scholarly journals Mechanisms and modifiers of methylmercury-induced neurotoxicity

2012 ◽  
Vol 1 (1) ◽  
pp. 32-38 ◽  
Author(s):  
Stephanie J. B. Fretham ◽  
Samuel Caito ◽  
Ebany J. Martinez-Finley ◽  
Michael Aschner
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Environmental Factors ◽  
Genetic Polymorphisms ◽  
Experimental Studies ◽  
Mehg Exposure ◽  
Complete Understanding ◽  
Cellular Processes ◽  
Gene Environment ◽  
Genetic And Environmental Factors

Abstract The neurotoxic consequences of methylmercury (MeHg) exposure have long been known, however a complete understanding of the mechanisms underlying this toxicity is elusive. Recent epidemiological and experimental studies have provided mechanistic insights into the contribution of genetic and environmental factors that interact with MeHg to modify toxicity. This review will outline cellular processes directly and indirectly affected by MeHg, including oxidative stress, cellular signaling and gene expression, and discuss epigenetic modifications, genetic polymorphisms and gene–environment interactions capable of modifying MeHg neurotoxicity.

scholarly journals Impact of Gene–Environment Interactions on Cancer Development

2020 ◽  
Vol 17 (21) ◽  
pp. 8089
Author(s):  
Ariane Mbemi ◽  
Sunali Khanna ◽  
Sylvianne Njiki ◽  
Clement G. Yedjou ◽  
Paul B. Tchounwou
Keyword(s):  
Environmental Factors ◽  
Scientific Evidence ◽  
Critical Role ◽  
Experimental Studies ◽  
Joint Effect ◽  
Human Diseases ◽  
Nucleotide Polymorphisms ◽  
Gene Environment ◽  
Genetic And Environmental Factors ◽  
The Impact

Several epidemiological and experimental studies have demonstrated that many human diseases are not only caused by specific genetic and environmental factors but also by gene–environment interactions. Although it has been widely reported that genetic polymorphisms play a critical role in human susceptibility to cancer and other chronic disease conditions, many single nucleotide polymorphisms (SNPs) are caused by somatic mutations resulting from human exposure to environmental stressors. Scientific evidence suggests that the etiology of many chronic illnesses is caused by the joint effect between genetics and the environment. Research has also pointed out that the interactions of environmental factors with specific allelic variants highly modulate the susceptibility to diseases. Hence, many scientific discoveries on gene–environment interactions have elucidated the impact of their combined effect on the incidence and/or prevalence rate of human diseases. In this review, we provide an overview of the nature of gene–environment interactions, and discuss their role in human cancers, with special emphases on lung, colorectal, bladder, breast, ovarian, and prostate cancers.

Obesity: epigenetic regulation – recent observations

2015 ◽  
Vol 6 (3) ◽  
pp. 163-175 ◽  
Author(s):  
Marlene Remely ◽  
Ana Laura de la Garza ◽  
Ulrich Magnet ◽  
Eva Aumueller ◽  
Alexander G. Haslberger
Keyword(s):  
Animal Models ◽  
Environmental Factors ◽  
Epigenetic Regulation ◽  
Special Importance ◽  
Epigenetic Mechanisms ◽  
Transgenerational Inheritance ◽  
Obesity Gene ◽  
Epigenetic Modifiers ◽  
Gene Environment ◽  
Genetic And Environmental Factors

AbstractGenetic and environmental factors, especially nutrition and lifestyle, have been discussed in the literature for their relevance to epidemic obesity. Gene-environment interactions may need to be understood for an improved understanding of the causes of obesity, and epigenetic mechanisms are of special importance. Consequences of epigenetic mechanisms seem to be particularly important during certain periods of life: prenatal, postnatal and intergenerational, transgenerational inheritance are discussed with relevance to obesity. This review focuses on nutrients, diet and habits influencing intergenerational, transgenerational, prenatal and postnatal epigenetics; on evidence of epigenetic modifiers in adulthood; and on animal models for the study of obesity.

scholarly journals Impact of Genetic and Environmental Factors on hsCRP Concentrations and Response to Therapeutic Agents

2009 ◽  
Vol 55 (2) ◽  
pp. 256-264 ◽  
Author(s):  
Jian Shen ◽  
Jose M Ordovas
Keyword(s):  
Environmental Factors ◽  
Genetic Polymorphisms ◽  
Genetic Variants ◽  
Inflammatory Marker ◽  
Lipid Lowering ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Fenofibrate Treatment ◽  
Genetic And Environmental Factors ◽  
The Impact

Abstract Background: Inflammation plays an instrumental role in all stages of atherosclerosis. High-sensitivity C-reactive protein (hsCRP), a systemic inflammatory marker, has been gaining recognition as an independent risk factor for cardiovascular disease (CVD). Both baseline hsCRP concentrations and drug-induced hsCRP changes are highly variable and potentially subject to genetic regulation. Content: This review summarizes the current studies examining the effect of genetic and environmental factors on baseline plasma hsCRP concentrations, with a main focus on C-reactive protein, pentraxin-related (CRP) genetic polymorphisms and various dietary components that affect hsCRP concentrations. We also address the association of CRP genetic variations with CVD risk, a relationship that may support or refute the causality of CRP in the atherosclerotic process. Moreover, we discuss the impact of CRP genetic polymorphisms on hsCRP changes in response to 3-week fenofibrate treatment in the genetic intervention of the Genetics of Lipid Lowering Drugs and Diet Network study. Summary: Genetic variants on the CRP locus and other loci and dietary and lifestyle factors are responsible for the interindividual variability of plasma hsCRP concentrations. CRP genetic variants further influence differing plasma hsCRP response after 3-week fenofibrate treatment in patients with metabolic syndrome. Future studies focusing on the influence and interaction of genetic variation on the hsCRP response to dietary and other behavior modification as well as drug treatment could have important implications for the development of more personalized preventive and therapeutic approaches to reduce CVD.

scholarly journals How Nonshared Environmental Factors Come to Correlate with Heredity

2020 ◽  
Author(s):  
Christopher Beam ◽  
Patrizia Pezzoli ◽  
Jane Mendle ◽  
S. Alexandra Burt ◽  
Michael C. Neale ◽  
...  
Keyword(s):  
Environmental Factors ◽  
Genetic Models ◽  
Future Research ◽  
Longitudinal Models ◽  
Behavioral Genetic ◽  
Relative Contribution ◽  
Environment Effects ◽  
Gene Environment ◽  
Genetic And Environmental Factors ◽  
Over Time

Conventional longitudinal behavioral genetic models estimate the relative contribution of genetic and environmental factors to stability and change of traits and behaviors. Longitudinal models rarely explain the processes that generate observed differences between genetically and socially related individuals. We propose that exchanges between people and their environments (i.e., phenotype-environment effects) can explain the emergence of observed differences over time. Such models, however, require violation of the independence assumption of standard behavioral genetic models, that is, uncorrelated genetic and environmental factors (Beam & Turkheimer, 2013; de Kort, Dolan, & Boomsma, 2012; Dolan, De Kort, Van Beijsterveldt, Bartels, & Boomsma, 2014). We review how specification of phenotype-environment effects contributes to understanding observed changes in genetic variability over time and longitudinal correlations among nonshared environmental factors. We then provide an example using 30 days of positive and negative affect scores from an all-female sample of twins. Results demonstrate that the phenotype-environment effects explain how heritability estimates fluctuate as well as how nonshared environmental factors persist over time. We discuss possible mechanisms underlying change in gene-environment correlation over time, the advantages and challenges of including gene-environment correlation in longitudinal twin models, and recommendations for future research.

scholarly journals Early-onset Alzheimer's disease in Scotland: environmental and familial factors

2001 ◽  
Vol 178 (S40) ◽  
pp. s53-s59 ◽  
Author(s):  
Lawrence J. Whalley
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Environmental Factors ◽  
Disease Model ◽  
Environmental Data ◽  
Paternal Age ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Genetic And Environmental Factors

BackgroundAlzheimer's disease (AD) is a common, complex, age-related disorder in which both genetic and environmental factors are important.AimsTo integrate recent studies on genetic and environmental factors in AD into a multi-factorial disease model.MethodDisease models to explain gene-environment interaction in cardiovascular disease are related to observations on AD.ResultsInformative, community-based studies on the genetic epidemiology of AD are rare. Putative risk factors from the Scottish studies include increased paternal age in AD men and coal mining as paternal occupation in both AD and vascular dementia. Migration effects suggest that environmental factors in high-incidence AD areas are important during adult life.ConclusionsThe studies summarised do not provide sufficient data to support a single comprehensive disease model of gene-environment interaction in AD. Future studies will require very large (≥600) sample sizes, molecular genetic analysis, and environmental data that span neurodevelopment and the period between disease onset and appearance of clinical symptoms.

scholarly journals Modeling Obesity and Its Associated Disorders in Drosophila

Physiology ◽  
2013 ◽  
Vol 28 (2) ◽  
pp. 117-124 ◽  
Author(s):  
Irene Trinh ◽  
Gabrielle L. Boulianne
Keyword(s):  
Public Health ◽  
Heart Disease ◽  
Environmental Factors ◽  
Health Problem ◽  
Public Health Problem ◽  
Major Public Health Problem ◽  
Complex Disorder ◽  
Gene Environment ◽  
Life Threatening ◽  
Genetic And Environmental Factors

In recent years, obesity has been recognized as a major public health problem due to its increased prevalence in both children and adults and its association with numerous life-threatening complications including diabetes, heart disease, hypertension, and cancer. Obesity is a complex disorder that is the result of the interaction between predisposing genetic and environmental factors. However, the precise nature of these gene-gene and gene-environment interactions remains unclear. Here, we will describe recent studies demonstrating how fruit flies can be used to identify and characterize the mechanisms underlying obesity and to establish models of obesity-associated disorders.

scholarly journals Etiology of Parkinson's Disease

2003 ◽  
Vol 30 (S1) ◽  
pp. S10-S18 ◽  
Author(s):  
Zhigao Huang ◽  
Raúl de la Fuente-Fernández ◽  
A. Jon Stoessl
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Environmental Factors ◽  
Neurodegenerative Disorders ◽  
Caffeine Intake ◽  
Genetic Mutations ◽  
Abnormal Protein ◽  
Relative Contribution ◽  
Genetic And Environmental Factors

There is growing recognition that Parkinson's disease (PD) is likely to arise from the combined effects of genetic predisposition as well as largely unidentified environmental factors. The relative contribution of each varies from one individual to another. Even in situations where more than one family member is affected, the predominant influence may be environmental. Although responsible for only a small minority of cases of PD, recently identified genetic mutations have provided tremendous insights into the basis for neurodegeneration and have led to growing recognition of the importance of abnormal protein handling in Parkinson's as well as other neurodegenerative disorders. Abnormal protein handling may increase susceptibility to oxidative stress; conversely, numerous other factors, including oxidative stress and impaired mitochondrial function can lead to impaired protein degradation. A limited number of environmental factors are known to be toxic to the substantia nigra; in contrast, some factors such as caffeine intake and cigarette smoking may protect against the development of PD, although the mechanisms are not established. We review the various genetic and environmental factors thought to be involved in PD, as well as the mechanisms that contribute to selective nigral cell death.

scholarly journals THE INTERACTION OF GENETIC AND ENVIRONMENTAL FACTORS IN THE CONTROL OF AMYLASE GENE EXPRESSION IN DROSOPHILA MELANOGASTER

Genetics ◽  
1986 ◽  
Vol 114 (3) ◽  
pp. 943-954
Author(s):  
Bernhard F Benkel ◽  
Donal A Hickey
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Environmental Factors ◽  
Molecular Basis ◽  
Amylase Activity ◽  
Glucose Repression ◽  
Amylase Gene ◽  
Dietary Effects ◽  
Eukaryotic Gene ◽  
Genetic And Environmental Factors

ABSTRACT A number of previous studies have established that amylase activity can vary between Drosophila strains which are maintained under identical laboratory conditions. In addition, we have recently shown that all strains examined so far are subject to glucose repression of amylase activity. In this study, we show that the degree of glucose repression can vary between strains. Moreover, the glucose repression effect is much more pronounced in larvae than in adult flies. Our results lead to the conclusion that the strain-specific differences in activity and the dietary effects are not independent phenomena. These results have implications for the interpretation of many studies on amylase activity variation, including those experiments which have been designed to link amylase activity variations with fitness differences in nature. A question that naturally arises concerns the molecular basis for these strain-specific variations in the degree of glucose repression of this eukaryotic gene.

scholarly journals Transcriptome Sequencing Reveals Widespread Gene-Gene and Gene-Environment Interactions

2014 ◽  
Author(s):  
Alfonso Buil ◽  
Andrew A Brown ◽  
Tuuli Lappalainen ◽  
Ana Viñuela ◽  
Matthew N Davies ◽  
...  
Keyword(s):  
Gene Expression ◽  
Genetic Architecture ◽  
Intermediate Step ◽  
Specific Expression ◽  
Relative Contribution ◽  
Regulatory Variants ◽  
Gene Environment ◽  
Genetic And Environmental Factors ◽  
Proper Estimation ◽  
In Cis

Understanding the genetic architecture of gene expression is an intermediate step to understand the genetic architecture of complex diseases. RNA-seq technologies have improved the quantification of gene expression and allow to measure allelic specific expression (ASE)1-3. ASE is hypothesized to result from the direct effect of cis regulatory variants, but a proper estimation of the causes of ASE has not been performed to date. In this study we take advantage of a sample of twins to measure the relative contribution of genetic and environmental effects on ASE and we found substantial effects of gene x gene (GxG) and gene x environment (GxE) interactions. We propose a model where ASE requires genetic variability in cis, a difference in the sequence of both alleles, but the magnitude of the ASE effect depends on trans genetic and environmental factors that interact with the cis genetic variants. We uncover large GxG and GxE effects on gene expression and likely complex phenotypes that currently remain elusive.

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