Long-term consumption of recycled cooking oil induces cell death and tissue damage

被引:2
|
作者
Zhu, Shudong [1 ,2 ]
Zhu, Yan [1 ,3 ]
Li, Hao [2 ]
Wang, Qiuwen [2 ]
Wang, Kuansong [4 ]
Baska, Katelynn [5 ]
Zhang, Dianzheng [5 ]
机构
[1] Nantong Univ, Sch Med, 19 Qixiu Rd, Nantong, Jiangsu, Peoples R China
[2] Cent South Univ, Sch Life Sci, Dept Biochem & Mol Biol, Changsha, Peoples R China
[3] Xuzhou Hlth Res Inst Co Ltd, Xuzhou, Jiangsu, Peoples R China
[4] Cent South Univ, Xiangya Hosp, Dept Pathol, Changsha, Peoples R China
[5] Philadelphia Coll Osteopath Med, Dept Biomed Sci, Philadelphia, PA USA
来源
FASEB JOURNAL | 2021年 / 35卷 / 02期
关键词
apoptosis; C57; mice; DNA damage; recycled cooking oil; toxicity; DNA-DAMAGE;
D O I
10.1096/fj.202000825R
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Recycled cooking oil (RCO) is widely used in many small restaurants. However, the health risk posed by long-term consumption of RCO is unclear. In this study, C57 mice were treated with RCO for 34 weeks. Organ coefficients of the liver, stomach, and kidney were found to be decreased. H&E staining revealed overt lesions in the pancreas, liver, kidney, esophagus, duodenum, and ileum of RCO-treated mice. Immunohistochemistry showed significant DNA damage in the duodenum and ileum and apoptosis in the lungs of the RCO-treated mice. Immunoblotting showed elevated levels of gamma-H2AX, Bcl-2/Bax, TNF alpha, cleaved Caspase-3 and poly ADP-ribose polymerase (PARP). Increased levels of lactate dehydrogenase (LDH) and decreased levels of succinate dehydrogenase (SDH) were also detected. These findings suggest that long-term consumption of RCO produces various toxicities in mice with important implications for humans. DNA damage followed by mitochondria-associated apoptosis, and necrosis is likely to contribute to the toxicities.
引用
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页数:11
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