Martin Hélène, Uring-Lambert Béatrice, Adrian Markus, Lahlou Abdeslam, Bonet Alexandre, Demougeot Céline, Devaux Sylvie, Laurant Pascal, Richert Lysiane, Berthelot Alain
Laboratoire de Toxicologie Cellulaire, EA 2SBP, UFR des sciences médicales et pharmaceutiques, Besançon, France.
Magnes Res. 2008 Jun;21(2):124-30.
In the present study, we investigated the effect of long-term dietary Mg intake on the rate of oxidative stress, apoptosis and ageing in rat livers. To address this issue, rats were fed diets containing either a moderately deficient (0.15 g Mg/kg diet), a standard (0.8 g Mg/kg diet) or a high (3.2 g Mg/kg diet) Mg dose for two years. It is noteworthy that a higher percentage of animal mortality was observed in the lowest Mg diet, as compared to the other groups. Oxidative stress and antioxidant status were evaluated by measuring different enzyme activities, among which glutathione peroxidase activity was significantly reduced when Mg content was decreased in the diet. Moreover, we obtained an activation of caspase-3 and a higher lipid peroxidation in the Mg-deficient group, as compared to the Mg standard group, while no changes in Mg-supplemented group were observed, in accordance with our previously published data in primary cultures of rat hepatocytes (Martin et al., J Nutr 2003). Telomere shortening was measured in rat livers, as a marker of ageing. We found that telomere length was decreased in old animals, as compared to young animals confirming that telomere shortening correlated well with ageing events. Moreover, in old animals, we obtained a decrease of telomere length in the Mg-deficient group, as compared to the other groups. Taken together, our results show that a long-term chronic Mg deficiency led to oxidative stress, apoptosis and an acceleration of ageing in rat livers.
在本研究中，我们调查了长期膳食镁摄入量对大鼠肝脏氧化应激率、细胞凋亡和衰老的影响。为解决这一问题，将大鼠喂食含适度缺乏（0.15克镁/千克饮食）、标准（0.8克镁/千克饮食）或高剂量（3.2克镁/千克饮食）镁的饮食，持续两年。值得注意的是，与其他组相比，在最低镁饮食组中观察到更高比例的动物死亡。通过测量不同的酶活性来评估氧化应激和抗氧化状态，其中当饮食中镁含量降低时，谷胱甘肽过氧化物酶活性显著降低。此外，与镁标准组相比，我们在缺镁组中观察到半胱天冬酶-3的激活和更高的脂质过氧化，而在补充镁组中未观察到变化，这与我们先前在大鼠肝细胞原代培养中的发表数据一致（Martin等人，《营养学杂志》2003年）。在大鼠肝脏中测量端粒缩短，作为衰老的标志物。我们发现，与年轻动物相比，老年动物的端粒长度缩短，证实端粒缩短与衰老事件密切相关。此外，在老年动物中，与其他组相比，我们在缺镁组中观察到端粒长度减少。综上所述，我们的结果表明，长期慢性缺镁会导致大鼠肝脏氧化应激、细胞凋亡和衰老加速。
