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利用衰老相关分泌表型蛋白 30 敲除小鼠作为维生素 C 合成缺陷模型鉴定维生素 C 和维生素 E 的组织特异性相互作用。

Determination of tissue-specific interaction between vitamin C and vitamin E using senescence marker protein-30 knockout mice as a vitamin C synthesis deficiency model.

机构信息

Molecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology, Tokyo173-0015, Japan.

Institute of Life Innovation Studies, Toyo University, Gunma374-0193, Japan.

出版信息

Br J Nutr. 2022 Sep 28;128(6):993-1003. doi: 10.1017/S0007114521004384. Epub 2021 Nov 2.

DOI:10.1017/S0007114521004384
PMID:34725010
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9381305/
Abstract

Vitamin E (-tocopherol; VE) is known to be regenerated from VE radicals by vitamin C (L-ascorbic acid; VC) . However, their interaction in various tissues is still unclear. Therefore, we alternatively examined the interaction of VC and VE by measurement of their concentrations in various tissues of senescence marker protein-30 (SMP30) knockout (KO) mice as a VC synthesis deficiency model. Male SMP30-KO mice were divided into four groups (VC+/VE+, VC+/VE-, VC-/VE+ and VC-/VE-), fed diets with or without 500 mg/kg VE and given water with or without 1·5 g/l VC . Then, VC and VE concentrations in the plasma and various tissues were determined. Further, gene expression levels of transporters associated with VC and VE, such as -tocopherol transfer protein (-TTP) and sodium-dependent vitamin C transporters (SVCTs), were examined. These results showed that the VE levels in the VC-depleted (VC-/VE+) group were significantly lower than those in the VC+/VE+ group in the liver and heart; the VC levels in the VE-depleted (VC+/VE-) group were significantly lower than those in the VC+/VE+ group in the kidneys. The -TTP gene expression in the liver and kidneys was decreased by VC and/or VE depletion. Moreover, SVCT1 gene expression in the liver was decreased by both VC and VE depletion. In conclusion, these results indicate that VC spares VE mainly in the liver and heart and that VE spares VC in the kidneys of SMP30-KO mice. Thus, interaction between VC and VE is likely to be tissue specific.

摘要

维生素 E（-生育酚；VE）已知可由维生素 C（L-抗坏血酸；VC）从 VE 自由基中再生。然而，它们在各种组织中的相互作用仍不清楚。因此，我们通过检测衰老标志物蛋白-30（SMP30）敲除（KO）小鼠（VC 合成缺陷模型）各种组织中 VC 和 VE 的浓度，交替研究了 VC 和 VE 的相互作用。雄性 SMP30-KO 小鼠分为四组（VC+/VE+、VC+/VE-、VC-/VE+和 VC-/VE-），分别喂食含或不含 500mg/kg VE 的饮食，并给予含或不含 1.5g/l VC 的水。然后，测定血浆和各种组织中的 VC 和 VE 浓度。此外，还检查了与 VC 和 VE 相关的转运体的基因表达水平，如 -生育酚转移蛋白（-TTP）和钠离子依赖型维生素 C 转运体（SVCTs）。这些结果表明，在肝脏和心脏中，VC 耗尽（VC-/VE+）组的 VE 水平明显低于 VC+/VE+组；在肾脏中，VE 耗尽（VC+/VE-）组的 VC 水平明显低于 VC+/VE+组。肝脏和肾脏中的 -TTP 基因表达因 VC 和/或 VE 耗竭而降低。此外，SVCT1 基因在肝脏中的表达因 VC 和 VE 耗竭而降低。总之，这些结果表明 VC 主要在肝脏和心脏中节省 VE，而 VE 在 SMP30-KO 小鼠的肾脏中节省 VC。因此，VC 和 VE 之间的相互作用可能是组织特异性的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aba0/9381305/3fc0339139a8/S0007114521004384_fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aba0/9381305/5462a94d30e9/S0007114521004384_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aba0/9381305/6a1c268930be/S0007114521004384_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aba0/9381305/5ed04a76064a/S0007114521004384_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aba0/9381305/bde9f56de062/S0007114521004384_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aba0/9381305/52e57687e814/S0007114521004384_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aba0/9381305/3fc0339139a8/S0007114521004384_fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aba0/9381305/5462a94d30e9/S0007114521004384_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aba0/9381305/6a1c268930be/S0007114521004384_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aba0/9381305/5ed04a76064a/S0007114521004384_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aba0/9381305/bde9f56de062/S0007114521004384_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aba0/9381305/52e57687e814/S0007114521004384_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aba0/9381305/3fc0339139a8/S0007114521004384_fig6.jpg

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