富含黄酮类物质膳食干预对不同GST基因型个体氧化损伤相关指标的影响

Effects of flavonoid-rich diet intervention on body oxidative damage related biomarkers in the health subjects with different GST genotype

目的 观察不同GSTT1/GSTM1基因型个体机体氧化损伤相关生化指标对富含黄酮类物质膳食干预敏感性的差异.方法 募集GSTT1-/GSTM1-和GSTT1＋/GSTM1＋基因型的21-23岁健康成年人志愿者各13人进行膳食干预实验.根据当地的饮食习惯并结合中国居民膳食指南,选择黄酮类物质含量丰富的蔬菜和水果汁作为干预食物编制食谱.所有受试者经消洗期和适应膳后进入2周的饮食干预试验.收集受试对象在膳食干预前、干预1周、2周时的外周血和晨尿.试剂盒法测定血浆丙二醛（malondialdehyde,MDA）、谷胱甘肽（glutathione,GSH）含量及红细胞超氧化物歧化酶（superoxide dismutase,SOD）、谷胱甘肽硫转移酶（Glutathione-S-transferase,GST）、谷胱甘肽过氧化物酶（reduced glutathione,GSH-Px）活性;酶联免疫试剂盒法检测尿液中8-羟基脱氧鸟苷（8-OH-dG）含量.结果 膳食干预前,两组人群血浆MDA、GSH水平及红细胞SOD、GST及GSH-Px酶活性,差异无统计学意义.膳食干预1周时,GSTM1＋/GSTT1＋组血浆MDA水平比GSTM1-/GSTT1-组明显降低,差异有统计学意义.膳食干预2周后,2组人群血浆MDA水平均显著降低,与干预前相比差异有统计学意义.膳食干预对2组人群血浆GSH水平及红细胞SOD酶活性无明显影响,但可诱导GSH-Px酶的活性.对红细胞GST酶活性的影响存在GST基因型差异.膳食干预可以明显增加GSTM1＋/GSTT1＋组人群红细胞GST酶活性,且与干预前相比,差异有统计学意义;而GSTM1-/GSTT1-组GST酶活性有升高趋势,但与干预前相比,差异无统计学意义.干预前,2组人群尿液中8-OH-dG的含量差异无统计学意义,膳食干预2周时,两组人群尿液中8-OH-dG的含量表现为降低趋势,但与干预前相比差异无统计学意义.结论 不同GSTT1/GSTM1基因型个体氧化损伤相关指标对富含黄酮类物质膳食干预的反应不同.

Objective To study the response of body oxidative damage related biomarkers to flavonoid-rich diet intervention in healthy subjects with different GST genotypes. Methods Totally 26 healthy adults （21 -23 years old） with the GSTTI -/GSTM1-or GSTTI ＋/ GSTM1 ＋ genotype were enrolled to participate in the flavonoid-rich diet intervention. The venous blood and urine samples were collected at the baseline, 1 and 2 weeks after the dietary intervention. Experimental kits were used for detecting the plasma MDA, GSH levels, and erythrocyte SOD, GST and GSH-Px enzyme activities. ELISA Kit was applied to detect the urinary 8-OH-dG level. Results No significant differences of plasma MDA, GSH levels and erythrocyte SOD, GST and GSH-Px activities were found at the baseline between GSTT1/GSTM1 genotype groups. After dietary intervention for 1 week, the plasma MDA level in GSTM1 ＋/GSTT1 ＋ group had a significant decrease than the baseline and that in GSTM1-/GSTTI-group, while, after intervention for 2 weeks, the MDA level in GSTT1-/ GSTMl-group began to decrease to lower than that in the baseline. Two weeks of flavonoid-rich food intervention had no effects on the plasma GSH level and erythrocyte SOD enzyme activity, but increase in GSH-Px activity was found in both groups. Significant increase in GSH-Px activities were detected in GSTM1 ＋/GSTT1 ＋ and GSTM1-/GSTTI-groups. The response of erythrocyte GST activity was GST genotype dependent. Dietary intervention significantly increased erythrocyte GST activity in the GSTM1 ＋/GSTT1 ＋ group; however, no influence was detected in GSTM1-/GSTTI-group. The content of urinary 8-OH-dG presented a decrease trend after dietary intervention for 2 weeks, however, no statistical significance was found. Conclusion Oxidative damage related biomarkers of the subjects with different GSTT1/GSTM1 genotypes had different responses to the flavonoid-rich diet.