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Intake of Trans-Fat Diet With Prenatal Bisphenol A Exposure Induce Global DNA Methylation in Rats Offspring

Abulehia H, Mohd Nor NS, Sheikh Abdul Kadir SH

Birth Defects Res, 2025 Feb;117(2):e2450.
PMID: 39953946 DOI: 10.1002/bdr2.2450

BACKGROUND: Bisphenol A (BPA) is a ubiquitous industrial compound found in an enormous variety of consumer goods such as plastics, epoxy resins, and thermal paper. Despite its widespread usage, the effects of BPA on the risk and development of metabolic syndrome are not fully understood. Prenatal exposure to BPA has been shown to disrupt the development of offspring's metabolically active tissues and increase their susceptibility to the adverse consequences of a trans-fat diet (TFD).
METHODS: In this experiment, pregnant rats (n = 18) were randomly separated into three groups. These groups were treated from pregnancy day (PD) 2 to PD 21. Subsequently, the male offspring of these rats were provided either a normal-diet (ND) or a TFD from 3rd postnatal week (PNW) to 14th PNW. Then, protein expression of PPAR-γ and global DNA methylation were assessed in the adult rat offspring that were exposed to in utero BPA and subjected to postnatal TFD intake.
RESULTS: The study findings have shown that there was no association between prenatal exposure to BPA and/or TFD consumption and PPAR-γ protein expression within all the study groups in the liver tissue. On the other hand, changes at the molecular level, as reflected by the global DNA hypermethylation induced by prenatal BPA and postnatal TFD intake in adult male SD rat offspring (PNW 14).
CONCLUSIONS: This study underscores the potential impact of prenatal BPA exposure and postnatal TFD intake on epigenetic regulation, as evidenced by global DNA hypermethylation, despite no observable changes in PPAR-γ protein expression. These findings suggest that early-life environmental exposures may predispose individuals to metabolic disruptions, including diabetes and obesity, in adulthood or future generations.

Matched MeSH terms: Maternal Exposure/adverse effects
Fulltext Association between biomass fuel use and maternal report of child size at birth--an analysis of 2005-06 India Demographic Health Survey data

Sreeramareddy CT, Shidhaye RR, Sathiakumar N

BMC Public Health, 2011;11:403.
PMID: 21619613 DOI: 10.1186/1471-2458-11-403

BACKGROUND: Observational epidemiological studies and a systematic review have consistently shown an association between maternal exposure to biomass smoke and reduced birth weight. Our aim was to further test this hypothesis.
METHODS: We analysed the data from 47,139 most recent singleton births during preceding five years of 2005-06 India Demographic Health Survey (DHS). Information about birth weight from child health card and/or mothers' recall) was analysed. Since birth weight was not recorded for nearly 60% of the reported births, maternal self-report of child's size at birth was used as a proxy. Fuel type was classified as high pollution fuels (wood, straw, animal dung, and crop residues kerosene, coal and charcoal), and low pollution fuels (electricity, liquid petroleum gas (LPG), natural gas and biogas). Univariate and multivariable logistic regression models were developed using SURVEYLOGISTIC procedure in SAS system. We used three logistic regression models in which child factors, maternal factors and demographic factors were added step-by-step to the main exposure variable. Adjusted Odds Ratios (AORs) and their 95% CI were calculated. A p-value less than 0.05 was considered as significant.
RESULTS: Child's birth weight was available for only 19,270 (41%) births; 3113 from health card and 16,157 from mothers' recall. For available data, mean birth weight was 2846.5 grams (SD = 684.6). Children born in households using high pollution fuels were 73 grams lighter than those born in households using low pollution fuels (mean birth weight 2883.8 grams versus 2810.7 grams, p < 0.001). Use of biomass fuels was associated with size at birth. Unadjusted OR was 1.41 (95% CI, 1.27 1.55). Adjusted OR after controlling for child factors was 1.41 (95% CI 1.29, 1.57). AOR after controlling for both child and maternal factors was 1.21 (95% CI 1.06, 1.32). In final model AOR was 1.07 (95% 0.94, 1.22) after controlling for child, maternal and demographic factors. Gender, birth order, mother's BMI, haemoglobin level and education were significant in all three models.
CONCLUSIONS: Use of biomass fuels is associated with child size at birth. Future studies should investigate this association using more direct methods for measurement of exposure to smoke emitted from biomass fuels and birth weight.

Matched MeSH terms: Maternal Exposure/adverse effects*
Early life secondhand smoke exposure assessed by hair nicotine biomarker may reduce children's neurodevelopment at 2years of age

Mohamed NN, Loy SL, Lim PY, Al Mamun A, Jan Mohamed HJ

Sci Total Environ, 2018 Jan 01;610-611:147-153.
PMID: 28803192 DOI: 10.1016/j.scitotenv.2017.08.030

Exposure to secondhand smoke (SHS) can affect fetal brain development as well as subsequent neurodevelopment. This study aimed to determine the association between prenatal and postnatal SHS exposure with children's neurodevelopment at 2years of age. Among 107 mother-child pairs from a Malaysia prospective cohort, prenatal and postnatal SHS exposure was determined based on maternal and child hair nicotine concentrations. Multiple linear regressions were used to determine the association between prenatal and postnatal levels of nicotine in maternal and children's' hair with children's neurodevelopment. After adjustment for confounders, prenatal nicotine concentration levels were negatively associated with communication (β=-2.059; p=0.015) and fine motor skills (β=-2.120; p=0.002) while postnatal nicotine concentration levels were inversely associated with fine motors (β=-0.124; p=0.004) and problem solving skills (β=-0.117; p=0.013). In conclusion, this study suggests that early life exposure to SHS may affect children's neurodevelopment.

Matched MeSH terms: Maternal Exposure/adverse effects*
Adverse effects of melatonin on rat pups of Wistar-Kyoto dams receiving melatonin supplementation during pregnancy

Singh HJ, Keah LS, Kumar A, Sirajudeen KN

Exp. Toxicol. Pathol., 2012 Nov;64(7-8):751-2.
PMID: 21354772 DOI: 10.1016/j.etp.2011.01.011

This report documents an incidental finding during a study investigating the effects of melatonin supplementation on the development of blood pressure in SHR. Administration of 10 mg/kg/day of melatonin in drinking water during pregnancy to Wistar-Kyoto (WKY) dams caused a loss of more than 50% of the pups by the age of three weeks and 95% by the age of 6 weeks. There was no maternal morbidity or mortality in the two strains or death of any of the SHR pups. No obvious physical defects were present but mean body weight was lower in the surviving WKY rats when compared to that of melatonin supplemented SHR or non-supplemented WKY pups. The reason for the high mortality in WKY pups is uncertain and appears to be strain if not batch specific. There is a need for caution in its use, particularly during pregnancy, and clearly necessitates more detailed studies.

Matched MeSH terms: Maternal Exposure/adverse effects*
Maternal dexamethasone exposure inhibits the gonadotropin-releasing hormone neuronal movement in the preoptic area of rat offspring

Lim WL, Soga T, Parhar IS

Dev Neurosci, 2014;36(2):95-107.
PMID: 24713635 DOI: 10.1159/000360416

Migration and final positioning of gonadotropin-releasing hormone (GnRH) neurons in the preoptic area (POA) is critical for reproduction. It is known that maternal dexamethasone (DEX) exposure impairs reproductive function and behaviour in the offspring. However, it is still not known whether maternal DEX exposure affects the postnatal GnRH neurons in the offspring. This study determined the neuronal movement of enhanced green fluorescent protein (EGFP)-tagged GnRH neurons in slice culture of postnatal day 0 (P0), P5 and P50-60 transgenic male rats. Effect of maternal DEX treatment on EGFP-GnRH neuronal movement and F-actin distribution on GnRH neurons at P0 stage were studied. Time-lapse analysis of P0 and P5 EGFP-GnRH neurons displayed active cellular movement within the POA compared to young adult P50-60 stages, suggesting possible fine-tuning movement for positioning of early postnatal GnRH neurons. The DEX-treated EGFP-GnRH neurons demonstrated decreased motility in the POA and reduced F-actin distribution in the GnRH neurons at 60 h culture compared to the vehicle-treated. These results suggest that the P0 GnRH neuronal movement in the POA is altered by maternal DEX exposure, which possibly disrupts the fine-tuning process for positioning and development of early postnatal GnRH neurons in the brain, potentially linked to reproductive dysfunction in adulthood.

Matched MeSH terms: Maternal Exposure/adverse effects*
Fulltext Prenatal exposure to serotonin reuptake inhibitors and congenital heart anomalies: an exploratory pharmacogenetics study

Daud ANA, Bergman JEH, Kerstjens-Frederikse WS, van der Vlies P, Hak E, Berger RMF, et al.

Pharmacogenomics, 2017 Jul;18(10):987-1001.
PMID: 28639488 DOI: 10.2217/pgs-2017-0036

AIM: To explore the role of pharmacogenetics in determining the risk of congenital heart anomalies (CHA) with prenatal use of serotonin reuptake inhibitors.
METHODS: We included 33 case-mother dyads and 2 mother-only (child deceased) cases of CHA in a case-only study. Ten genes important in determining fetal exposure to serotonin reuptake inhibitors were examined: CYP1A2, CYP2C9, CYP2C19, CYP2D6, ABCB1, SLC6A4, HTR1A, HTR1B, HTR2A and HTR3B.
RESULTS: Among the exposed cases, polymorphisms that tended to be associated with an increased risk of CHA were SLC6A4 5-HTTLPR and 5-HTTVNTR, HTR1A rs1364043, HTR1B rs6296 and rs6298 and HTR3B rs1176744, but none reached statistical significance due to our limited sample sizes.
CONCLUSION: We identified several polymorphisms that might potentially affect the risk of CHA among exposed fetuses, which warrants further investigation.

Matched MeSH terms: Maternal Exposure/adverse effects*