Nuclear factor-erythroid 2-related factor-2 (Nrf2) is an important modulator of cellular responses against Cd in mammalian cells. However, whether such modulation is conserved in Marsupenaeus japonicas remains unknown.In our study, the shrimps were injected with dsRNA targeting Nrf2 at 4 μg g⁻¹ body weight (b.w.) or sulforaphane (SFN) at 5 μg g⁻¹ b.w., and then were exposed to 40 mg L⁻¹ CdCl₂ for 48 h. After Nrf2 knockdown, the Cd content increased, but decreased in the SFN group. This suggested that Nrf2 could promote Cd excretion. A terminal deoxynulceotidyl transferase nick-end-labeling (TUNEL) assay revealed that the Nrf2 knockdown increased the number of apoptotic cells in M. japonicas, while SFN decreased the number of apoptotic cells. After Nrf2 knockdown, the total antioxidant capacity (T-AOC), superoxide dismutase (Sod) activity, and related gene expression decreased significantly, while the malondialdehyde (MDA) content increased remarkably. By contrast, SFN injection alleviated the oxidative stress, as evidenced by increased T-AOC, Sod activity, sod mRNA expression and a reduced MDA content. Similarly, detoxification related enzyme activities (ethoxyresorufin O-deethylase and glutathione-S-transferase (GST)) and their corresponding gene expressions (cyp3a (cytochrome P450 family 3 subfamily A) and gst) were suppressed in the ds-Nrf2 injection group, while they were elevated in the SFN group. In addition, ds-Nrf2 activated mitochondrial apoptotic pathway, as evidenced the mRNA and protein levels of caspase-3, Bcl2 associated X protein (Bax), and p53, while SFN treatment suppressed them. These results displayed that in M. japonicus Cd-induced cellular oxidative damage probably acts via the Nrf2 pathway.

核因子-类胡萝卜素2相关因子2（Nrf2）是哺乳动物细胞中针对Cd的细胞反应的重要调节剂。然而，这样的调制是否在保守的囊对虾粳稻遗体unknown.In我们的研究中，进行了虾用dsRNA靶向注射的Nrf2以4μg克^-1体重（BW）或萝卜硫素（SFN）以5μg克^-1体重，和然后暴露于40 mg L ^-1 CdCl ₂中48 h。后Nrf2的击倒，镉含量增加，但SFN组下降。这表明Nrf2可以促进Cd的排泄。终端脱氧核糖核苷酸转移酶缺口末端标记（TUNEL）分析显示Nrf2敲低增加了日本粳稻中凋亡细胞的数量，而SFN减少了凋亡细胞的数量。敲低Nrf2后，总抗氧化能力（T-AOC），超氧化物歧化酶（Sod）活性和相关基因表达显着下降，而丙二醛（MDA）含量显着增加。相比之下，SFN注射减轻了氧化应激，这可以通过增加T-AOC，Sod活性，sod mRNA表达和降低MDA含量来证明。同样，与排毒有关的酶活性（乙氧基resorufin O-脱乙基酶和谷胱甘肽-S-转移酶（GST））及其相应的基因表达（cyp3a（细胞色素P450家族3亚家族A）和gst）在ds-Nrf2注射组中被抑制，而在SFN组中则升高。此外，ds-Nrf2激活了线粒体的凋亡途径，证明caspase-3，Bcl2相关X蛋白（Bax）和p53的mRNA和蛋白水平，而SFN处理抑制了它们的表达。这些结果表明，在日本支原体中， Cd诱导的细胞氧化损伤可能通过Nrf2途径起作用。