Nicotinamide-induced mouse embryo developmental defect rescued by resveratrol and I-CBP112.
Mol Reprod Dev
; 87(9): 1009-1017, 2020 09.
Article
en En
| MEDLINE
| ID: mdl-32818292
ABSTRACT
Cell cycle of mouse embryo could be delayed by nicotinamide (NAM). Histone H3 lysine 56 (H3K56ac) acetylation plays an important role in mammalian genomic stability and the function of this modification in mouse embryos is not known. Hence, we designed to study the effects of NAM-induced oxidative stress on the developmental ability of mouse embryos, on the acetylation of H3K56ac and the possible functions of this modification related to mouse embryo development. Treatment with NAM (10, 20, or 40 mmol/L for 24 or 48 hr) during in vitro culture significantly decreased developmental rate of blastocyst (24 hr 90.2 vs. 81.2, 43.2, and 18.2, with p > .05, p < .01, respectively; 48 hr 89.3 vs. 53.2%, 12.1%, and 0% with p < .05, respectively). NAM treatment (20 mmol/L) for 6 and 31 hr resulted in increased intracellular reactive oxygen species levels in two-cell embryos, and apoptotic cell numbers in blastocysts. Resveratrol (RSV) and I-CBP112 rescued the 20 mmol/L NAM-induced embryo developmental defects. RSV and I-CBP112 increased the level of Sirt1 and decreased the level of H3K56ac induced by NAM in two-cell embryos (p < .05). These data suggest that NAM treatment decreases the expression of Sirt1, which induces high levels of H3K56 acetylation that may be involved in oxidative stress-induced mouse embryo defects, which can be rescued by RSV and I-CBP112.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Oxazepinas
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Piperidinas
/
Niacinamida
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Desarrollo Embrionario
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Resveratrol
Límite:
Animals
Idioma:
En
Revista:
Mol Reprod Dev
Asunto de la revista:
BIOLOGIA MOLECULAR
/
MEDICINA REPRODUTIVA
Año:
2020
Tipo del documento:
Article
País de afiliación:
China