Retinol-induced changes in the phosphorylation levels of histones and high mobility group proteins from Sertoli cells

Moreira, José Cláudio Fonseca; Dal‐Pizzol, Felipe; Rocha, Adriana Brondani da; Klamt, Fábio; Ribeiro, Nede Carlos; Ferreira, C.J.S.; Bernard, Elena Aida

doi:10.1590/s0100-879x2000000300005

Cited by 16 publications

(3 citation statements)

References 32 publications

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“…Although more studies should be conducted, all these molecules are able to induce epigenetic changes. Thus, ascorbate promotes widespread DNA demethylation in human embryonic stem cells (Chung et al, 2010), whereas retinol alters histone phosphorylation levels in rat Sertoli cells (Moreira et al, 2000). Vitamin E, lipoic acid and conjugated linoleic acids (CLA) require deeper analysis, although molecular modeling studies of all of them suggest a putative role as HDAC inhibitors (Dashwood and Ho, 2007).…”

Section: Different Minerals Have Been Associated With Changes In Epigmentioning

confidence: 99%

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

Milagro

Mansego

Miguel

et al. 2013

Molecular Aspects of Medicine

251

161

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Nutritional factors play a life-long role in human health. Indeed, there is growing evidence that one of the mechanisms by which nutrients and bioactive compounds affect metabolic traits is epigenetics. Complex interactions among food components and histone modifications, DNA methylation, non-coding RNA expression and chromatin remodeling factors lead to a dynamic regulation of gene expression that controls the cellular phenotype. Although perinatal period is the time of highest phenotypic plasticity, contributing largely to developmental programming, also during adulthood there is evidence about a nutritional influence on epigenetic regulation. Similarly to type 2 diabetes, hypertension, atherosclerosis and other metabolic disorders, obesity predisposition and weight loss outcomes have been repeatedly associated to changes in epigenetic patterns. Different non-nutritional risk factors that usually accompany obesity seem also to be involved in these epigenetic modifications, especially hyperglycemia, inflammation, hypoxia and oxidative stress. There are currently three major objectives in epigenetic research in relation to obesity: to search for epigenetic biomarkers to predict future health problems or detect the individuals at most risk, to understand the obesity-related environmental factors that could modulate gene expression by affecting epigenetic mechanisms, and to study novel therapeutic strategies based on nutritional or pharmacological agents that can modify epigenetic marks. At this level, the major tasks are: development of robust epigenetic biomarkers of weight regulation, description of those epigenetic marks more susceptible to be modified by dietary exposures, identification of the active ingredients (and the doses) that alter the epigenome, assessment of the real importance of other obesity-related factors on epigenetic regulation, determination of the period of life in which best results are obtained, and understanding of the importance of the inheritance of these epigenetic marks.

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Section: Different Minerals Have Been Associated With Changes In Epigmentioning

confidence: 99%

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

Milagro

Mansego

Miguel

et al. 2013

Molecular Aspects of Medicine

251

161

View full text Add to dashboard Cite

show abstract

“…The fatty acids family, including EPA, DHA, and butyrate acetate propionate also affect n-6 and n-3 fatty acid metabolism, as well as inflammation via DNA methylation and histone acetylation [ 39 40 41 42 ]. In addition, vitamins such as retinol, tocopherols, and ascorbate impact the antioxidant process via histone acetylation and DNA methylation [ 40 43 44 ]. Of particular note, minor nutrient-mediated DNA methylation is primarily modified by the folate-methionine cycle.…”

Section: Discussionmentioning

confidence: 99%

Physiologic and epigenetic effects of nutrients on disease pathways

2023

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BACKGROUND/OBJECTIVES Epigenetic regulation by nutrients can influence the development of specific diseases. This study sought to examine the effect of individual nutrients and nutrient families in the context of preventing chronic metabolic diseases via epigenetic regulation. The inhibition of lipid accumulation and inflammation by nutrients including proteins, lipids, vitamins, and minerals were observed, and histone acetylation by histone acetyltransferase (HAT) was measured. Correlative analyses were also performed. MATERIALS/METHODS Nutrients were selected according to information from the Korean Ministry of Food and Drug Safety. Selected nutrient functionalities, including the attenuation of fatty acid-induced lipid accumulation and lipopolysaccharide-mediated acute inflammation were evaluated in mouse macrophage Raw264.7 and mouse hepatocyte AML-12 cells. Effects of the selected nutrients on in vitro HAT inhibition were also evaluated. RESULTS Nitric oxide (NO) production correlated with HAT activity, which was regulated by the amino acids group, suggesting that amino acids potentially contribute to the attenuation of NO production via the inhibition of HAT activity. Unsaturated fatty acids tended to attenuate inflammation by inhibiting NO production, which may be attributable to the inhibition of in vitro HAT activity. In contrast to water-soluble vitamins, the lipid-soluble vitamins significantly decreased NO production. Water- and lipid-soluble vitamins both exhibited significant inhibitory activities against HAT. In addition, calcium and manganese significantly inhibited lipid accumulation, NO production, and HAT activity. CONCLUSIONS Several candidate nutrients and their family members may have roles in the prevention of diseases, including hepatic steatosis and inflammation-related diseases (i.e., nonalcoholic steatohepatitis) via epigenetic regulation. Further studies are warranted to determine which specific amino acids, unsaturated fatty acids and lipid-soluble vitamins or specific minerals influence the development of steatosis and inflammatory-related diseases.

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“…This can cause DNA breaks by directly attacking the deoxyribose [48]. Retinol also changes the organization and function of chromatin, thus altering the on-and off-switching of transcriptionally-active regions of DNA in rat Sertoli cells [49], as well as increasing DNA fragmentation in Chinese hamster lung fibroblasts and inducing DNA breaks, cell cycle progression and increasing the numbers of proliferative foci in terminally differentiated rat Sertoli cells [50]. All of these mechanisms might be involved in the observed genotoxic actions of the novel compounds in CHO cells.…”

Section: Discussionmentioning

confidence: 99%

Synthetic Diphenylacetylene-Based Retinoids Induce DNA Damage in Chinese Hamster Ovary Cells without Altering Viability

et al. 2022

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All-trans-retinoic acid (ATRA), the active metabolite of vitamin A, plays a pivotal role in cell differentiation, proliferation and embryonic development. It is an effective therapy for dermatological disorders and malignancies. ATRA is prone to isomerization and oxidation, which can affect its activity and selectivity. Novel diphenylacetylene-based ATRA analogues with increased stability can help to overcome these problems and may offer significant potential as therapeutics for a variety of cancers and neurodegenerative diseases, including amyotrophic lateral sclerosis. Here, we investigated the effects of these retinoids on cell viability and genotoxicity in the widely used model system of the rapidly proliferating Chinese hamster ovary cell line. DC360 is a fluorescent ATRA analogue and DC324 is a non-active derivative of DC360. EC23, DC525, DC540, DC645, and DC712 are promising analogues with increased bioactivity. The cytotoxic activity of the compounds was evaluated by ATP assay and DNA damage was tested by comet assay. No cytotoxicity was observed in the 10−6–10−5 M concentration range. All compounds induced DNA migration similar to ATRA, but DC324, DC360 and EC23 did so to a greater extent, particularly at higher concentrations. We believe that retinoid receptor-independent genotoxicity is a general characteristic of these compounds; however, further studies are needed to identify the molecular mechanisms and understand their complex biological functions.

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Retinol-induced changes in the phosphorylation levels of histones and high mobility group proteins from Sertoli cells

Cited by 16 publications

References 32 publications

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

Physiologic and epigenetic effects of nutrients on disease pathways

Synthetic Diphenylacetylene-Based Retinoids Induce DNA Damage in Chinese Hamster Ovary Cells without Altering Viability

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