion as an alternative route for MDA elimination in fish. Our results suggest that the decreased MDA levels after exposure of lambari to diesel oil pollutant probably reflects an association between enhanced antioxidant protection, MDA metabolism, and MDA excretion in water.
丙二醛(MDA)水平的升高通常被认为是脂质过氧化的指标,脂质过氧化是由鱼类暴露于污染物所引起的氧化应激损伤导致的。然而,也有报道称,在接触外源性物质后 MDA 水平会降低,这种效应主要归因于抗氧化防御的增强。在本研究中,我们评估了污染物介导的 MDA 降低是否与抗氧化增强有关,或者与肝脏和鳃中的醛脱氢酶(ALDH)对 MDA 的代谢有关,研究对象是暴露于柴油(0.001、0.01 和 0.1 mL/L)的蓝脂鲤(Astyanax altiparanae)。暴露于柴油的蓝脂鲤肝脏中的 MDA 水平降低。肝脏中的抗氧化酶,如过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx)的活性没有变化,而葡萄糖-6-磷酸脱氢酶(G6PDH)的活性降低。相比之下,肝脏中的总谷胱甘肽(tGSH)水平和谷胱甘肽 S-转移酶(GST)的活性增加,这部分支持了对脂质过氧化的抗氧化保护。更重要的是,ALDH 活性呈浓度依赖性增加,与 MDA 水平呈负相关,表明 ALDH 对 MDA 的代谢。在鳃中,柴油暴露增加了 MDA 和脂质氢过氧化物的水平,并促进了抗氧化防御的增加,表明发生了氧化应激。有趣的是,在鳃中未检测到 ALDH 活性,这支持了 MDA 通过鳃直接排泄到水中的可能性。对暴露于柴油的水族箱中的水进行 MDA 分析显示,与对照水族箱相比,MDA 水平升高。进行了第二次实验,其中鱼被腹膜内注射 MDA(10 mg/kg),并在 1、6 和 12 小时后进行分析。MDA 注射导致肝 MDA 水平呈时间依赖性降低,不改变 ALDH、CAT、GPx 和 GST 活性,降低 G6PDH 活性和 tGSH 水平。在鳃中,MDA 注射后 1 小时 MDA 水平略有增加,但不改变 GPx、G6PDH 和 GST 活性。MDA 注射还增强了鳃中的 CAT 活性和 tGSH 水平。注射 MDA 后 1、6 和 12 小时,水中的 MDA 浓度逐渐增加,支持 MDA 作为鱼类 MDA 消除的替代途径直接排泄的假设。我们的结果表明,蓝脂鲤暴露于柴油污染物后 MDA 水平降低可能反映了增强的抗氧化保护、MDA 代谢和 MDA 在水中排泄之间的关联。