The effects of alcohol on rat placenta

Akay, M. Turan; Koçkaya, E. Arzu

doi:10.1002/cbf.1175

Cited by 22 publications

(14 citation statements)

References 17 publications

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“…Decidual diameter was decreased in certain regions. Placental hypertrophy has been reported as a compensatory reaction to intrauterine growth restriction (IUGR) under an unfavorable maternal environment such as maternal hemorrhage [72], uterine vessel ligation [73], and indomethacin [74] or ethanol exposure [75]. …”

Section: Discussionmentioning

confidence: 99%

Chromium VI − Induced developmental toxicity of placenta is mediated through spatiotemporal dysregulation of cell survival and apoptotic proteins

Banu

Stanley

Sivakumar

et al. 2017

Reproductive Toxicology

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Environmental contamination with hexavalent chromium (CrVI) is a growing problem both in the U.S and developing countries. CrVI is a heavy-metal endocrine disruptor; women working in Cr industries exhibit an increased incidence of premature abortion and infertility. The current study was designed to understand the mechanism of CrVI toxicity on placental cell survival/death pathways. Pregnant mothers were treated with or without CrVI (50 ppm K2Cr2O7) through drinking water from gestational day (GD) 9.5–14.5, and placentas were analyzed on GD 18.5. Results indicated that CrVI increased apoptosis of trophoblasts, vascular endothelium of the metrial glands and yolk sac epithelium through caspase-3 and p53-dependent pathways. CrVI increased apoptosis in labyrinth and basal zones in a caspase-3-independent manner via AIF, and through an ATM-p53-NOXA-PUMA-p27 network. CrVI downregulated cell survival proteins Bcl-2, Bcl-XL and XIAP in the placenta. CrVI disrupts placental histoarchitecture and increases cell death by spatiotemporal modulation of apoptotic signaling.

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Section: Discussionmentioning

confidence: 99%

Chromium VI − Induced developmental toxicity of placenta is mediated through spatiotemporal dysregulation of cell survival and apoptotic proteins

Banu

Stanley

Sivakumar

et al. 2017

Reproductive Toxicology

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“…The average peak blood acetaldehyde concentration is in the range 26–43 µM [12], [15], [16], [34], [42], [43]. Pharmacological studies in animals have used as much as 50–100 mM ethanol administered daily [19]. We have shown that ethanol or acetaldehyde at clinically relevant concentrations (≤40 mM and ≤40 µM respectively) has adverse effects on two key aspects of trophoblast function: proliferation and nutrient transport.…”

Section: Discussionmentioning

confidence: 99%

“…Placental development is significantly altered with increased placental weight in rats following chronic high ethanol (20%v/v) liquid diet [19], [23], [24]. This increase is accompanied by trophoblast morphological irregularities and altered blood vessel development in the nutrient-exchanging labyrinth zone [19]. In sheep on a high ethanol diet, placental transport of system A-dependent α-amino isobutyric acid is reduced [25].…”

Section: Introductionmentioning

confidence: 99%

Detrimental Effects of Ethanol and Its Metabolite Acetaldehyde, on First Trimester Human Placental Cell Turnover and Function

et al. 2014

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Fetal alcohol spectrum disorder (FASD) describes developmental issues from high maternal alcohol intake, which commonly results in fetal growth restriction and long term morbidity. We aimed to investigate the effect of alcohol and acetaldehyde, on the first trimester placenta, the period essential for normal fetal organogenesis. Normal invasion and establishment of the placenta during this time are essential for sustaining fetal viability to term. We hypothesise that alcohol (ethanol) and acetaldehyde have detrimental effects on cytotrophoblast invasion, turnover and placental function. Taurine is an important amino acid for neuronal and physiological development, and so, its uptake was assayed in cells and placental explants exposed to alcohol or acetaldehyde. First trimester villous explants and BeWo cells were treated with 0, 10, 20, 40 mM ethanol or 0, 10, 20, 40 µM acetaldehyde. The invasive capacity of SGHPL4, a first trimester extravillous cytotrophoblast cell line, was unaffected by ethanol or acetaldehyde (p>0.05; N = 6). The cells in-cycle were estimated using immunostaining for Ki67. Proliferating trophoblast cells treated with ethanol were decreased in both experiments (explants: 40% at 20 mM and 40 mM, p<0.05, N = 8–9) (cell line: 5% at 20 mM and 40 mM, p<0.05, N = 6). Acetaldehyde also reduced Ki67-positive cells in both experiments (explants at 40 µM p<0.05; N = 6) (cell line at 10 µM and 40 µM; p<0.05; N = 7). Only in the cell line at 20 µM acetaldehyde demonstrated increased apoptosis (p<0.05; N = 6). Alcohol inhibited taurine transport in BeWo cells at 10 mM and 40 mM (p<0.05; N = 6), and in placenta at 40 mM (p<0.05; N = 7). Acetaldehyde did not affect taurine transport in either model (P<0.05; N = 6). Interestingly, system A amino acid transport in placental explants was increased at 10 µM and 40 µM acetaldehyde exposure (p<0.05; N = 6). Our results demonstrate that exposure to both genotoxins may contribute to the pathogenesis of FASD by reducing placental growth. Alcohol also reduces the transport of taurine, which is vital for developmental neurogenesis.

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“…In spontaneously hypertensive rats, it is induced in response to a poor capacity of the uteroplacental unit for transferring glucose to fetuses 38 . Drug- and chemical-induced compensatory placental hypertrophy is reported in indomethacin-exposed rats 39 and ethanol-exposed rats 40,41 . Secondly, placental hypertrophy is detected in the intact uterus with a decreased number of corpora luteum, implantation sites and fetuses (less than six fetuses in rats) 42 as an implantation-related reaction.…”

Section: Histopathology Of the Placenta In The Ratmentioning

confidence: 99%

“…14). In animal experiments, placental necrosis is induced by such things as valproate acid 50 , chlorpromazine 51 , glucocorticoid 52 , streptozotocin 53 , cadmium 54 , ethanol 40 , lead acetate 55 , diethylstilbestrol, estrogen, tobacco, adrenomedullin antagonist, cocaine and vitamin E-deficiency. Histopathologically, placental necrosis appears more commonly in the trophoblasts in the labyrinth zone.…”

Section: Histopathology Of the Placenta In The Ratmentioning

confidence: 99%

Toxicological Pathology in the Rat Placenta

et al. 2011

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The placenta grows rapidly for a short period with high blood flow during pregnancy and has multifaceted functions, such as its barrier function, nutritional transport, drug metabolizing activity and endocrine action. Consequently, the placenta is a highly susceptible target organ for drug- or chemical-induced adverse effects, and many placenta-toxic agents have been reported. However, histopathological examination of the placenta is not generally performed, and the placental toxicity index is only the placental weight change in rat reproductive toxicity studies. The placental cells originate from the trophectoderm of the embryo and the endometrium of the dam, proliferate and differentiate into a variety of tissues with interaction each other according to the development sequence, resulting in formation of a placenta. Therefore, drug- or chemical-induced placental lesions show various histopathological features depending on the toxicants and the exposure period, and the pathogenesis of placental toxicity is complicated. Placental weight assessment appears not to be enough to evaluate placental toxicity, and reproductive toxicity studies should pay more attention to histopathological evaluation of placental tissue. The detailed histopathological approaches to investigation of the pathogenesis of placental toxicity are considered to provide an important tool for understanding the mechanism of teratogenicity and developmental toxicity with embryo lethality, and could benefit reproductive toxicity studies.

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The effects of alcohol on rat placenta

Cited by 22 publications

References 17 publications

Chromium VI − Induced developmental toxicity of placenta is mediated through spatiotemporal dysregulation of cell survival and apoptotic proteins

Chromium VI − Induced developmental toxicity of placenta is mediated through spatiotemporal dysregulation of cell survival and apoptotic proteins

Detrimental Effects of Ethanol and Its Metabolite Acetaldehyde, on First Trimester Human Placental Cell Turnover and Function

Toxicological Pathology in the Rat Placenta

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