Caffeine suppresses the expression of the Bcl-2 mRNA in BeWo cell culture and rat placenta

Nomura, Keiko; Saito, Shigeno; Ide, Kazunao; Kamino, Yoshikazu; Sasahara, Hiroshige; Nakamoto, Tetsuo; Abiko, Yoshimitsu

doi:10.1016/j.jnutbio.2003.12.007

Cited by 12 publications

(1 citation statement)

References 48 publications

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“…It is known that Bcl-2 and Bax are important apoptosis-related genes and that a balance in their expression is crucial for the structure and function of the placenta and that a disturbance in this balance may even affect pregnancy outcome. 26 Saito et al 27 demonstrated that caffeine can affect the expression of certain genes (such as Bcl-2 and Bax) in placental cells, especially in the trophoblast. p53 is a tumour suppressor gene that is widely expressed in normal cytotroblasts and syncytiotrophoblasts 28 and causes apoptosis by upregulating the expression of Bax and downregulating the expression of Bcl-2.…”

Section: Discussionmentioning

confidence: 99%

Role of p53‐dependent placental apoptosis in the reproductive and developmental toxicities of caffeine in rodents

Huang

Zhou

Ping

et al. 2012

Clin Exp Pharma Physio

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The aim of the present study was to evaluate the role of placental apoptosis in mediating the reproductive and developmental toxicity of caffeine in rodents. Female Kunming mice were treated with caffeine (60, 120 and 240 mg/kg per day) before and during pregnancy. The conception rate, maternal bodyweight gain, placental weight and indices of fetal developmental, including the rate of intrauterine growth retardation (IUGR; i.e. the actual number of fetuses exhibiting IUGR as a percentage of the total number of fetuses), were determined on gestational day (GD) 18. Female Wistar rats were treated with caffeine (20, 60 and 180 mg/kg per day) from GD11 to GD20. The IUGR rate, maternal plasma angiotensin (Ang) II and prolactin concentrations, placental pathology, expression of angiotensin AT(1) and AT(2) receptors and apoptosis-related proteins were measured on GD20. In mice, caffeine treatment dose-dependently reduced the total conception rate, delayed conception and decreased maternal bodyweight gain, placental weight, fetal bodyweight and fetal body and tail lengths, whereas the IUGR rate was increased. In rats, caffeine treatment dose-dependently decreased placental weight and fetal bodyweight and increased the IUGR rate. Abnormal placental structures and decreased maternal plasma prolactin concentrations were observed following 180 mg/kg per day caffeine treatment, which resulted in increases in renin-angiotensin system (RAS) activity, including maternal plasma AngII concentrations and placental AT(1B) and AT(2) receptor expression, and Bax and p53 expression, but decreases in placental Bcl-2 expression. On the basis of the results of the present study, it appears that caffeine ingestion has detrimental effects on the reproductive system and fetal development in rodents that are associated with chronic activation of the maternal and placental RAS, and induction of p53-dependent placental apoptosis.

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Section: Discussionmentioning

confidence: 99%

Role of p53‐dependent placental apoptosis in the reproductive and developmental toxicities of caffeine in rodents

Huang

Zhou

Ping

et al. 2012

Clin Exp Pharma Physio

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Evaluation of the reproductive and developmental risks of caffeine

Brent

Christian

Diener

2011

Birth Defects Research Pt B

120

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A risk analysis of in utero caffeine exposure is presented utilizing epidemiological studies and animal studies dealing with congenital malformation, pregnancy loss, and weight reduction. These effects are of interest to teratologists, because animal studies are useful in their evaluation. Many of the epidemiology studies did not evaluate the impact of the “pregnancy signal,” which identifies healthy pregnancies and permits investigators to identify subjects with low pregnancy risks. The spontaneous abortion epidemiology studies were inconsistent and the majority did not consider the confounding introduced by not considering the pregnancy signal. The animal studies do not support the concept that caffeine is an abortafacient for the wide range of human caffeine exposures. Almost all the congenital malformation epidemiology studies were negative. Animal pharmacokinetic studies indicate that the teratogenic plasma level of caffeine has to reach or exceed 60 µg/ml, which is not attainable from ingesting large amounts of caffeine in foods and beverages. No epidemiological study described the “caffeine teratogenic syndrome.” Six of the 17 recent epidemiology studies dealing with the risk of caffeine and fetal weight reduction were negative. Seven of the positive studies had growth reductions that were clinically insignificant and none of the studies cited the animal literature. Analysis of caffeine's reproductive toxicity considers reproducibility and plausibility of clinical, epidemiological, and animal data. Moderate or even high amounts of beverages and foods containing caffeine do not increase the risks of congenital malformations, miscarriage or growth retardation. Pharmacokinetic studies markedly improve the ability to perform the risk analyses. Birth Defects Res (Part B) 92:152–187, 2011. © 2011 Wiley-Liss, Inc.

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Intrauterine Programming and Effects of Caffeine

Jiao

Kou

et al. 2017

Diet, Nutrition, and Fetal Programming

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Caffeine suppresses the expression of the Bcl-2 mRNA in BeWo cell culture and rat placenta

Cited by 12 publications

References 48 publications

Role of p53‐dependent placental apoptosis in the reproductive and developmental toxicities of caffeine in rodents

Role of p53‐dependent placental apoptosis in the reproductive and developmental toxicities of caffeine in rodents

Evaluation of the reproductive and developmental risks of caffeine

Intrauterine Programming and Effects of Caffeine

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