• Journal of Nutrition and Health
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• v.55 no.3
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• pp.321-329
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• 2022

Riboflavin and its derivatives, flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), are key components of mitochondrial energy metabolism and oxidation-reduction reactions. Proposed dietary reference intakes for Koreans (KDRIs), that is, estimated average requirements (EARs), for riboflavin, based on current knowledge of riboflavin and riboflavin derivative levels, and glutathione reductase activity, are 1.3 mg/d for men aged 19-64 years and 1.0 mg/d for women aged 19-64 years. By applying a coefficient of variance of 10%, reference nutrient intakes (RNIs) were set at 1.5 mg/d for men aged 19-64 years and 1.2 mg/d for women aged 19-64 years. Likewise, EARs and RNIs of riboflavin intake were proposed for all age groups and women in specific life stages such as pregnancy. Mean adult riboflavin intake for adults aged ≥ 19 years was 1.69 mg/d in Korea National Health and Nutrition Examination Survey (KNHANES) 2020, which was 124.9% of EAR according to the 2020 KDRIs. In the 2015-2017 KNHANES study, the mean riboflavin intake from foods and supplements was 2.79 mg/d for all age groups, and 32.7% of individuals consumed less riboflavin than EAR according to the 2020 KDRIs. For those that used supplements, mean intakes were 1.50 mg/d for riboflavin from foods, 10.26 mg/d from supplements, and 11.76 mg/d from food and supplements, and 5.5% of individuals consumed less riboflavin than EAR. Although the upper limit of riboflavin has not been established, the merits of increasing supplement use warrant further consideration. Also, additional epidemiologic and intervention studies are required to explore the role of riboflavin in the etiology of chronic diseases.

• Journal of Life Science
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• v.23 no.10
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• pp.1230-1238
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• 2013

The regulatory effect of the tumor-suppressor protein p53 on the apoptogenic activity of $17{\alpha}$-estradiol ($17{\alpha}-E_2$) was compared between HCT116 ($p53^{+/+}$) and HCT116 ($p53^{-/-}$) cells. When the HCT116 ($p53^{+/+}$) and HCT116 ($p53^{-/-}$) cells were treated with $2.5{\sim}10{\mu}M$ $17{\alpha}-E_2$ for 48 h or with $10{\mu}M$for various time periods, cytotoxicity and an apoptotic sub-$G_1$ peak were induced in the HCT116 ($p53^{+/+}$) cells in a dose- and time-dependent manner. However, the HCT116 ($p53^{-/-}$) cells were much less sensitive to the apoptotic effect of $17{\alpha}-E_2$. Although $17{\alpha}-E_2$ induced aberrant mitotic spindle organization and incomplete chromosome congregation at the equatorial plate, $G_2/M$ arrest was induced to a similar extent in both cell types. In addition, $17{\alpha}-E_2$-induced activation of Bak and Bax, ${\Delta}{\Psi}m$ loss, and PARP degradation were more dominant in the HCT116 ($p53^{+/+}$) than in the HCT116 ($p53^{-/-}$) cells. In accordance with enhancement of p53 phosphorylation (Ser-15) and p53 levels, p21 and Bax levels were elevated in the HCT116 ($p53^{+/+}$) cells treated with $17{\alpha}-E_2$. The HCT116 ($p53^{-/-}$) cells exhibited barely or undetectable levels of p21 and Bax, regardless of $17{\alpha}-E_2$ treatment. On the other hand, although the level of Bcl-2 was slightly lower in the HCT116 ($p53^{+/+}$) than in the HCT116 ($p53^{-/-}$) cells, it remained relatively constant after the $17{\alpha}-E_2$ treatment. Together, these results show that among the components of the $17{\alpha}-E_2$-induced apoptotic-signaling pathway, which proceeds through mitotic spindle defects causing mitotic arrest, subsequent activation of Bak and Bax and the mitochondria-dependent caspase cascade, leading to PARP degradation, $17{\alpha}-E_2$-induced activation of Bak and Bax is the upstream target of proapoptotic action of p53.