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103. Effects of dibenzothiophene, a sulfur‐containing heterocyclic aromatic hydrocarbon, and its alkylated congener, 2,4,7‐trimethyldibenzothiophene, on placental trophoblast cell function.

Author

Raez‐Villanueva, Sergio, Perono, Genevieve A., Jamshed, Laiba, Thomas, Philippe J., and Holloway, Alison C.

Subjects
AROMATIC compounds, POLYCYCLIC aromatic hydrocarbons, GAS well drilling, ESTRADIOL, POLYCYCLIC aromatic compounds, CELL physiology, TROPHOBLAST, PROGESTERONE receptors
Abstract

Worldwide demand for petroleum products has resulted in increased oil and gas activities in many countries. Conventional and unconventional oil and gas extraction, production, and transport lead to increased levels of petroleum‐derived polycyclic aromatic hydrocarbons (PAHs) in the environment. PAH exposure has profound effects on reproduction by affecting pathways involved in placental trophoblast cell function and impairing normal placental development and function—key contributors to reproductive success. However, other components found in petroleum and wastewaters from oil and gas extraction, including the sulfur‐containing heterocyclic aromatic compounds such as dibenzothiophene (DBT) and its alkylated derivatives, may also impact reproductive success. The goal of this study was to examine the effect of exposure to DBT, a compound commonly detected in the environment, and one of its alkylated analogues, 2,4,7‐trimethyldibenzothiophene (2,4,7‐DBT), on steroidogenic and angiogenic pathways critical for mammalian development in placental trophoblast cells (HTR‐8/SVneo cells). 2,4,7‐DBT but not DBT increased estradiol output in association with increased tube‐like formation (surrogate for angiogenesis). These changes in angiogenesis did not appear to be related to altered expression of the key placental angiogenic gene targets (ANGPTL4, VEGFA, and PGF). Neither compound showed a concentration related effect on progesterone synthesis or its receptor expression. Our results suggest that 2,4,7‐DBT can disrupt key pathways important for placental trophoblast function and highlight the importance of determining the impact of exposure to both parent and alkylated compounds. Further, these data suggest that exposure to sulfur‐containing heterocyclic aromatic compounds may lead to placental dysfunction and impact reproductive success at environmentally relevant levels. Proximity to oil and gas extraction sites has been associated with impaired reproductive success. Oil and gas extraction is associated with increased detection of dibenzothiophene, a sulfur‐containing heterocyclic aromatic compound, and its alkylated congeners in abiotic matrices and wildlife. We demonstrated that 2,4,7‐trimethyldibenzothiophene but not dibenzothiophene caused dysregulated estradiol output and angiogenesis in placental cells. As these outcomes are linked with placental dysfunction, these results highlight the importance of considering the impact of alkylated polycyclic aromatic compounds on mammalian reproduction. [ABSTRACT FROM AUTHOR]

Published
2021
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104. Maternal Nicotine Exposure Leads to Augmented Expression of the Antioxidant Adipose Tissue Triglyceride Lipase Long-Term in the White Adipose of Female Rat Offspring

Author

Barra, Nicole, VanDuzer, Taylor, Holloway, Alison C, and Hardy, Daniel B

Subjects
Atgl, Pharmacology, adipose, DOHaD, Medical Physiology, nutritional and metabolic diseases, Pharmacy and Pharmaceutical Sciences, nicotine
Abstract

Globally, approximately 10-25% of women smoke during pregnancy. Since nicotine is highly addictive, women may use nicotine containing products like nicotine replacement therapies for smoking cessation, but the long-term consequences of early life exposure to nicotine remain poorly defined. Our laboratory has previously demonstrated that maternal nicotine exposed (MNE) rat offspring exhibit hypertriglyceridemia due to increased hepatic de novo lipogenesis. Hypertriglyceridemia may also be attributed to impaired white adipose tissue (WAT) lipid storage; however, the effects of MNE on WAT are not completely understood. We hypothesize that nicotine-induced alterations in adipose function (e.g. lipid storage) underlie dyslipidemia in MNE adults. Female 6 month old rats exposed to nicotine during gestation and lactation exhibited significantly decreased visceral adipocyte cell area by 40%, attributed, in part, to a 3-fold increase in adipose triglyceride lipase (ATGL) protein expression compared to vehicle. Given ATGL has antioxidant properties and in utero nicotine exposure promotes oxidative stress in various tissues, we next investigated if there was evidence of increased oxidative stress in MNE WAT. At both 3 weeks and 6 months, MNE offspring expressed 37-48% higher protein levels of SOD1 and SOD2 in WAT. Since oxidative stress can induce inflammation, we examined the inflammatory profile of WAT and found increased expression of cytokines (IL-1β, TNFα, and IL-6) by 44-61% at 6 months. Collectively, this suggests that the expression of WAT ATGL may be induced to counter MNE-induced oxidative stress and inflammation. However, higher levels of ATGL would further promote lipolysis in WAT, culminating in impaired lipid storage and long-term dyslipidemia.

Published
2018

108. Prenatal nicotine exposure leads to decreased histone H3 lysine 9 (H3K9) methylation and increased p66shcexpression in the neonatal pancreas

Author

Raez-Villanueva, Sergio, Debnath, Amrita, Hardy, Daniel B., and Holloway, Alison C.

Abstract

AbstractPrenatal exposure to nicotine, tobacco’s major addictive constituent, has been shown to reduce birth weight and increases apoptosis, oxidative stress, and mitochondrial dysfunction in the postnatal pancreas. Given that upregulated levels of the pro-oxidative adapter protein p66shcis observed in growth-restricted offspring and is linked to beta-cell apoptosis, the goal of this study was to investigate whether alterations in p66shcexpression underlie the pancreatic deficits in nicotine-exposed offspring. Maternal administration of nicotine in rats increased p66shcexpression in the neonatal pancreas. Similarly, nicotine treatment augmented p66shcexpression in INS-1E pancreatic beta cells. Increased p66shcexpression was also associated with decreased histone H3 lysine 9 methylation. Finally, nicotine increased the expression of Kdm4c, a key histone lysine demethylase, and decreased Suv39h1, a critical histone lysine methyltransferase. Collectively, these results suggest that upregulation of p66shcthrough posttranslational histone modifications may underlie the reported adverse outcomes of nicotine exposure on pancreatic function.

Published
2022
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109. A risk of bias instrument for non-randomized studies of exposures:A users' guide to its application in the context of GRADE

Author

Morgan, Rebecca L., Thayer, Kristina A., Santesso, Nancy, Holloway, Alison C., Blain, Robyn, Eftim, Sorina E., Goldstone, Alexandra E., Ross, Pam, Ansari, Mohammed, Akl, Elie, Filippini, Tommaso, Hansell, Anna, Meerpohl, Joerg J., Mustafa, Reem A., Verbeek, Jos, Vinceti, Marco, Whaley, Paul Alexander, Schunemann, Holger J., GRADE Working Group, Morgan, Rebecca L., Thayer, Kristina A., Santesso, Nancy, Holloway, Alison C., Blain, Robyn, Eftim, Sorina E., Goldstone, Alexandra E., Ross, Pam, Ansari, Mohammed, Akl, Elie, Filippini, Tommaso, Hansell, Anna, Meerpohl, Joerg J., Mustafa, Reem A., Verbeek, Jos, Vinceti, Marco, Whaley, Paul Alexander, Schunemann, Holger J., and GRADE Working Group

Abstract

The objective of this paper is to explain how to apply, interpret, and present the results of a new instrument to assess the risk of bias (RoB) in non-randomized studies (NRS) dealing with effects of environmental exposures on health outcomes. This instrument is modeled on the Risk Of Bias In Non-randomized Studies of Interventions (ROBINS-I) instrument. The RoB instrument for NRS of exposures assesses RoB along a standardized comparison to a randomized target experiment, instead of the study-design directed RoB approach. We provide specific guidance for the integral steps of developing a research question and target experiment, distinguishing issues of indirectness from RoB, making individual-study judgments, and performing and interpreting sensitivity analyses for RoB judgments across a body of evidence. Also, we present an approach for integrating the RoB assessments within the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) framework to assess the certainty of the evidence in the systematic review. Finally, we guide the reader through an overall assessment to support the rating of all domains that determine the certainty of a body of evidence using the GRADE approach.

Published
2019

110. Early-life chemical exposures and risk of metabolic syndrome

Author

De Long,Nicole E and Holloway,Alison C

Subjects
Targets and Therapy [Diabetes, Metabolic Syndrome and Obesity]
Abstract

Nicole E De Long,Alison C Holloway Department of Obstetrics and Gynecology, McMaster University, Hamilton, ON, Canada Abstract: The global prevalence of obesity has been increasing at a staggering pace, with few indications of any decline, and is now one of the major public health challenges worldwide. While obesity and metabolic syndrome (MetS) have historically thought to be largely driven by increased caloric intake and lack of exercise, this is insufficient to account for the observed changes in disease trends. There is now increasing evidence to suggest that exposure to synthetic chemicals in our environment may also play a key role in the etiology and pathophysiology of metabolic diseases. Importantly, exposures occurring in early life (in utero and early childhood) may have a more profound effect on life-long risk of obesity and MetS. This narrative review explores the evidence linking early-life exposure to a suite of chemicals that are common contaminants associated with food production (pesticides; imidacloprid, chlorpyrifos, and glyphosate) and processing (acrylamide), in addition to chemicals ubiquitously found in our household goods (brominated flame retardants) and drinking water (heavy metals) and changes in key pathways important for the development of MetS and obesity. Keywords: obesity, pesticides, polybrominated diphenyl ethers, heavy metals, acrylamide, endocrine-disrupting chemicals

Published
2017

111. Association of urinary polycyclic aromatic hydrocarbons and obesity in children aged 3–18: Canadian Health Measures Survey 2009–2015.

Author

Bushnik, Tracey, Wong, Suzy L., Holloway, Alison C., and Thomson, Errol M.

Abstract

Polycyclic aromatic hydrocarbons (PAHs) may contribute to obesity. Childhood obesity is a strong predictor of adult obesity and morbidity; however, the relationship between PAHs and obesity in young children (e.g., aged 3–5) has not been studied. We examined the association between urinary PAH metabolites and measures of obesity in children. We analyzed data from 3667 children aged 3–18 years who participated in the Canadian Health Measures Survey (CHMS, 2009–2015). We ran separate multivariable linear models to estimate the association between quartiles of PAH metabolites and each of body mass index (BMI) percentile, waist circumference (WC), and waist-to-height ratio (WHtR) in the total population, as well as in the age subgroups 3–5, 6–11, and 12–18, adjusting for age, sex, ethnicity, education, income quintile, diet, creatinine, and exposure to environmental tobacco smoke. A multinomial logistic regression model estimated adjusted odds ratios for risk of central obesity. BMI, WC, and WHtR were positively associated with total PAH and naphthalene metabolites in the total population aged 3–18 and in age groups 6–11 and 12–18. In 3–5 year olds, WHtR, but not BMI, was significantly associated with total PAH, naphthalene, and phenanthrene metabolites. Overall, those in the highest quartile for naphthalene or total PAH metabolites had three times greater odds of having central obesity compared with those in the lowest quartile. Urinary PAH metabolites are associated with WHtR, an indicator of central obesity and predictor of health risks associated with obesity, in children as young as 3–5. [ABSTRACT FROM AUTHOR]

Published
2020
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116. Intrapartum antibiotics for GBS prophylaxis alter colonization patterns in the early infant gut microbiome of low risk infants

Author

Stearns, Jennifer C., primary, Simioni, Julia, additional, Gunn, Elizabeth, additional, McDonald, Helen, additional, Holloway, Alison C., additional, Thabane, Lehana, additional, Mousseau, Andrea, additional, Schertzer, Jonathan D., additional, Ratcliffe, Elyanne M., additional, Rossi, Laura, additional, Surette, Michael G., additional, Morrison, Katherine M., additional, and Hutton, Eileen K., additional

Published
2017
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120. Early Life Exposures and the Development of the Infant Gut Microbiome: A Review.

Author

Li, Jenifer, Dizzell, Sara E., Jones, Sara L., Kanji, Sarah, Lau, Jennifer T., Mousseau, Andrea, Yousuf, Efrah I., Holloway, Alison C., Ratcliffe, Elyanne M., Stearns, Jennifer C., Morrison, Katherine, and Hutton, Eileen K.

Subjects
ANTIBIOTICS, BACTEROIDES, BIFIDOBACTERIUM, BREASTFEEDING, CHILDBIRTH, CULTURES (Biology), DELIVERY (Obstetrics), HOST-bacteria relationships, MEDICAL databases, INFORMATION storage & retrieval systems, MEDICAL information storage & retrieval systems, MATERNAL health services, EVALUATION of medical care, MEDLINE, PREGNANCY, PREGNANT women, PRENATAL care, VAGINA, SYSTEMATIC reviews, GUT microbiome, PRENATAL exposure delayed effects, CHILDREN
Abstract

Copyright of Canadian Journal of Midwifery Research & Practice is the property of Canadian Association of Midwives and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2019

122. Effect of 17[Beta]-estradiol on the expression of somatostatin genes in rainbow trout (Oncorhynchus mykiss)

Author

HOLLOWAY, ALISON C., MELROE, GREGORY T., EHRMAN, MELISSA M., REDDY, P. KONDA, LEATHERLAND, JOHN F., and SHERIDAN, MARK A.

Subjects
Physiology -- Research, Estradiol -- Physiological aspects, Gene expression -- Research, Somatostatin -- Research, Biological sciences
Abstract

Holloway, Allison C., Gregory T. Melroe, Melissa M. Ehrman, P. Konda Reddy, John F. Leatherland, and Mark A. Sheridan. Effect 17[Beta]-estradiol on the expression of somatostatin genes in rainbow trout (Oncorhynchus mykiss). Am J Physiol Regulatory Integrative Comp Physiol 279: R389-R393, 2000.--In the present study, the effects of 17[Beta]-estradiol ([E.sub.2]) treatment on the expression of preprosomatostatin (PPSS) I, PPSS II', and PPSS II' mRNA in the hypothalamus and endocrine pancreas (Brockmann body), as well as the effects of [E.sub.2] treatment on plasma somatostatin (SS)-14 and -25 concentrations in sexually immature rainbow trout (Oncorhynchus mykiss), were investigated. [E.sub.2] treatment significantly (P [is less than] 0.001) depressed both plasma SS-14 and SS-25. In the hypothalamus, [E.sub.2] treatment significantly (P [is less than] 0.001) decreased the levels of PPSS I and PPSS II' mRNA. However, there was no effect of [E.sub.2] treatment on PPSS II' mRNA levels. In the pancreas, [E.sub.2] treatment had no significant effect on the levels of either PPSS II' mRNA or PPSS II' mRNA. However, [E.sub.2] treatment significantly (P [is less than] 0.005) decreased levels of PPSS I mRNA. Thes data suggest that [E.sub.2] acts, in part, to increase plasma growth hormone levels in rainbow trout by decreasing the endogenous inhibitory somatostatinergic tone by inhibiting plasma levels of both SS-14 abd SS-25 and hypothalamic levels of mRNA encoding these proteins. differential gene regulation

Published
2000

123. Angiogenesis in the Placenta: The Role of Reactive Oxygen Species Signaling

Author

Pereira, Robyn D., De Long, Nicole E., Wang, Ruijun C., Yazdi, Fereshteh T., Holloway, Alison C., and Raha, Sandeep

Subjects
Article Subject, embryonic structures
Abstract

Proper placental development and function are central to the health of both the mother and the fetus during pregnancy. A critical component of healthy placental function is the proper development of its vascular network. Poor vascularization of the placenta can lead to fetal growth restriction, preeclampsia, and in some cases fetal death. Therefore, understanding the mechanisms by which uterine stressors influence the development of the placental vasculature and contribute to placental dysfunction is of central importance to ensuring a healthy pregnancy. In this review we discuss how oxidative stress observed in maternal smoking, maternal obesity, and preeclampsia has been associated with aberrant angiogenesis and placental dysfunction resulting in adverse pregnancy outcomes. We also highlight that oxidative stress can influence the expression of a number of transcription factors important in mediating angiogenesis. Therefore, understanding how oxidative stress affects redox-sensitive transcription factors within the placenta may elucidate potential therapeutic targets for correcting abnormal placental angiogenesis and function.

Published
2015
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125. A comparison of intestinal microbiota in a population of low-risk infants exposed and not exposed to intrapartum antibiotics: The Baby & Microbiota of the Intestine cohort study protocol

Author

Simioni, Julia, primary, Hutton, Eileen K., additional, Gunn, Elizabeth, additional, Holloway, Alison C., additional, Stearns, Jennifer C., additional, McDonald, Helen, additional, Mousseau, Andrea, additional, Schertzer, Jonathan D., additional, Ratcliffe, Elyanne M., additional, Thabane, Lehana, additional, Surette, Michael G., additional, and Morrison, Katherine M., additional

Published
2016
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127. Polyphenol-Rich Extract of Syzygium cumini Leaf Dually Improves Peripheral Insulin Sensitivity and Pancreatic Islet Function in Monosodium L-Glutamate-Induced Obese Rats

Author

Sanches, Jonas R., primary, França, Lucas M., additional, Chagas, Vinicyus T., additional, Gaspar, Renato S., additional, dos Santos, Kayque A., additional, Gonçalves, Luciana M., additional, Sloboda, Deborah M., additional, Holloway, Alison C., additional, Dutra, Richard P., additional, Carneiro, Everardo M., additional, Cappelli, Ana Paula G., additional, and Paes, Antonio Marcus de A., additional

Published
2016
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129. Effect of Atypical Antipsychotics on Fetal Growth: Is the Placenta Involved?

Author

Raha, Sandeep, Taylor, Valerie H., and Holloway, Alison C.

Subjects
Article Subject
Abstract

There is currently considerable uncertainty regarding prescribing practices for pregnant women with severe and persistent psychiatric disorders. The physician and the mother have to balance the risks of untreated psychiatric illness against the potential fetal toxicity associated with pharmacological exposure. This is especially true for women taking atypical antipsychotics. Although these drugs have limited evidence for teratological risk, there are reports of altered fetal growth, both increased and decreased, with maternal atypical antipsychotic use. These effects may be mediated through changes in the maternal metabolism which in turn impacts placental function. However, the presence of receptors targeted by atypical antipsychotics in cell lineages present in the placenta suggests that these drugs can also have direct effects on placental function and development. The signaling pathways involved in linking the effects of atypical antipsychotics to placental dysfunction, ultimately resulting in altered fetal growth, remain elusive. This paper focuses on some possible pathways which may link atypical antipsychotics to placental dysfunction.

Published
2012
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130. Human Cytochrome P450 Liability Studies of trans-Dihydronarciclasine: A Readily Available, Potent, and Selective Cancer Cell Growth Inhibitor

Author

McNulty, James, Thorat, Amol, Vurgun, Nesrin, Nair, Jerald J., Makaji, Emilija, Crankshaw, Denis J., Holloway, Alison C., and Pandey, Siyaram

Abstract

The cytochrome P45O activities of the naturally occurring Amaryllidaceae alkaloid narciclasine (3), isolated from Narcissus pseudonarcissus,and synthetic derivative trans-dihydronarciclasine (5) are reported. While narciclasine was found to possess potent inhibitory activity to human CYP3A4, its dihydro analogue was inactive. This study revealed that the C1−C10b double bond is required for inhibition of this crucial metabolizing enzyme. Compound 5also demonstrated no inhibition of the related human cytochromes CYP19 and CYP1A1. This study elevates the status of trans-dihydronarciclasine (5) as a highly privileged, readily available molecule, with potent and selective anticancer activity.

Published
2024
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134. Interleukin-15 Modulates Adipose Tissue by Altering Mitochondrial Mass and Activity

Author

Barra, Nicole G., primary, Palanivel, Rengasamy, additional, Denou, Emmanuel, additional, Chew, Marianne V., additional, Gillgrass, Amy, additional, Walker, Tina D., additional, Kong, Josh, additional, Richards, Carl D., additional, Jordana, Manel, additional, Collins, Stephen M., additional, Trigatti, Bernardo L., additional, Holloway, Alison C., additional, Raha, Sandeep, additional, Steinberg, Gregory R., additional, and Ashkar, Ali A., additional

Published
2014
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140. Adverse Fetal and Neonatal Outcomes Associated with a Life-Long High Fat Diet: Role of Altered Development of the Placental Vasculature

Author

Hayes, Emily K., primary, Lechowicz, Anna, additional, Petrik, Jim J., additional, Storozhuk, Yaryna, additional, Paez-Parent, Sabrina, additional, Dai, Qin, additional, Samjoo, Imtiaz A., additional, Mansell, Margaret, additional, Gruslin, Andree, additional, Holloway, Alison C., additional, and Raha, Sandeep, additional

Published
2012
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