Displaying publications 1 - 20 of 33 in total

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  1. Abd Aziz CB, Ahmad Suhaimi SQ, Hasim H, Ahmad AH, Long I, Zakaria R
    J Integr Med, 2019 Jan;17(1):66-70.
    PMID: 30591413 DOI: 10.1016/j.joim.2018.12.002
    OBJECTIVE: This study was done to determine whether Tualang honey could prevent the altered nociceptive behaviour, with its associated changes of oxidative stress markers and morphology of the spinal cord, among the offspring of prenatally stressed rats.

    METHODS: Pregnant rats were divided into three groups: control, stress, and stress treated with Tualang honey. The stress and stress treated with Tualang honey groups were subjected to restraint stress from day 11 of pregnancy until delivery. Ten week old male offspring (n = 9 from each group) were given formalin injection and their nociceptive behaviours were recorded. After 2 h, the rats were sacrificed, and their spinal cords were removed to assess oxidative stress activity and morphology. Nociceptive behaviour was analysed using repeated measures analysis of variance (ANOVA), while the levels of oxidative stress parameters and number of Nissl-stained neurons were analysed using a one-way ANOVA.

    RESULTS: This study demonstrated that prenatal stress was associated with increased nociceptive behaviour, changes in the oxidative stress parameters and morphology of the spinal cord of offspring exposed to prenatal stress; administration of Tualang honey reduced the alteration of these parameters.

    CONCLUSION: This study provides a preliminary understanding of the beneficial effects of Tualang honey against the changes in oxidative stress and neuronal damage in the spinal cord of the offspring of prenatally stressed rats.

    Matched MeSH terms: Prenatal Exposure Delayed Effects/metabolism; Prenatal Exposure Delayed Effects/physiopathology*
  2. Abdelwahab SI, Abdul AB, Devi N, Taha MM, Al-zubairi AS, Mohan S, et al.
    Exp. Toxicol. Pathol., 2010 Sep;62(5):461-9.
    PMID: 19581075 DOI: 10.1016/j.etp.2009.06.005
    Cervical cancer is the second most common cause of cancer death in women. We have demonstrated previously that zerumbone (ZER) has an anti-cancer effect towards human cervical cancer cells (HeLa).
    Matched MeSH terms: Prenatal Exposure Delayed Effects
  3. Adamu HA, Imam MU, Ooi DJ, Esa NM, Rosli R, Ismail M
    BMC Complement Altern Med, 2017 Jan 21;17(1):67.
    PMID: 28109299 DOI: 10.1186/s12906-017-1571-0
    The development of insulin resistance is multifactorial, with maternal pre- and postnatal nutrition having significant influences. In this regard, high fat diet (HFD) feeding in pregnancy has been shown to increase risks of metabolic diseases. Thus, we investigated the effects of supplementation of HFD with germinated brown rice (GBR) and GBR-derived gamma oryzanol-rich extract (OE) on insulin resistance and its epigenetic implications in pregnant rats and their offsprings.
    Matched MeSH terms: Prenatal Exposure Delayed Effects*
  4. Andi Asri AA, Lim BK, Lim YK, A Latiff L
    Singapore Med J, 2016 Aug;57(8):470.
    PMID: 27549741 DOI: 10.11622/smedj.2016138
    Matched MeSH terms: Prenatal Exposure Delayed Effects
  5. Brunekreef B, Von Mutius E, Wong GK, Odhiambo JA, Clayton TO, ISAAC Phase Three Study Group
    Int J Epidemiol, 2012 Jun;41(3):753-61.
    PMID: 22287135 DOI: 10.1093/ije/dyr216
    Associations between early life exposure to farm animals and respiratory symptoms and allergy in children have been reported in developed countries, but little is known about such associations in developing countries.
    Matched MeSH terms: Prenatal Exposure Delayed Effects/epidemiology
  6. Chaudhuri JD
    Indian J Med Sci, 2000 Oct;54(10):425-31.
    PMID: 11262858
    It can be concluded that alcohol is definitely harmful to the developing fetus. The effect can manifest in various ways, the most extreme of which is a condition called Fetal Alcohol Syndrome (FAS). The diagnosis of maternal alcoholism leading onto cases of FAS is difficult due to absence of accurate diagnostic tests. The diagnosis of FAS in a child is easier by a proper examination. There is no specific treatment of FAS in a child. The only management is by institution of corrective and rehabilitative measures. The exact mechanism of the teratogenic action of alcohol is not known. It is probably due to the harmful effect of alcohol on the epiblast layer of the bilaminar germ disc. In the absence of adequate knowledge regarding FAS, not much can be done to remedy the deleterious effects of alcohol. Hence, a word of advice to all pregnant women is to avoid drinking during pregnancy.
    Matched MeSH terms: Prenatal Exposure Delayed Effects
  7. Cherian SB, Bairy KL, Rao MS
    Indian J Exp Biol, 2009 Nov;47(11):893-9.
    PMID: 20099462
    With a view to examine the effect of chronic maternal stress on cognitive function in the offspring during young age, pregnant Wistar rats were subjected to restraint stress from embryonic day 11 till delivery. Male and female pups born to these stressed rats were subjected to passive avoidance test on postnatal day 30 and 31. Results were compared with rats of the same age and sex born to control mothers, which were not stressed. The results showed that prenatal maternal restraint stress impairs the memory retention during young age in both sexes. The memory retention deficit induced by maternal restraint stress was evident in the decreased latency to enter the dark compartment of passive avoidance apparatus by the rats born to stressed mothers. The observed behavioral deficit may be due to the insult of stress on the developing hippocampus, a structure of the brain concerned with learning and memory. The results suggest that prolonged prenatal stress leads to long lasting malfunction in the behavioral development during young age in both male and female young rats. However when compared to their respective stress naïve controls, it seems evident that prenatal restraint stress has a less effect on females which could be due to their oesterogenic effects. These data reinforce the view that prenatal stress affects cognitive development in a sex-specific manner.
    Matched MeSH terms: Prenatal Exposure Delayed Effects*
  8. Dantham P, Nuvvula S, Ismail AF, Akkilagunta S, Mallineni SK
    Dent Med Probl, 2024;61(2):209-216.
    PMID: 38668708 DOI: 10.17219/dmp/156655
    BACKGROUND: Several risk factors contribute to the development of dental caries in children, including sociodemographic, dietary, oral hygiene-related and other miscellaneous factors. Maternal smoking was highly associated with dental caries when compared to smoking by fathers or other household members.

    OBJECTIVES: The aim of the study was to determine the prevalence of dental caries and their association with exposure to environmental tobacco smoke (ETS) among 5- to 10-year-old students attending private and government schools.

    MATERIAL AND METHODS: A cross-sectional analytical study was conducted among schoolchildren. Data was collected from the primary caregivers using a pre-tested form to assess the ETS exposure under 5 domains based on history: antenatal exposure; exposure during the index period; exposure in the school neighborhood; exposure in restaurants/roadside stalls; and exposure in bus stops/railway stations. Dental caries was assessed based on the World Health Organization (WHO) guidelines from 1997. The association was reported using prevalence ratios (PRs) (95% confidence interval (CI)).

    RESULTS: Data was obtained from 211 schoolchildren attending government (39.8%) and private schools (60.2%). The overall prevalence (95% CI) of dental caries was 49.3% (42.5-56.1%). Among all the risk factors evaluated in the study, exposure to ETS was associated with a significantly increased risk of dental caries. The adjusted prevalence ratio (APR) of ETS exposure varied with the mother's educational status and high sugar exposure, although this was statistically insignificant.

    CONCLUSIONS: The prevalence of dental caries among schoolchildren aged 5 to 10 years in the city was moderate and similar to the national average. Among the risk factors assessed in the study, antenatal exposure to ETS was found to significantly increase the prevalence of dental caries by 41% after adjusting for other factors. Therefore, it is important to educate parents on the causal role of ETS exposure in dental caries.

    Matched MeSH terms: Prenatal Exposure Delayed Effects/epidemiology
  9. Daud AN, Bergman JE, Kerstjens-Frederikse WS, Groen H, Wilffert B
    Int J Mol Sci, 2016 Aug 13;17(8).
    PMID: 27529241 DOI: 10.3390/ijms17081333
    Serotonin reuptake inhibitors (SRIs) are often prescribed during pregnancy. Previous studies that found an increased risk of congenital anomalies, particularly congenital heart anomalies (CHA), with SRI use during pregnancy have created concern among pregnant women and healthcare professionals about the safety of these drugs. However, subsequent studies have reported conflicting results on the association between CHA and SRI use during pregnancy. These discrepancies in the risk estimates can potentially be explained by genetic differences among exposed individuals. In this review, we explore the potential pharmacogenetic predictors involved in the pharmacokinetics and mechanism of action of SRIs, and their relation to the risk of CHA. In general, the risk is dependent on the maternal concentration of SRIs and the foetal serotonin level/effect, which can be modulated by the alteration in the expression and/or function of the metabolic enzymes, transporter proteins and serotonin receptors involved in the serotonin signalling of the foetal heart development. Pharmacogenetics might be the key to understanding why some children exposed to SRIs develop a congenital heart anomaly and others do not.
    Matched MeSH terms: Prenatal Exposure Delayed Effects/chemically induced*; Prenatal Exposure Delayed Effects/genetics*
  10. 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: Prenatal Exposure Delayed Effects/chemically induced*; Prenatal Exposure Delayed Effects/genetics
  11. David P, Subramaniam K
    PMID: 19452514 DOI: 10.1002/bdra.20593
    Clinical studies and research in animals have established that alcohol consumption during pregnancy produces irreversible developmental anomalies. Deficits in fine motor performance are often noted in infants diagnosed with fetal alcohol syndrome. However, the effects of alcohol on the spinal motoneurons have not been examined. In this study, the morphometric alterations in spinal motoneurons were assessed as a result of prenatal alcohol exposure.
    Matched MeSH terms: Prenatal Exposure Delayed Effects/chemically induced*; Prenatal Exposure Delayed Effects/pathology
  12. Ellis L, Lykins A, Hoskin A, Ratnasingam M
    J Sex Med, 2015 Dec;12(12):2364-77.
    PMID: 26663858 DOI: 10.1111/jsm.13070
    According to neurohormonal theory, prenatal androgens are key determinants of sexual orientation. As a reputed marker for prenatal androgens, the 2D:4D finger length ratio has been used in more than a dozen studies to test the hypothesis that prenatal androgens influence sexual orientation. Findings have been very inconsistent.
    Matched MeSH terms: Prenatal Exposure Delayed Effects/metabolism
  13. Ellis L, Das S
    Int J Offender Ther Comp Criminol, 2013 Aug;57(8):966-84.
    PMID: 22514238 DOI: 10.1177/0306624X12440564
    There is little doubt that family factors can influence involvement in delinquency, although the full nature and extent of their influences remain unclear. In recent decades, testosterone has been increasingly implicated as a contributor to adolescent offending. The present study sought to determine whether two important types of familial factors--parental socioeconomic status and amicable parent-child relationships--are interacting with testosterone (and possibly other androgens) to affect delinquency. A large sample of North American college students self-reported their involvement in eight categories of delinquency along with self-ratings of various androgen-promoted traits (e.g., muscularity and low-deep voice), parental social status, and the quality of the relationships they had with parents. In both sexes, parent-child relationships and androgens were significantly associated with delinquency but parental social status was not. Factor analysis revealed that the authors' measures of all four categories of variables exhibited strong loadings onto their respective factors. Androgens and amicable parent-child relationships were associated with delinquency but parental social status was not. About one third of the influence of parent-child relationships on delinquency appeared to be attributable to androgens. Findings are discussed from the perspective of the evolutionary neuroandrogenic theory of delinquent and criminal behavior.
    Matched MeSH terms: Prenatal Exposure Delayed Effects/blood
  14. Ellis L, Widmayer A, Das S
    Crim Behav Ment Health, 2012 Dec;22(5):325-35.
    PMID: 22696101 DOI: 10.1002/cbm.1828
    BACKGROUND: Several studies have reported significant positive correlations between smoking during pregnancy by mothers and the involvement of their offspring in criminal/delinquent behaviour later in life, but these findings have been described as modest and the criminality based on official conviction statistics.
    AIMS: We sought to verify this relationship and probe for more details on the basis of self-reported offending among college students.
    METHODS: Independently completed questionnaires were collected from 6332 students and their mothers. The students provided information about their delinquent acts, if any, according to eight categories. Their mothers provided retrospective reports of their smoking habits, if any, during pregnancy.
    FINDINGS: Mothers who recalled having smoked during pregnancy were significantly more likely than non-smoking mothers to have offspring who self-reported engaging in some types of delinquency. This relationship was more evident for female offspring than for male offspring and was most pronounced for illegal drug use by the offspring. There was, however, no relationship between offspring offending and estimated number of cigarettes smoked by mothers, month of pregnancy when smoked or consistency of smoking throughout pregnancy.
    CONCLUSION: Overall, our study confirms that maternal smoking during pregnancy is associated with offspring involvement in delinquency, but the lack of critical timing or dose-response relationships between maternal smoking and later offspring delinquency cast doubt on the possibility that the associations are due to teratogenic effects of tobacco smoke.
    Study site: college students at 20 US and two Canadian universities
    Matched MeSH terms: Prenatal Exposure Delayed Effects/psychology*
  15. Ellis L, Skorska MN, Bogaert AF
    Laterality, 2017 Mar;22(2):157-180.
    PMID: 26932806 DOI: 10.1080/1357650X.2016.1151024
    BACKGROUND: Some evidence suggests that prenatal androgens influence both handedness and sexual orientation. This study sought to clarify how androgens, handedness, and sexual orientation are interrelated.

    METHODS: Data were obtained from large samples of students enrolled at universities in Malaysia and the US, including self-reported information on handedness, sexual orientation, and five somatic markers of prenatal androgen exposure (2D:4D, height, strength, muscularity, and athletic ability). Factor analysis of these somatic markers yielded two factors: a muscular coordination and a bone growth factor.

    RESULTS: In women, but not in men, ambidextrousness was more prevalent among those with homosexual tendencies. Modest and often complex associations were found between the androgen factors and handedness. Clear links between the androgen factors and sexual orientation were found, especially for muscular coordination. For males and females, intermediate sex-typical androgen exposure was associated with heterosexual preferences.

    CONCLUSIONS: Ambidextrousness appears to be somewhat more common among females with homosexual tendencies, but left-handedness is nearly as strongly associated with heterosexual preferences, particularly in males, as is right-handedness. Factors indicative of prenatal androgen exposure are associated with sexual orientation in theoretically predictable ways, especially for muscular coordination, but associations between prenatal androgens and handedness are complex.

    Matched MeSH terms: Prenatal Exposure Delayed Effects*
  16. George, Mitchel Constance, Murthy, Krishna Dilip, Zainal Arifin Mustapha
    MyJurnal
    Prenatal exposure to chronic stress during critical periods of foetal development produces depression, attention and learning deficits, hormonal imbalances and affects the brain. The effect of prenatal restraint-stress on the postnatal developmental milestones, anthropometric measurements, and the body, brain and adrenal gland weights of the pups were examined and compared with the unrestrained control and the restrained group under the pyramid at postnatal day 10 and 21. Pregnant rats were restrained (9h/day) from gestation day 7 until parturition. Results showed significant delay in the milestones by one day in the restraint control (RC) compared to the unrestrained normal control (NC), while pups of the restrained pyramid (RP) group did not show the delay. Significant decreases in the anthropometric measurements, body and brain weights in RC group were observed at both postnatal days, while the RP group results matched with the NC group. Significant increase in the adrenal weights was found in the RC group compared to NC group and not the RP group. Results suggest prenatal restraint-stress definitely hampers the developmental milestones, anthropometric measurements, and body and brain weights of the young offspring. Results suggest, pyramid environment counteracts and protects the deleterious effects of chronic prenatal stress.
    Matched MeSH terms: Prenatal Exposure Delayed Effects
  17. Haron MN, Mohamed M
    Andrologia, 2016 Jun;48(5):525-31.
    PMID: 26289766 DOI: 10.1111/and.12473
    Exposure to prenatal stress is associated with impaired reproductive function in male rat offspring. Honey is traditionally used by the Malays for enhancement of fertility. The aim of this study was to determine the effect of honey on reproductive system of male rat offspring exposed to prenatal restraint stress. Dams were divided into four groups (n = 10/group): control, honey, stress and honey + stress groups. Dams from honey and honey + stress groups received oral honey (1.2 g kg(-1) body weight) daily from day 1 of pregnancy, meanwhile dams from stress and honey + stress groups were subjected to restraint stress (three times per day) from day 11 of pregnancy until delivery. At 10 weeks old, each male rat offspring was mated with a regular oestrus cycle female. Male sexual behaviour and reproductive performance were evaluated. Then, male rats were euthanised for assessment on reproductive parameters. Honey supplementation during prenatal restraint stress significantly increased testis and epididymis weights as well as improved the percentages of abnormal spermatozoa and sperm motility in male rat offspring. In conclusion, this study might suggest that supplementation of honey during pregnancy seems to reduce the adverse effects of restraint stress on reproductive organs weight and sperm parameters in male rat offspring.
    Matched MeSH terms: Prenatal Exposure Delayed Effects/pathology; Prenatal Exposure Delayed Effects/physiopathology*; Prenatal Exposure Delayed Effects/prevention & control*
  18. Jayachandra S, D'Souza UJ
    J Environ Sci Health B, 2014;49(4):271-8.
    PMID: 24502214 DOI: 10.1080/03601234.2014.868287
    The objective of this research is to study the possible reproductive adverse effects of diazinon on rat offspring exposed in utero and during lactation. Twenty-four Sprague-Dawley female rats (10-12 week old) were randomly assigned to four groups, each consisting of six rats. Group 1 served as the control and these rats were given normal saline orally. Rats in groups 2, 3, and 4 were administered diazinon, dissolved in saline at 10, 15, 30 mg/ kg(-1) body weight, per oral, once daily, during mating, pregnancy and lactation. The male offsprings were examined at puberty and adulthood for body weight, testis weight, epididymis weight, sperm count, motility and morphology, pituitary-gonadal hormone levels. At 30 mg kg(-1) dose, the male offsprings showed a decrease in testicular weight, sperm count, motility, with an increase in abnormal sperm percentage and a decline in pituitary-gonadal hormones, at puberty. Upon attaining adulthood, there was a decrease in testicular weight, sperm count and motility with an increase in abnormal sperm percentage and a decrease in pituitary hormone level. There was evidence of some adverse reproductive effects on the male offspring at the 15 mg/ kg(-1) dose. Most of the adverse effects were irreversible and were evident at both puberty and adulthood in the offsprings, although a few parameters reverted to the normal growth pattern. Diazinon is a reproductive toxicant for male offsprings if exposed during prenatal and postnatal phases.
    Matched MeSH terms: Prenatal Exposure Delayed Effects/metabolism; Prenatal Exposure Delayed Effects/physiopathology*
  19. Jayachandra S, D'Souza UJ
    PMID: 23758154
    The objective of this study was to study the possible reproductive adverse effects of the diazinon on rat offspring exposed in utero and during lactation. Dams were gavaged daily (10, 15, and 30 mg/kg) before mating, during mating, and during pregnancy and lactation in separate groups. Reproductive outcome data of dams were examined. Body weight, testis weight, testicular marker enzyme activities (alkaline phosphatase, acid phosphatase, lactate dehydrogenase, and glucose-6-phosphate dehydrogenase), qualitative and quantitative testicular and epididymal histology, and immunohistochemisty for 3-β-hydroxysteroid dehydrogenase (HSD) were examined in male offspring at puberty and adulthood. The 30-mg/kg dose induced significant adverse effects at both puberty and adulthood in offspring. At puberty the male offspring showed a decrease in testicular weight, degenerative changes, and 3-β-HSD. Moreover, an increase in activity of alkaline and acid phosphatase also was observed. At adulthood, there was a decrease in testicular weight and 3-β-HSD with an increase in the levels of testicular marker enzyme. There was evidence of some adverse reproductive effects in male offspring at the 15-mg/kg dose. Most of the adverse effects were irreversible and were evident at both puberty and adulthood in offspring, although a few parameters reverted back to the normal growth pattern. Hence, diazinon is a reproductive toxicant in male offspring, which caused significant damage to the testes when exposed during prenatal and postnatal life.
    Matched MeSH terms: Prenatal Exposure Delayed Effects/chemically induced*; Prenatal Exposure Delayed Effects/metabolism; Prenatal Exposure Delayed Effects/pathology
  20. Karisnan K, Mahzabin T, Bakker AJ, Song Y, Noble PB, Pillow JJ, et al.
    Am J Physiol Regul Integr Comp Physiol, 2018 04 01;314(4):R523-R532.
    PMID: 29212808 DOI: 10.1152/ajpregu.00150.2017
    The preterm diaphragm is functionally immature compared with its term counterpart. In utero inflammation further exacerbates preterm diaphragm dysfunction. We hypothesized that preterm lambs are more vulnerable to in utero inflammation-induced diaphragm dysfunction compared with term lambs. Pregnant ewes received intra-amniotic (IA) injections of saline or 10 mg lipopolysaccharide (LPS) 2 or 7 days before delivery at 121 days (preterm) or ∼145 days (term) of gestation. Diaphragm contractile function was assessed in vitro. Plasma cytokines, diaphragm myosin heavy chain (MHC) isoforms, and oxidative stress were evaluated. Maximum diaphragm force in preterm control lambs was significantly lower (22%) than in term control lambs ( P < 0.001). Despite similar inflammatory cytokine responses to in utero LPS exposure, diaphragm function in preterm and term lambs was affected differentially. In term lambs, maximum force after a 2-day LPS exposure was significantly lower than in controls (by ~20%, P < 0.05). In preterm lambs, maximum forces after 2-day and 7-day LPS exposures were significantly lower than in controls (by ~30%, P < 0.05). Peak twitch force after LPS exposure was significantly lower in preterm than in controls, but not in term lambs. In term lambs, LPS exposure increased the proportion of MHC-I fibers, increased twitch contraction times, and increased fatigue resistance relative to controls. In preterm diaphragm, the cross-sectional area of embryonic MHC fibers was significantly lower after 7-day versus 2-day LPS exposures. We conclude that preterm lambs are more vulnerable to IA LPS-induced diaphragm dysfunction than term lambs. In utero inflammation exacerbates diaphragm dysfunction and may increase susceptibility to postnatal respiratory failure.
    Matched MeSH terms: Prenatal Exposure Delayed Effects*
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