User:Ramankalaic/sandbox

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Transgenerational epigenetic effects of substance use[edit]

An epigenetic trait is a heritable phenotype arising from chromosomal changes in the absence of DNA sequence alterations.[1] Epigenetic changes can occur over the lifetime of an individual, affecting their own gene expression, but can also occur in an individual's germline cells, transmitting modifications in gene expression to descendants.[2] Lamarckian inheritance, which is the idea of transmitting acquired characteristics to progeny, had fallen out of favor prior to epigenetic understanding due to an inability to link environmental exposure to sequence changes in DNA.[2] Many different modifications can be made to DNA without changing the sequence, such as methylation, acetylation, phosphorylation, in addition to histone modifications.[3]

Transgenerational epigenetic inheritance occurs when epigenetic information is transferred through the germline in the absence of direct environmental exposure.[4] Substance use has been tied to phenotypic effects in progeny, but many of these associations are due to use during pregnancy, altering the intrauterine environment directly.[5] These are not considered to be truly transgenerational epigenetic effects, as the epigenetic changes would be due to direct exposure to the substance via maternal blood or environment, and not the transmission of epigenetic modifications in the germ cells.[4] Fetal alcohol spectrum disorders are an example of this kind of phenotype.[6] Transgenerational changes in epigenetics regarding pre-pregnancy parental behaviours of both sexes have recently been a focus of attention.[7] It appears that age of onset, intensity, and duration of an individual's substance use behaviour can affect the epigenetic changes elicited in themselves and/or future generations.[8][9][10][11] Association studies in humans and laboratory experiments using rodents have shown possible transgenerational epigenetic effects associated with the use of various substances.

Tobacco smoking[edit]

Smoking of tobacco has been associated with epigenetic changes of certain genes across the lifespan, with modifications varying depending on intensity and length of use,[12] ethnicity,[13] and the age of onset of the smoking behaviour.[8] An analysis of maternal smoking effects has concluded that smoking during pregnancy was more responsible for observed effects in progeny than maternal smoking prior to pregnancy.[5] It's been shown in rats that when females are exposed to nicotine neonatally or in utero, their offspring exhibited insulin resistance and increased blood pressure, despite not having been exposed to nicotine themselves.[14] Paternal smoking in childhood (before the age of 11) has been linked to greater BMI in male, but not female, offspring.[7]

Opiates[edit]

The use of prescription opiates by teenage girls has significantly increased since 2004.[15] In rats, maternal adolescent opiate exposure changed offspring μ-opioid receptor (OPRM1) expression in the ventral tegmental area, with a more pronounced effect in male offspring.[15] Offspring adults and their progeny also displayed sex-specific changes in social and emotional functioning, as well as altered responses to morphineCite error: A <ref> tag is missing the closing </ref> (see the help page). Differential effects on progeny based on their sex has been observed in paternal mice exposed to alcohol.[16] This sex difference involved increased behavioural sensitivity and reduced alcohol drinking in sons but not daughters.[16]

Cocaine[edit]

Outside of the brain, cocaine concentration is highest in the testes of male mice, where it can bind to spermatozoa, making paternal exposure effects on offspring hard to discern between direct exposure and transgenerational epigenetic effects in first generation progeny.[7] Voluntary cocaine ingestion by rat fathers increased BDNF expression in the male, but not female, offspring Prefrontal cortex, resulting in a resistance to cocaine's reinforcing effects.[7] Male offspring also had increased association of acetylated Histone H3 with BDNF promoters.[7] DNA methyltransferase-1 expression was decreased in the seminiferous tubules of testis in rats that used cocaine; together with histone acetylation, this finding provides a possible mechanism for transgenerational epigenetic inheritance.[7] Offspring of cocaine using fathers exhibited deteriorated attention and spatial working memory, particularly in female progeny.[7] These findings corresponded to offspring of exposed mice, so direct exposure of sperm to cocaine may be causing these effects rather than heritable epigenetic changes.

References[edit]

  1. ^ Berger SL, Kouzarides T, Shiekhattar R., Shilatifard A (2009). "An operational definition of epigenetics". Genes Dev. 23: 781-783. doi:10.1101/gad.1787609. PMID 19339683.
  2. ^ a b Szyf M (2014). "Lamarck revisited: epigenetic inheritance of ancestral door fear conditioning". Nature Neuroscience 17: 2-4. doi:10.1038/nn.3603. PMID 24369368.
  3. ^ Weinhold B (2006). "Epigenetics: The science of change". Environ Health Perspect. 114(3): A160-A167. PMC 1392256
  4. ^ a b Nilsson E, Skinner MK (2014). "Chapter 2: Definition of epigenetic transgenerational inheritance and biological impacts". Transgenerational Epigenetics: 11-16. doi:10.1016/B978-0-12-405944-3.00002-7
  5. ^ a b Joubert BR, Haberg SE, Bell DA, Nilsen RM, Vollset SE, Midttun O, Ueland PM, Wu MC, Nystad W, Peddada SD, London SJ (2014). "Maternal smoking and DNA methylation in newborns: In utero effect or epigenetic inheritance?". Cancer Epidemiol Biomarkers Prev, 23(6): 1007-1017. doi: 10.1158/1055-9965.EPI-13-125.
  6. ^ Mead EA, Sarkar DK (2 June 2014). "Fetal alcohol spectrum disorders and their transmission through genetic and epigenetic mechanisms". Front. Genet. 5: 154. doi:10.3389/fgene.2014.00154. PMC 4040491
  7. ^ a b c d e f g Vassoler M, Byrnes EM, Pierce RC (2014). "The impact of exposure to addictive drugs on future generations: Physiological and behavioural effects". Neuropharmacology 76: 269-275. doi:10.1016/j.neuropharm.2013.06.016.
  8. ^ a b Soubrey A, Verbeke G, Hoyo C. (8 October 2014). "The legacy of paternal smoking Do early paternal exposures to lifestyle factors such as smoking increase the risk of chronic diseases in the offspring?". European Journal of Human Genetics 22: 1341-1342. doi:10.1038/ejhg.2014.206.
  9. ^ Fodor A, Timar J, Zelena D. (28 May 2013). "Behavioral effects of perinatal opioid exposure". Life Sciences 104(1-2): 1-8. doi:10.1016/j.lfs.2014.04.006
  10. ^ Szutorisz H, Dinieri JA, Sweet E, Egervari G, Michaelides M, Carter JM, Ren Y, Miller ML, Blitzer RD, Hurd YL (May 2014). "Parental THC exposure leads to compulsive heroin-seeking and altered striatal synaptic plasticity in the subsequent generation". Neuropsychopharmacology 39(6): 1315-1323. doi:10.1038/npp.2013.352
  11. ^ Byrnes JJ, Babb JA, Scanlan VF, Byrnes EM (17 March 2011). "Adolescent opioid exposure in female rats: Transgenerational effects on morphine analgesia and anxiety-like behaviour in adult offspring". Behavioural Brain Research 216(1): 200-205. doi:10.1016/j.bbr.2010.11.059.
  12. ^ Barrett JR (February 2014). "A smoking Gun? Epigenetic markers of tobacco use history". Environ Health Perspect. 122(2): A56. doi:10.1289/ehp.122-A56
  13. ^ Elliott HR, Tillin T, McArdle WL, Ho K, Duggirala A, Frayling TM, Smith GD, Hughes AD, Chaturvedi N, Relton CL (2014). "Differences in smoking associated DNA methylation patterns in South Asians and Europeans". Clinical Epigenetics 6:4. doi:10.1186/1868-7083-6-4.
  14. ^ Holloway AC, Cuu DQ, Morrison KM, Gerstein HC, Tarnopolsky MA (June 2007). "Transgenerational effects of fetal and neonatal exposure to nicotine". Endocrine 31(3): 254-259. doi:10.1007/s12020-007-0043-6.
  15. ^ a b Vassoler FM, Johnson-Collins NL, Carini LM, Byrnes EM (2014). "Next generation effects of female adolescent morphine exposure: sex-specific alterations in response to acute morphine emerge before puberty". Behavioural Pharmacology 25(2): 173-181. doi:10.1097/FBP.0000000000000032
  16. ^ a b Finegersh A, Homanics GE (2014). "Paternal Alcohol Exposure Reduces Alcohol Drinking and Increases Behavioral Sensitivity to Alcohol Selectively in Male Offspring". PLoS ONE 9(6): e99078. doi:10.1371/journal.pone.0099078
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