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首页> 外文期刊>Metallomics. integrated biometal science >An in vitro examination of selenium-cadmium antagonism using primary cultures of rainbow trout (Oncorhynchus mykiss) hepatocytes
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An in vitro examination of selenium-cadmium antagonism using primary cultures of rainbow trout (Oncorhynchus mykiss) hepatocytes

机译：使用虹鳟鱼（Oncorhynchus mykiss）肝细胞原代培养物对硒-镉拮抗作用的体外研究

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摘要

The present study evaluated the ameliorative properties of selenium (Se) against cadmium (Cd)-induced oxidative stress, using isolated rainbow trout (Oncorhynchus mykiss) hepatocytes in primary culture as the model experimental system. Cadmium (Cd) is known to induce cytotoxic effects by disrupting cellular oxidative homeostasis. On the other hand, selenium (Se) is an essential component of biological antioxidative machinery, and thus may provide protection against the toxic insults of Cd by augmenting the cellular antioxidant response. However, Se, when present above the threshold concentration, can also induce reactive oxygen species (ROS) generation and cause oxidative damage. In this experiment, trout hepatocytes in primary culture were exposed to 100 mu M Cd, alone or in combination with different concentrations (25-500 mu M) of selenite (SeO32-) or selenomethionine (SeMet) for 48 h. Our findings indicated that both chemical forms of Se, at the lowest concentration used (25 mu M), significantly reduced Cd-induced cytotoxicity (measured as cell viability). In contrast, Se at higher concentrations (>= 50 mu M) did not offer any protection against a Cd induced decrease in cell viability. The reduced cytotoxicity of Cd in the presence of 25 mu M selenite or SeMet was associated with reduced intracellular ROS production, recovery of the cellular thiol status (ratio of reduced and oxidized glutathione), and amelioration in the activities of major enzymatic antioxidants (superoxide dismutase, catalase, and glutathione peroxidase). Co-treatment of hepatocytes with Cd and pharmacological antioxidants (TEMPO and NAC) also reduced Cd-induced oxidative stress in trout hepatocytes. This provided further evidence that Se likely ameliorates Cd toxicity via different antioxidative mechanisms.
机译：本研究使用原代培养的虹鳟（Oncorhynchus mykiss）肝细胞作为模型实验系统，评估了硒（Se）对镉（Cd）诱导的氧化应激的改善特性。已知镉（Cd）通过破坏细胞氧化稳态来诱导细胞毒性作用。另一方面，硒（Se）是生物抗氧化机制的重要组成部分，因此可以通过增强细胞的抗氧化剂反应来提供抗Cd毒性伤害的保护作用。但是，当硒的含量超过阈值浓度时，硒也会引起活性氧（ROS）生成并引起氧化损伤。在该实验中，将原代培养的鳟鱼肝细胞单独或与不同浓度（25-500μM）的亚硒酸盐（SeO32-）或硒代蛋氨酸（SeMet）组合暴露于100μM Cd中48 h。我们的发现表明，两种化学形式的最低浓度（25μM）的Se均可显着降低Cd诱导的细胞毒性（以细胞生存力衡量）。相反，较高浓度（> = 50μM）的Se对Cd诱导的细胞活力降低没有任何保护作用。在25μM亚硒酸盐或SeMet存在下，镉的细胞毒性降低与细胞内ROS的产生减少，细胞硫醇状态的恢复（谷胱甘肽还原和氧化的比率）以及主要酶抗氧化剂（超氧化物歧化酶）活性的改善有关。 ，过氧化氢酶和谷胱甘肽过氧化物酶）。肝细胞与镉和药理抗氧化剂（TEMPO和NAC）的共同处理也减少了鳟鱼肝细胞中镉诱导的氧化应激。这提供了进一步的证据，表明硒可能通过不同的抗氧化机制改善了镉的毒性。

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