适度增加饮食锌可改善DNA损伤、氧化应激、免疫功能和蛋白质水平
2016年12月21日,美国营养学会官方期刊《美国临床营养杂志》在线发表奥克兰儿童医院研究所的研究报告,发现每天在饮食中适度额外摄入4mg锌可能对机体健康有长期积极影响,同时还有助于防止感染和疾病的发生,摄入锌的水平相当于某些强化作物中的锌水平,如含锌水稻和含锌小麦,这些强化作物可以加入营养缺乏地区的体弱、营养不良人群饮食,有助于维持人群机体健康。
锌遍布机体,能够促进机体多种功能发挥,在优化儿童生长过程中发挥关键作用,同时也能确保机体免疫系统健康。此外,锌还可有效抑制机体炎症和氧化应激的发生,而机体炎症和氧化应激与许多癌症以及慢性心血管疾病发生直接相关。
在世界各地,很多家庭都食用抛光大米、精制小麦、精制面粉,这些食物能够为机体提供基本能量供给,但是不能提供足够微量营养素,如锌。锌是大约3000种不同蛋白质的必要组成部分,可影响蛋白质在细胞中的调节方式,当缺乏足量的锌,机体对DNA进行修复的能力就会丧失。
该随机对照研究共入组18位男性,为期6周,前2周每天食用6mg锌,后4周每天食用10mg锌,为了减少锌的吸收,在初始阶段将植酸盐加入饮食。每天进食前后测定锌稳态指标,包括总吸收锌、可交换锌池、血浆和细胞锌浓度、锌转运蛋白基因表达、其他代谢指标(包括DNA损伤、炎症、氧化应激),通过计算DNA链断裂测定锌对人类机体代谢的影响,利用DNA损伤指标检测适度水平的锌对个体健康的影响,这是一种不同于传统方法的新型方法,传统方法通过测定血浆锌水平或者根据个体生长迟缓和病态表现评估机体的锌水平。
结果发现,随着饮食锌增加,总吸收锌增加,但是血浆锌浓度、可交换锌池、红细胞和白细胞锌浓度、锌转运蛋白表达不变。然而,白细胞DNA链断裂随着饮食锌增加而减少,并且在饮食锌增加后,参与DNA修复、抗氧化、免疫功能的蛋白质水平恢复。
该研究首次发现,饮食中的锌水平适度增加,能够降低机体的氧化应激和DNA损伤,对于机体健康有重要的影响,或许能够提供测定锌对机体健康重要性的策略,同时也能证明基于食物的干预措施可有效改善微量营养素缺乏人群的健康。该研究评估了基于食物的解决策略对改善机体营养不良的关键作用,利用生物强化方法或许能够持久有效地解决人群机体锌缺乏的状况。
Am J Clin Nutr. 2016 Dec 21. [Epub ahead of print]
A moderate increase in dietary zinc reduces DNA strand breaks in leukocytes and alters plasma proteins without changing plasma zinc concentrations.
Zyba SJ, Shenvi SV, Killilea DW, Holland TC, Kim E, Moy A, Sutherland B, Gildengorin V, Shigenaga MK, King JC.
Nutrition and Metabolism Center, Children's Hospital Oakland Research Institute, Oakland, CA.
BACKGROUND: Food fortification has been recommended to improve a population's micronutrient status. Biofortification techniques modestly elevate the zinc content of cereals, but few studies have reported a positive impact on functional indicators of zinc status.
OBJECTIVE: We determined the impact of a modest increase in dietary zinc that was similar to that provided by biofortification programs on whole-body and cellular indicators of zinc status.
DESIGN: Eighteen men participated in a 6-wk controlled consumption study of a low-zinc, rice-based diet. The diet contained 6 mg Zn/d for 2 wk and was followed by 10 mg Zn/d for 4 wk. To reduce zinc absorption, phytate was added to the diet during the initial period. Indicators of zinc homeostasis, including total absorbed zinc (TAZ), the exchangeable zinc pool (EZP), plasma and cellular zinc concentrations, zinc transporter gene expression, and other metabolic indicators (i.e., DNA damage, inflammation, and oxidative stress), were measured before and after each dietary-zinc period.
RESULTS: TAZ increased with increased dietary zinc, but plasma zinc concentrations and EZP size were unchanged. Erythrocyte and leukocyte zinc concentrations and zinc transporter expressions were not altered. However, leukocyte DNA strand breaks decreased with increased dietary zinc, and the level of proteins involved in DNA repair and antioxidant and immune functions were restored after the dietary-zinc increase.
CONCLUSIONS: A moderate 4-mg/d increase in dietary zinc, similar to that which would be expected from zinc-biofortified crops, improves zinc absorption but does not alter plasma zinc. The repair of DNA strand breaks improves, as do serum protein concentrations that are associated with the DNA repair process.
This trial was registered at clinicaltrials.gov as NCT02861352.
KEYWORDS: DNA repair; antioxidant; inflammation; zinc biomarkers; zinc fortification
PMID: 28003206
PII: ajcn135327
DOI: 10.3945/ajcn.116.135327