Hydrocarbons (jet fuel JP-8) induce epigenetic transgenerational inheritance of obesity, reproductive disease and sperm epimutations

Tracey, Rebecca; Manikkam, Mohan; Guerrero-Bosagna, Carlos; Skinner, Michael K.

doi:10.1016/j.reprotox.2012.11.011

Cited by 202 publications

(191 citation statements)

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“…There was a significant increase in ovarian disease in transgenerational F3 generation DDT and vinclozolin lineage rats at one year of age compared to F3 generation controls (Figure 1). Previous studies have shown that transgenerational increases in ovarian disease were detected following exposures to plastic derived compounds bisphenol A (BPA) and phthalates (DBT & DEHP) [26], dioxin (TCCD) [25], pesticides permethrin and DEET [27], jet fuel hydrocarbons [28], and methoxychlor [29], with nearly 100% disease frequency. Therefore, the transgenerational inheritance of increased ovarian disease can occur after exposure to a variety of environmental toxicants.…”

Section: Resultsmentioning

confidence: 99%

Environmental toxicant induced epigenetic transgenerational inheritance of ovarian pathology and granulosa cell epigenome and transcriptome alterations: ancestral origins of polycystic ovarian syndrome and primary ovarian insufficiency

et al. 2018

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Two of the most prevalent ovarian diseases affecting women’s fertility and health are Primary Ovarian Insufficiency (POI) and Polycystic Ovarian Syndrome (PCOS). Previous studies have shown that exposure to a number of environmental toxicants can promote the epigenetic transgenerational inheritance of ovarian disease. In the current study, transgenerational changes to the transcriptome and epigenome of ovarian granulosa cells are characterized in F3 generation rats after ancestral vinclozolin or DDT exposures. In purified granulosa cells from 20-day-old F3 generation females, 164 differentially methylated regions (DMRs) (P < 1 x 10−6) were found in the F3 generation vinclozolin lineage and 293 DMRs (P < 1 x 10−6) in the DDT lineage, compared to controls. Long noncoding RNAs (lncRNAs) and small noncoding RNAs (sncRNAs) were found to be differentially expressed in both the vinclozolin and DDT lineage granulosa cells. There were 492 sncRNAs (P < 1 x 10−4) in the vinclozolin lineage and 1,085 sncRNAs (P < 1 x 10−4) in the DDT lineage. There were 123 lncRNAs and 51 lncRNAs in the vinclozolin and DDT lineages, respectively (P < 1 x 10−4). Differentially expressed mRNAs were also found in the vinclozolin lineage (174 mRNAs at P < 1 x 10−4) and the DDT lineage (212 mRNAs at P < 1 x 10−4) granulosa cells. Comparisons with known ovarian disease associated genes were made. These transgenerational epigenetic changes appear to contribute to the dysregulation of the ovary and disease susceptibility that can occur in later life. Observations suggest that ancestral exposure to toxicants is a risk factor that must be considered in the molecular etiology of ovarian disease.

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Section: Resultsmentioning

confidence: 99%

Environmental toxicant induced epigenetic transgenerational inheritance of ovarian pathology and granulosa cell epigenome and transcriptome alterations: ancestral origins of polycystic ovarian syndrome and primary ovarian insufficiency

et al. 2018

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“…Differential methylation of genome-wide DMRs in sperm gene promoters of F3 generation Rat Maternal exposure to jet fuel JP-8 hydrocarbon during pregnancy [292] Increased primordial follicle loss and kidney, prostate, pubertal and polycystic ovarian abnormalities [103] Higher methylation in IGF2 P3 in maternal blood than in cord blood, and higher IGF2 P2 methylation in cord blood than in maternal blood. P2 and P3 methylation correlated with serum levels of vitamin B12 in mother's blood, but not in cord blood P2 methylation correlated with mother's smoking history and weight gain during pregnancy Human Survey of folic acid intake before and during pregnancy using self-administered questionnaire, and association with methylation levels of IGF2/H19 DMRs in cord blood [104] Decreased methylation levels at the H19 DMR with increasing folic acid intake before and during pregnancy…”

Section: Hypomethylation Of the Pancreatic Il13ra2 Genementioning

confidence: 99%

“…[280][281][282][283][284] Other commonly available environmental and air pollutants including pesticides, agricultural chemicals, and others have also been shown to induce extensive epigenetic changes that are inherited transgenerationally with consequent increases in the risk of adult NCCDs. [285][286][287][288][289][290][291][292] From the beginning of the industrial revolution, humans have undoubtedly been exposed to a wide range of chemicals and environmental pollutants that could have programed the risk of many diseases in different communities. Moreover, at the beginning of the industrial revolution no legislations were available to control the industrial production of many pollutants or the use of chemicals to manufacture materials for domestic use as we have today.…”

Section: Smoking Alcohol Pollutants and Other Environmental Chemicalsmentioning

confidence: 99%

The Impact of Traditional Food and Lifestyle Behavior on Epigenetic Burden of Chronic Disease

Imam

Ismail

2017

Global Challenges

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There are already extensive reviews on the global burden of NCCDs in the public domain. [1][2][3][4][5][6] The consensus that can be surmised from the available data on NCCDs is that their overall prevalence appears to be rising globally and the projections indicate an upward trend. Epidemiological transition data suggests that the morbidity and mortality rate from these diseases is far more than that of communicable diseases in the developed world [7] and a similar trend is now occurring in the low to medium income countries (LMICs). [8] Among the NCCDs, cardiovascular diseases (CVDs) are the leading causes of morbidity and mortality, followed closely by metabolic diseases like Noncommunicable chronic diseases (NCCDs) are the leading causes of morbidity and mortality globally. The mismatch between present day diets and ancestral genome is suggested to contribute to the NCCDs burden, which is promoted by traditional risk factors like unhealthy diets, physical inactivity, alcohol and tobacco. However, epigenetic evidence now suggests that cumulatively inherited epigenetic modifications may have made humans more prone to the effects of present day lifestyle factors. Perinatal starvation was widespread in the 19th century. This together with more recent events like increasing consumption of western and low fiber diets, smoking, harmful use of alcohol, physical inactivity, and environmental pollutants may have programed the human epigenome for higher NCCDs risk. In this review, on the basis of available epigenetic data it is hypothesized that transgenerational effects of lifestyle factors may be contributing to the current global burden of NCCDs. Thus, there is a need to reconsider prevention strategies so that the subsequent generations will not have to pay for our sins and those of our ancestors. Cardiovascular DiseasesDr. M. U. Imam

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“…Epidemiologically, the majority of environmental factors, including geographical regions, stress, nutrition and toxicants, affect malignant diseases by inducing epigenetic modifications (8). Additionally, the environmental factors include race, climate, life style, diet, nutritional factors (9), airborne polycyclic aromatic hydrocarbons (10), toxicants (e.g., cocaine) (11), alcohol (5), fungicides or pesticides (e.g., dicofol and vinclozolin) (12), aflatoxin (13), bacteria (e.g., Helicobacter Pylori), viruses (e.g., hepatitis virus) (14), heavy metal exposure (e.g., cadmium, arsenic) (15) and endocrine disruptors (e.g., bisphenol-A) (16).…”

Section: Environment Factors and The How To Influence Epigenetic Modimentioning

confidence: 99%

Epigenetic actions of environmental factors and promising drugs for cancer therapy (Review)

Bai

Zhu

et al. 2017

Oncol Lett

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Abstract.Carcinogenesis is known to be primarily associa ted with gene mutations. Recently, increasing evidence has suggested that epigenetic events also serve crucial roles in tumor etiology. Environmental factors, including nutrition, toxicants and ethanol, are involved in carcinogenesis through inducing epigenetic modifications, such as DNA methylation, histone deacetylase and miRNA regulation. Studying epigenetic mechanisms has facilitated the development of early diagnostic strategies and potential therapeutic avenues. Modulation at the epigenetic level, including reversing epigenetic modifications using targeted drugs, has demonstrated promise in cancer therapy. Therefore, identifying novel epigenetic biomarkers and therapeutic targets has potential for the future of cancer therapy. The present review discusses the environmental factors involved in epigenetic modifications and potential drug candidates for cancer therapy.

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Hydrocarbons (jet fuel JP-8) induce epigenetic transgenerational inheritance of obesity, reproductive disease and sperm epimutations

Cited by 202 publications

References 69 publications

Environmental toxicant induced epigenetic transgenerational inheritance of ovarian pathology and granulosa cell epigenome and transcriptome alterations: ancestral origins of polycystic ovarian syndrome and primary ovarian insufficiency

Environmental toxicant induced epigenetic transgenerational inheritance of ovarian pathology and granulosa cell epigenome and transcriptome alterations: ancestral origins of polycystic ovarian syndrome and primary ovarian insufficiency

The Impact of Traditional Food and Lifestyle Behavior on Epigenetic Burden of Chronic Disease

Epigenetic actions of environmental factors and promising drugs for cancer therapy (Review)

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