Vitamin E Reversed Apoptosis of Cardiomyocytes Induced by Exposure to High Dose Formaldehyde During Mice Pregnancy

Wu, Dongyuan; Jiang, Zhirong; Gong, Bing; Dou, Yue; Song, Mingxuan; Song, Xiaoxia; Tian, Yu

doi:10.1536/ihj.16-279

Cited by 14 publications

(6 citation statements)

References 31 publications

(35 reference statements)

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“…Of note, treating dams with vitamin E isomer α-Tocopherol prior to the inflammatory insult completely prevented endothelial apoptosis and fetal demise, likely due to the attenuation of placental inflammation. Vitamin E exerts its broad cytoprotective effects as an antioxidant by scavenging reactive oxygen species, inhibiting caspase activity 56,57 , and reducing inflammation [58][59][60][61] . Although the WHO reports no beneficial effect of routine vitamin E supplementation for women with or without a high risk pregnancy 62 , our study suggests that acute vitamin E therapy may be specifically beneficial in pregnancies with underlying inflammation when the women are receiving iron supplementation.…”

Section: Discussionmentioning

confidence: 99%

Iron-dependent apoptosis causes embryotoxicity in inflamed and obese pregnancy

et al. 2021

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Iron is essential for a healthy pregnancy, and iron supplementation is nearly universally recommended, regardless of maternal iron status. A signal of potential harm is the U-shaped association between maternal ferritin, a marker of iron stores, and risk of adverse pregnancy outcomes. However, ferritin is also induced by inflammation and may overestimate iron stores during inflammation or infection. In this study, we use mouse models to determine whether maternal iron loading, inflammation, or their interaction cause poor pregnancy outcomes. Only maternal exposure to both iron excess and inflammation, but not either condition alone, causes embryo malformations and demise. Maternal iron excess potentiates embryo injury during both LPS-induced acute inflammation and obesity-induced chronic mild inflammation. The adverse interaction depends on TNFα signaling, causes apoptosis of placental and embryo endothelium, and is prevented by anti-TNFα or antioxidant treatment. Our findings raise important questions about the safety of indiscriminate iron supplementation during pregnancy.

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Section: Discussionmentioning

confidence: 99%

Iron-dependent apoptosis causes embryotoxicity in inflamed and obese pregnancy

et al. 2021

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“…Injury caused by ischemia-reperfusion after reduction of testicular torsion led to the production of a large number of pro-inflammatory cytokines and cell adhesion molecules, thus causing severe ischemic tissue damage (24,25), which had a great impact on testicular function. After many testicle torsions and reductions, IL-1β and other cytokines were measured in the treatment of ischemia-reperfusion.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of hypothermia and vitamin E on spermatogenic function after reduction of testicular torsion in rats

Wang

Nie

et al. 2020

Exp Ther Med

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This study was designed to investigate the protective effect of hypothermia and vitamin E on spermatogenic function after reduction of testicular torsion in rats. Ninety-six pure inbred male SD rats were divided into group A, B, C and D according to the principle of body weight and birth similarity, with 24 rats in each group. Four groups of rats were respectively twisted on the left testis to establish unilateral testicular torsion rats. Rats in groups A, B, C, D were respectively given normal saline, hypothermia therapy, vitamin E therapy, and hypothermia and vitamin E therapy. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content of the four groups were detected, and the correlation levels of inflammatory factors IL-1β, hs-CRP and related sex hormones luteinizing hormone (LH), follicle-stimulating hormone (FSH), total testosterone (T) were detected by ELISA. Apoptosis of spermatogenic cells of testis in the four groups was detected by flow cytometry. SOD activity and MDA content in groups B, C and D were significantly higher than those in group A, MDA content was significantly lower than that in group A (P<0.05), SOD activity in group D was higher than that in groups B and C, while MDA content was lower than that in groups B and C (P<0.05). The levels of IL-1β and hs-CRP in group A were much higher than those in groups B, C and D (P<0.05). LH and FSH levels in group A were significantly higher than those in groups B, C and D (P<0.05), and in group D were significantly lower than those in groups B and C (P<0.05). Apoptosis rate of spermatogenic cells in group A was significantly higher than that in groups B, C and D (P<0.05). Hypothermia combined with vitamin E can reverse testicular injury in rats and reduce the apoptosis rate of spermatogenic cells.

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“…However, supplementation with vitamin E during pregnancy can reverse the systemic and cardiomyocyte toxicity induced by formaldehyde. This further reveals that the underlying mechanism of formaldehyde‐induced reproduction and developmental toxicity may occur through DNA, chromatin and cell damage (such as cell death or apoptosis) 80 …”

Section: Formaldehyde and Heart Developmentmentioning

confidence: 97%

The cellular function and molecular mechanism of formaldehyde in cardiovascular disease and heart development

Zhang

Yang

et al. 2021

J Cellular Molecular Medi

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As a common air pollutant, formaldehyde is widely present in nature, industrial production and consumer products. Endogenous formaldehyde is mainly produced through the oxidative deamination of methylamine catalysed by semicarbazide‐sensitive amine oxidase (SSAO) and is ubiquitous in human body fluids, tissues and cells. Vascular endothelial cells and smooth muscle cells are rich in this formaldehyde‐producing enzyme and are easily damaged owing to consequent cytotoxicity. Consistent with this, increasing evidence suggests that the cardiovascular system and stages of heart development are also susceptible to the harmful effects of formaldehyde. Exposure to formaldehyde from different sources can induce heart disease such as arrhythmia, myocardial infarction (MI), heart failure (HF) and atherosclerosis (AS). In particular, long‐term exposure to high concentrations of formaldehyde in pregnant women is more likely to affect embryonic development and cause heart malformations than long‐term exposure to low concentrations of formaldehyde. Specifically, the ability of mouse embryos to effect formaldehyde clearance is far lower than that of the rat embryos, more readily allowing its accumulation. Formaldehyde may also exert toxic effects on heart development by inducing oxidative stress and cardiomyocyte apoptosis. This review focuses on the current progress in understanding the influence and underlying mechanisms of formaldehyde on cardiovascular disease and heart development.

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Vitamin E Reversed Apoptosis of Cardiomyocytes Induced by Exposure to High Dose Formaldehyde During Mice Pregnancy

Cited by 14 publications

References 31 publications

Iron-dependent apoptosis causes embryotoxicity in inflamed and obese pregnancy

Iron-dependent apoptosis causes embryotoxicity in inflamed and obese pregnancy

Protective effect of hypothermia and vitamin E on spermatogenic function after reduction of testicular torsion in rats

The cellular function and molecular mechanism of formaldehyde in cardiovascular disease and heart development

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