Oxidized frying oil and its polar fraction fed to pregnant mice are teratogenic and alter mRNA expressions of vitamin A metabolism genes in the liver of dams and their fetuses

Huang, Chin-Fang; Lin, Yu-Shun; Chiang, Zong-Cian; Lu, Shui-Yuan; Kuo, Yueh‐Hsiung; Chang, Sunny Li‐Yun; Chao, Pei-Min

doi:10.1016/j.jnutbio.2014.01.005

Cited by 25 publications

(19 citation statements)

References 44 publications

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“…In accordance with our previous study, ingestion of PO in pregnant WT mice had no significant effect on early embryonic implantation, although it induced congenital malformations in offspring [4]. In addition, PO altered mRNA profiles of genes involved in RA metabolism.…”

Section: Discussionsupporting

confidence: 90%

“…In maternal and fetal livers, a PO diet suppressed Cyp1a1 regardless of genotype, in line with a suppression of AhR transactivation by PO as previously demonstrated in a reporter assay [4]. Though the mRNA levels of Pxr in FO (WT) dams and fetuses were the highest compared to their counterparts in other groups ( p -interaction < 0.05), Cyp3a11 was upregulated by PO diet in dams.…”

Section: Resultssupporting

confidence: 78%

“…We were apparently the first to propose that PO-mediated malformations were associated with perturbed RA metabolism in mothers and fetuses. Indeed, when pregnant mice were given PO throughout gestation, gene expression pattern for RA synthesis (e.g., Rdh10 , Dhrs4 , Raldh1 , and Raldh2 ) as well as RA catabolism (e.g., Cyp2c39 , Cyp26a1 , Cyp26b1 and Cyp26c1 ) in mothers and fetuses deviated from that of their peers (Figure 2 and [4]). Likewise, that the same enzyme families (alcohol dehydrogenase, short-chain dehydrogenase/reductase and RALDHs) were shared for alcohol metabolism and RA synthesis, alcohol might be a competitor for RA synthesis.…”

Section: Discussionmentioning

confidence: 99%

“…Oxidized frying oil (OFO) is essentially an environmental pollutant that can be regarded as a xenobiotic since it is foreign to the body, lipophilic and induces expression of detoxifying CYP450 monoxygenase and phase II conjugation enzymes to facilitate its own catabolism [3]. We recently reported that OFO, specifically, the polar fraction or polar compounds (PO), is teratogenic, and that this effect was associated with disturbed retinoic acid (RA) metabolism in pregnant mice and their fetuses [4]. Nevertheless, underlying mechanisms of disturbed RA metabolic gene expression by PO remain unknown.…”

Section: Introductionmentioning

confidence: 99%

“…We previously reported that PO is a major contributor to peroxisome proliferator-activated receptor α(PPARα) activation by OFO [4]. As a nuclear receptor, PPARα has a pivotal role in regulating systemic lipid homeostasis by modulating an array of target genes participating in lipid catabolism and lipoprotein assembly and transport [17].…”

Section: Introductionmentioning

confidence: 99%

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Peroxisome Proliferator-Activated Receptor α Activation Is Not the Main Contributor to Teratogenesis Elicited by Polar Compounds from Oxidized Frying Oil

Lin

et al. 2017

IJMS

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We previously reported that polar compounds (PO) in cooking oil are teratogenic and perturbed retinoic acid (RA) metabolism. Considering PO as a potent peroxisome proliferator-activated receptor α (PPARα) activator, this study aimed to investigate the role of PPARα in PO-induced teratogenesis and disturbance of RA metabolism. Female PPARα knockout or wild type mice were mated with males of the same genotype. Pregnant mice were fed a diet containing 10% fat from either fresh oil (FO) or PO from gestational day1 to day18, and killed at day18. The PO diet significantly increased the incidence of teratogenesis and fetal RA concentrations, regardless of genotype. Though PPARα deficiency disturbed maternal RA homeostasis, itself did not contribute to teratogenesis as long as FO diet was given. The mRNA profile of genes involved in RA metabolism was differentially affected by diet or genotype in mothers and fetuses. Based on hepatic mRNA levels of genes involved in xenobiotic metabolism, we inferred that PO not only activated PPARα, but also altered transactivity of other xenobiotic receptors. We concluded that PO-induced fetal anomalies and RA accumulation were independent of PPARα activation.

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Section: Discussionsupporting

confidence: 90%

Section: Resultssupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Peroxisome Proliferator-Activated Receptor α Activation Is Not the Main Contributor to Teratogenesis Elicited by Polar Compounds from Oxidized Frying Oil

Lin

et al. 2017

IJMS

Self Cite

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Toxicity of Lipid Oxidation Products Consumed in the Diet

Schaich

2020

Bailey's Industrial Oil and Fat Products

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Toxicity of food components is now under intense scrutiny as the public has become increasingly concerned about the safety of our food supply. Products of lipid oxidation and thermal degradation have long been suspected as potential toxins when consumed in the diet, and numerous changes induced by lipid oxidation products have been reported. However, animals have extensive endogenous protection mechanisms throughout the gastrointestinal system in the liver, and in all tissues, so presumed toxicity must be differentiated from normal physiological metabolism and detoxification. This article reevaluates whether and how oxidizing lipids consumed in foods may or may not be toxic, with focus on levels ingested, modification during digestion, absorption vs action only in the gut, physiological processing, effects of other diet components, and differentiating normal responses from actual toxicity. Recommended guidelines for future research are included.

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