Table 1.
Epigenetic modifications induced by alcohol and/or cannabinoids. A comprehensive table showing up to date contributions from the literature. The first column shows the group that carried out the research study, second column indicates the epigenetic modifications associated with alcohol and/or cannabinoids, and the last column indicates the experimental model and region used in the study.
| Alcohol | ||
|---|---|---|
| Group | Epigenetic Modifications | Experimental Model/Region of Study |
| Park et al. [49] | Increase in H3K9ac in hepatocytes | Acute alcohol exposure in rat hepatocytes |
| Kim and Shukla [51] | Increase in H3K9ac in stellate cells | Rat hepatic stellate cells |
| Park et al. [53] | Increase in association of class I alcohol dehydrogenase (ADH I) gene with H3K9ac, increase in HAT activity | Acute alcohol treatment in rat hepatocytes |
| Kim and Shukla [52] | Increase in H3K9ac in liver, lung spleen tissues | Acute in-vivo alcohol administration to rats |
| Lee and Shukla [54] | Increase in phosphorylation of H3 serine 10 and 28, along with nuclear activation of p38 MAP kinase | Acute ethanol treatment in rat hepatocytes |
| Pandey and Ugale [57] | Increase in H3 and H4 acetylation, decrease in HDAC activity at acute levels | Acute alcohol exposure in rats, study carried out in the amygdala region |
| Pascual [58] | Increase in H3K9ac and H4K12ac | Chronic intermittent ethanol administration in young rats, study carried out in frontal cortex region |
| Zhou [60] | Genome wide alteration in H3K4me3 in hippocampus | Human post mortem brain tissue from alcohol and cocaine users |
| Ponomarev [59] | Increase in H3K4me3 and associated DNA hypo methylation | Human autopsy brain samples from alcoholics and non-alcoholics |
| Agudelo [61] | Increase in HDAC 1 and 3 and HDAC activity along with increase in 5-HT3 | Acute alcohol treatment in CNS cells |
| LópezMoreno [62] | Differential modulation in HDACs 1–11 | Acute and chronic alcohol exposure in rats and human periphery. |
| Agudelo [63] | Increase in class I HDACs gene expression and differential modulation in HDAC protein expression | Acute alcohol treatment in primary monocyte derived dendritic cells in-vitro and from alcohol users |
| Asimes [74] | Alteration genome wide DNA methylation in alcohol-naïve offspring | Binge ethanol exposure in adolescent rats, study carried out in hypothalamus of offspring |
| Cannabinoids | ||
| Group | Epigenetic Modifications | Experimental Model/Region of Study |
| Khare [124] | Increase in HDAC3 expression causing dysregulation in genes for placental development | THC exposure in Human trophoblast cell line BeWo |
| Paradisi [99] | Modulation in DNA methylation at CB1 receptor | Anandamide exposure to keratinocytes |
| Tomasiewicz [125] | Decrease in H3K9me2 and me3 levels associated with Penk gene mRNA levels | THC exposure to adolescent rats and studies carried out in adult rat nucleus accumbens |
| DiNieri [126] | Increase in H3K9me2 and decrease in H3k4me3 at the Drd2 gene locus in offspring | in utero THC exposure to rats followed by studies in adult rat nucleus accumbens |
| Yang [100] | Modulation in multiple histone modification sites like H3K4me3, H3K9me3, H3K27me3, and H3K36me3 | THC exposure in differentiating mouse lymph node cells |
| Alcohol-Cannabinergic Pathway | ||
| Group | Epigenetic Modifications | Experimental Model/Region of Study |
| Subbanna [114] | Increase in H4K8ac, decrease in H3K9me by enhancing CB1R exon | Postnatal alcohol exposure in rats, studies carried out in neonatal brain. |
| Nagre [115] | Downregulation in DNMT1 and DNMT3A and impairment of DNA methylation, while CB1R knockout mice does not show the same deficits | Postnatal alcohol exposure and studies carried out in neonatal brain. |