Maternal Exposure to Ethanol During Pregnancy and Lactation Affects Glutamatergic System and Induces Oxidative Stress in Offspring Hippocampus

Cesconetto, Patrícia Acordi; Andrade, Camila Marques de; Cattani, Daiane; Domingues, Juliana Tonietto; Parisotto, Eduardo Benedetti; Filho, Danilo Wilhelm; Zamoner, Ariane

doi:10.1111/acer.12917

Cited by 17 publications

(7 citation statements)

References 48 publications

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“…Oxidative stress, which has been strongly implicated in congenital heart defect, is a potent apoptotic inducer (Wu et al 2016). In line with previous studies, as shown in the heart (Shirpoor et al 2015) and other tissues (Cesconetto et al 2016;Nogales et al 2017;Shirpoor et al 2014), we demonstrated that maternal ethanol exposure disrupted the oxidative balance in the myocardial tissue of the pups that was manifested by increasing the MDA and decreasing the TAC content.…”

Section: Discussionsupporting

confidence: 93%

Ethanol exposure in prenatal and early postnatal induced cardiac injury in rats: involvement of oxidative stress, Hsp70, ERK 1/2, JNK, and apoptosis in a 3-month follow-up study

Shirpoor

Gaderi

Naderi

2019

Cell Stress and Chaperones

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Alcohol exposure during pregnancy induces a wide range of structural and functional abnormalities in the fetal heart. However, the underlying mechanism of this phenomenon is not well known. This study was undertaken to elucidate probable mechanisms of myocardial damage induced by prenatal and early postnatal ethanol treatment. Pregnant Wistar rats received ethanol 4.5 g/kg BW once per day from the seventh day of gestation (GD7) throughout lactation. The oxidative stress injury of the myocardium in pups was evaluated by measuring levels of oxidative stress biomarkers. Histopathological examinations and Western blot were performed to evaluate histological features, apoptosis, and molecular alterations in the myocardial tissue of male pups on the postnatal day 21 (PN-21) and postnatal day 90 (PN-90). The results showed that maternal ethanol consumption caused oxidative stress (impaired total antioxidant capacity and malondialdehyde), histological changes, and apoptosis of the myocardium in the pups on PN-21 and PN-90. At the molecular levels, Western blot analysis revealed that ethanol modulated the protein expression of p-ERK1/2, p-JNK, and Hsp70 in the myocardial tissue of the pups after 21 and 90 days of birth compared with the controls. These findings revealed that maternal ethanol intake induced cardiac toxicity in part, mediated by oxidative stress and apoptosis in the pups. A further mechanism study revealed that ethanol enhanced ERK1/2 and JNK phosphorylation and Hsp70 protein expression.

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Section: Discussionsupporting

confidence: 93%

Ethanol exposure in prenatal and early postnatal induced cardiac injury in rats: involvement of oxidative stress, Hsp70, ERK 1/2, JNK, and apoptosis in a 3-month follow-up study

Shirpoor

Gaderi

Naderi

2019

Cell Stress and Chaperones

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“…Similar to previous studies using standard chow (29)(30)(31)(32) , maternal EtOH consumption during pregnancy decreased body (3.7% at PD3; 5.1% at PD7), brain (5.8%) and liver weights (5.7%) of pups born to dams fed chow, but these results did not reach statistical significance. In an earlier study, it was reported that maternal EtOH consumption from GD14 to GD19 significantly decreased body weight in fetuses but not in postnatal pups (33) .…”

Section: Effects Of Maternal Diet and Etoh On Birth Outcomessupporting

confidence: 79%

Differential effects of maternal diets on birth outcomes and metabolic parameters in rats after ethanol consumption during pregnancy

et al. 2020

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Maternal nutrition status plays an important role in the development of fetal alcohol spectrum disorders (FASD), but its direct evidence is lacking. This study compared a standard chow with a semi-purified energy-dense (E-dense) diet on birth and metabolic outcomes in rats after ethanol (EtOH) consumption during pregnancy. Pregnant Sprague–Dawley rats were randomised into four groups: chow (n 6), chow + EtOH (20 %, v/v) (n 7), E-dense (n 6) and E-dense + EtOH (n 8). Birth outcomes including litter size, body and organ weights were collected. Metabolic parameters were measured in dams and pups at postnatal day (PD) 7. Maternal EtOH consumption decreased body weights (P < 0·0001) and litter sizes (P < 0·05) in chow-fed dams. At PD7, pups born to dams fed the E-dense diet had higher body (P < 0·002) and liver weights (P < 0·0001). These pups also had higher plasma total cholesterol (P < 0·0001), TAG (P < 0·003) and alanine aminotransferase (P < 0·03) compared with those from chow-fed dams. Dams fed the E-dense diet had higher plasma total (P < 0·0001) and HDL-cholesterol (P < 0·0001) and lower glucose (P < 0·0001). EtOH increased total cholesterol (P < 0·03) and glucose (P < 0·05) only in dams fed the E-dense diet. Maternal exposure to the E-dense diet attenuated prenatal EtOH-induced weight loss and produced different metabolic outcomes in both dams and pups. While the long-lasting effects of these outcomes are unknown, this study highlights the importance of maternal diet quality for maternal health and infant growth and suggests that maternal nutrition intervention may be a potential target for alleviating FASD.

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“…In our study, we also tried to explore the relationship between energy metabolism and the decrease in learning and memory ability of rats. LDH and SDH are two important energy metabolism enzymes that can reflect changes in cellular energy metabolism [36][37][38] . Our research found that combined exposure with 1.5 GHz and 4.3 GHz microwave radiation was able to cause a decrease in the activities of LDH and SDH in the hippocampal tissue of rats.…”

Section: Discussionmentioning

confidence: 99%

Effects of 1.5 and 4.3 GHz microwave radiation on cognitive function and hippocampal tissue structure in Wistar rats

Zhu

Wang

et al. 2021

Sci Rep

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Previous studies have shown that single-frequency microwave radiation can lead to cognitive decline in rats. However, few studies have focused on the combined effects of irradiation with different frequencies of microwaves. Our research aimed to investigate the effects of 1.5 GHz and 4.3 GHz microwave radiation, singly and in combination, on cognitive function and hippocampal tissue structure in rats. A total of 140 male Wistar rats were randomly divided into 4 groups: the S group (sham radiation group), L10 group (10 mW/cm2 1.5 GHz group), C10 group (10 mW/cm2 4.3 GHz band group) and LC10 group (10 mW/cm2 1.5 and 4.3 GHz multi-frequency radiation group). For 1–28 days after microwave radiation, we analyzed the average escape latency for the Morris water maze task, electroencephalograms, change in hippocampal tissue structure and ultrastructure, content of the Nissl body in the hippocampus, and activities of lactate dehydrogenase and succinate dehydrogenase. Compared to the S group, all exposure groups showed varying degrees of learning and memory decline and hippocampal structural damage. The results showed that 1.5 GHz and 4.3 GHz microwave radiation was able to induce cognitive impairment and hippocampal tissue damage in rats and combined radiation with both frequencies caused more serious injuries, but none of these damaging effects varied with microwave frequency.

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Maternal Exposure to Ethanol During Pregnancy and Lactation Affects Glutamatergic System and Induces Oxidative Stress in Offspring Hippocampus

Cited by 17 publications

References 48 publications

Ethanol exposure in prenatal and early postnatal induced cardiac injury in rats: involvement of oxidative stress, Hsp70, ERK 1/2, JNK, and apoptosis in a 3-month follow-up study

Ethanol exposure in prenatal and early postnatal induced cardiac injury in rats: involvement of oxidative stress, Hsp70, ERK 1/2, JNK, and apoptosis in a 3-month follow-up study

Differential effects of maternal diets on birth outcomes and metabolic parameters in rats after ethanol consumption during pregnancy

Effects of 1.5 and 4.3 GHz microwave radiation on cognitive function and hippocampal tissue structure in Wistar rats

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