长期运动训练对外周血淋巴细胞DNA损伤和凋亡的影响及机制研究

Effects and mechanism of long-term exercise training on peripheral blood lymphocyte DNA damage and apoptosis

训练组(男子足球运动员,n=16)和对照组(男子大学生,n=16)在功率自行车上完成一次递增负荷力竭运动。运动前、运动后以及运动后24 h采集静脉血,测定外周血淋巴细胞计数、淋巴细胞凋亡率、羟自由基、8-羟基脱氧鸟嘌呤(8-OHdG)和8-氧鸟嘌呤DNA糖基化酶(OGG1)。结果发现,运动后即刻,训练组和对照组外周血淋巴细胞计数(P<0.01;P<0.05)、淋巴细胞凋亡率(P<0.05;P<0.01)、羟自由基(P<0.01;P<0.01)、8-OHdG(P<0.01;P<0.01)和OGG1(P<0.01;P<0.01)均高于运动前水平,而训练组OGG1升高幅度高于对照组(P<0.01),其他各指标升高幅度则均明显低于对照组(均为P<0.01)。运动后24h,对照组外周血淋巴细胞计数低于运动前(P<0.01),淋巴细胞凋亡率高于运动前(P<0.01),而训练组则恢复至运动前;两组8-OHdG(P<0.05;P<0.01)均高于运动前,但升高幅度明显低于对照组(P<0.01);OGG1在对照组恢复至运动前,而训练组仍高于运动前水平(P<0.05)。因此,长期运动训练通过降低氧化应激水平、提高DNA修复能力、减轻DNA氧化损伤,抑制运动性淋巴细胞凋亡。

Training group （male football athletes, n = 16） and control group （male normal undergraduate students, n = 16） performed a bout of incremental exhausted exercise test on cycle ergometer. Peripheral blood lymphocyte counts, apoptotic rate of leukocytes, hydroxy radical, 8- hydroxydeoxyguanosine （8 -OHdG） and 8 -oxoguanine DNA glycosylase （OGG1） were determined in venous blood before, immediately after and 24 h after exercise test. We found that although lymphocyte count（P 〈0. 01 ; P 〈0.05）, apoptotic rate（P 〈0. 05 ; P 〈0.01 ）, hydroxyl radical（P 〈 0. 01 ; P 〈 0.01 ）, 8 - OHdG （ P 〈 0. 01 ; P 〈 0.01 ） and OGG1 （ P 〈 0. 01 ; P 〈 0.01 ） increased immediately after exercise test in both groups, the change extent of OGG1 in training group was significantly higher than that of control group （P 〈0.01 ）, while that of other indexes were low- er than control group （ all P 〈 0.01 ）. After 24h, lymphocyte count was lower （P 〈 0.01 ）, apoptot- ic rate was higher（P 〈 0.01 ） than that of pre - exercise in control group, which were recovered in training group ; 8 - OHdG in both group were higher （ P 〈 0. 05 ; P 〈 0.01 ） than pre - exercise but elevation range in training group was lower than control group （P 〈 0.01 ） ; OGG1 recovered in control group, while higher than pre - exercise in training group （P 〈 0.05 ）. In conclusion, attenuated oxidative stress, improved DNA repair ability and decreased lymphocyte oxidative DNA damage could be the mechanism to prevent exercise induced lymphocytes apoptosis through long - term exercise training.