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.

中文翻译：

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暴露于柴油的鱼（Astyanax altiparanae）中的丙二醛水平降低：乙醛脱氢酶在肝脏中代谢和在水中排泄的证据。

丙二醛（MDA）含量升高通常被认为是脂质过氧化的指标，该脂质过氧化源自鱼暴露于污染物而引起的氧化应激损伤。但是，也有报告称异源生物暴露后MDA含量降低，这种作用主要归因于抗氧化剂防御能力的增强。在这项研究中，我们评估了污染物介导的MDA降低是否与抗氧化剂的增强或其在肝脏和暴露于柴油（0.001、0.01和0.1）的la（Astyanax altiparanae）g中的醛脱氢酶（ALDH）的代谢有关mL / L）。暴露于柴油的朗巴里肝脏中的MDA水平降低。肝脏中抗氧化酶，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6-磷酸葡萄糖脱氢酶（G6PDH）降低。相反，肝脏中总谷胱甘肽（tGSH）和谷胱甘肽S-转移酶（GST）的活性增加，这部分支持抗脂质过氧化的抗氧化剂保护。更重要的是，ALDH活性以浓度依赖性的方式增加，与MDA水平呈负相关，表明ALDH代谢MDA。在the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能力的增加，表明氧化应激。奇怪的是，AL中没有检测到ALDH活性，这支持了the直接在水中排泄MDA的可能性。对水中MDA的分析表明，鱼暴露于柴油中的水族箱中MDA含量增加，相较于控制水族箱。进行第二个实验，其中向鱼腹膜内注射MDA（10 mg / kg），并在1、6和12小时后进行分析。注射MDA会引起肝脏MDA水平的时间依赖性下降，不会改变ALDH，CAT，GPx和GST活性，并且会降低G6PDH活性和tGSH水平。在the中，注射MDA会在1小时后引起MDA水平的轻微增加，但不会改变GPx，G6PDH和GST的活性。MDA注射还增强了中的CAT活性和tGSH水平。水中MDA浓度在1、6和12小时后逐渐增加，这支持了直接MDA排泄作为鱼类中MDA消除的替代途径的假设。