后代
丙二醛
氧化应激
超氧化物歧化酶
哺乳期
血红素加氧酶
谷胱甘肽过氧化物酶
内分泌学
内科学
活性氧
肾
GPX1型
谷胱甘肽
化学
生物
生物化学
血红素
医学
怀孕
酶
遗传学
作者
Feng Gao,Zhiqiang Guo,Yanan Gao,Chuanqi Wang,Huiting Wang,Xinxin Yao,Baoming Shi
摘要
Abstract BACKGROUND Cooking oil is an indispensable component of the human diet. However, oils usually undergo thermal oxidation. Oxidized soybean oil (OSO) has been shown to have detrimental effects on humans and has emerged as a root cause of many chronic diseases. The objective of this work was to evaluate the effects of puerpera exposure to OSO on kidney damage in the mother and offspring using lactating rats as an experimental model. RESULTS Pathological sections and ultrastructure showed that OSO exposure resulted in various levels of damage to lactating rats and their offspring. OSO induced oxidative stress in the kidneys of lactating rats, as evidenced by increased levels of hydrogen peroxide, interleukin (IL)‐1 β , and IL‐8. OSO increased the activities of glutathione peroxidase and superoxide dismutase. OSO upregulated the expression of apoptosis‐related genes, nuclear factor‐erythroid 2‐related factor 2 (Nrf2), and nuclear factor κ B‐related inflammatory factor genes. In the offspring of the OSO‐exposed mothers, hydrogen peroxide, malondialdehyde, IL‐6, and tumor necrosis factor‐alpha contents were increased. Furthermore, OSO enhanced the levels of Nrf2, NAD(P)H quinone oxidoreductase 1, heme oxygenase 1, and p65 and decreased B‐cell lymphoma 2. CONCLUSION These findings indicated that the kidneys of two generations of rats were compromised by oxidative damage when fed OSO during lactation. This study provides evidence for increasing the genes expression of the Nrf2/heme oxygenase 1 pathway to alleviate the kidney damage caused by OSO in the mother and offspring. © 2021 Society of Chemical Industry.
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