Previous studies illustrated that gibel carp F strain displays better lipid mobilization and antioxidant ability and compared to the A strain. We therefore hypothesized that the F strain would exhibit superior defense to cadmium exposure. Comparative studies were conducted between A and F strains using plasma stress biomarkers, histological observations, and analysis of hepatic molecular events to examine exposure to waterborne Cd (11.9 mg L⁻¹) for 48 h and 96 h. Waterborne Cd exposure stimulated stress response and hepatic metallothionein mRNA induction in both gibel carp strains confirming exposure. Antioxidant responses were stimulated to counteract Cd toxicity, suggested by the upregulation of mRNA levels of genes associated with nuclear factor erythroid 2-related factor 2 (nrf2) signaling. Cd exposure induced endoplasmic reticulum (ER) stress, meanwhile, branches of genes in unfolded protein response (UPR) were activated. Slight time-dependent effects were implied by greater ER stress, UPR, and apoptosis signals with the duration of Cd exposure. Genotype-specific effects were identified, revealing that the F strain showed greater stress at 96 h exposure and higher antioxidant response compared to the A strain, as indicated by the mRNA levels of genes in nrf2 signaling. ER stress and UPR were also stronger in the F strain after Cd exposure. In contrast, the A strain showed higher autophagy and apoptosis response compared to the F strain. Collectively, combined autophagy and apoptosis were triggered under ER stress, which might serve as defense strategies in both gibel carp strains. The F strain showed greater antioxidant detoxification response and UPR to mitigate Cd toxicity, whereas excessive ER stress contributed to higher autophagy and apoptosis in the A strain. The present study uncovered the differential regulation and defense strategies in fish strains exposed to metal exposure.

先前的研究表明，与A株相比，吉贝尔F株显示出更好的脂质动员和抗氧化能力。因此，我们假设F菌株对镉的暴露具有更好的防御作用。使用血浆应激生物标记，组织学观察和肝分子事件分析在A和F菌株之间进行了比较研究，以检查48 h和96 h暴露于水性Cd（11.9 mg L ^-1）的情况。在两个长鳍金枪鱼品系中，水镉暴露刺激了应激反应和肝金属硫蛋白mRNA的诱导，证实了暴露。刺激抗氧化反应以抵消Cd毒性，这是由于与核因子红系2相关因子2（nrf2）信令。镉暴露引起内质网（ER）胁迫，同时，未折叠蛋白反应（UPR）中的基因分支被激活。随着镉暴露时间的延长，ER压力，UPR和凋亡信号暗示了时间依赖性。鉴定出了基因型特异性效应，表明与A菌株相比，F菌株在暴露96 h时表现出更大的压力和更高的抗氧化反应，如nrf2中基因的mRNA水平所示信号。暴露于Cd后的F菌株中ER应力和UPR也较强。相反，与F菌株相比，A菌株显示出更高的自噬和凋亡反应。总的来说，内质网应激下触发了自噬和细胞凋亡的结合，这可能是两种长鳍金枪鱼菌株的防御策略。F菌株表现出更大的抗氧化剂解毒反应和UPR以减轻Cd毒性，而过大的ER应力导致A菌株中较高的自噬和细胞凋亡。本研究揭示了暴露于金属暴露的鱼品系中的不同调控和防御策略。