With regards to cardiovascular health, frequent consumption of fried foods is discouraged, despite a lack of clear evidence of a direct link between eating oxidative frying oil (OFO) and cardiovascular diseases. In this study, male Sprague Dawley rats were exposed to diets containing fresh or fried soybean oil (groups C and O, respectively) from in utero to 28 weeks of age. A subset of rats in group O was supplemented with vitamin E (500 mg/kg of DL-α-tocopherol acetate; group OE) from 8 week of age onward to mitigate oxidative stress associated with OFO ingestion. Echocardiography, cardiac histology and indices associated with ATP production and calcium cycling in cardiac tissues were measured. Compared to group C, there was cardiac hypertrophy, fibrosis and diastolic dysfunction, in groups O and OE, with no differences between the latter two groups. Although cardiac mRNA levels of genes associated with mitochondrial biogenesis and function were increased, there were lower ATP concentrations and higher transcripts of uncoupling proteins in groups O and OE than in group C. In addition, decreases in phosphorylation of phospholamban and Ca²⁺/calmodulin-dependent protein kinase II activity, plus increased protein phosphatase 2A activity in groups O and OE, implied calcium cycling required for cardiac function was disrupted by OFO consumption. We concluded that long-term OFO exposure resulted in cardiac hypertrophy, fibrosis and diastolic dysfunction that was not mitigated by vitamin E supplementation. Underlying mechanisms were partly attributed to inefficient energy production via uncoupled phosphorylation and disrupted calcium cycling.

关于心血管健康，尽管缺乏明确的证据表明食用氧化性煎炸油 (OFO) 与心血管疾病之间存在直接联系，但不鼓励频繁食用油炸食品。在这项研究中，雄性 Sprague Dawley 大鼠在子宫内暴露于含有新鲜或油炸大豆油（分别为 C 组和 O 组）的饮食至 28 周龄。从 8 周龄开始，O 组中的一部分大鼠补充维生素 E（500 mg/kg DL-α-生育酚乙酸酯；OE 组），以减轻与 OFO 摄入相关的氧化应激。测量了超声心动图、心脏组织学和与心脏组织中 ATP 产生和钙循环相关的指标。与C组相比，O组和OE组出现心脏肥大、纤维化和舒张功能障碍，后两组无差异。尽管与线粒体生物发生和功能相关的基因的心脏 mRNA 水平有所增加，但与 C 组相比，O 组和 OE 组的 ATP 浓度较低，解偶联蛋白的转录本较高。此外，受磷蛋白和 Ca ^{2+的磷酸化降低}钙调蛋白依赖性蛋白激酶 II 活性，加上 O 组和 OE 组蛋白磷酸酶 2A 活性增加，暗示心脏功能所需的钙循环被 OFO 消耗破坏。我们得出结论，长期接触 OFO 会导致心脏肥大、纤维化和舒张功能障碍，而补充维生素 E 并不能减轻这种情况。潜在机制部分归因于通过非耦合磷酸化和破坏钙循环产生的低效能量产生。