Baek B S, Kwon H J, Lee K H, Yoo M A, Kim K W, Ikeno Y, Yu B P, Chung H Y
College of Pharmacy, Research Institute of Drug Development, Pusan National University, Korea.
Arch Pharm Res. 1999 Aug;22(4):361-6. doi: 10.1007/BF02979058.
One of the potential causes of age-related neuronal damage can be reactive oxygen species (ROS), as the brain is particularly sensitive to oxidative damage. In the present study, we investigated the effects of aging and dietary restriction (DR) on ROS generation, lipid peroxidation, and antioxidant enzymes in cerebrum, hippocampus, and cerebellum of 6-, 12-, 18-, and 24-month-old rats. ROS generation significantly increased with age in cerebrum of ad libitum (AL) rats. However, no significant age-difference was observed in hippocampus and cerebellum. DR significantly decreased ROS generation in cerebrum and cerebellum at 24-months. On the other hand, the increased lipid peroxidation of AL rats during aging was significantly reduced by DR in all regions. Our results further showed that catalase activity decreased with age in cerebellum of AL rats, which was reversed by DR, although SOD activity had little change by aging and DR in all regions. In a similar way, glutathione (GSH) peroxidase activity increased with age in cerebrum of AL rats, while DR suppressed it at 24-months. These data further support the evidence that the vulnerability to oxidative stress in the brain is region-specific.
与年龄相关的神经元损伤的潜在原因之一可能是活性氧(ROS),因为大脑对氧化损伤特别敏感。在本研究中,我们调查了衰老和饮食限制(DR)对6、12、18和24月龄大鼠大脑、海马体和小脑中ROS生成、脂质过氧化和抗氧化酶的影响。随意进食(AL)大鼠大脑中的ROS生成随年龄显著增加。然而,在海马体和小脑中未观察到显著的年龄差异。饮食限制在24个月时显著降低了大脑和小脑中的ROS生成。另一方面,饮食限制在所有区域都显著降低了衰老过程中AL大鼠脂质过氧化的增加。我们的结果进一步表明,AL大鼠小脑中过氧化氢酶活性随年龄降低,饮食限制使其逆转,尽管超氧化物歧化酶活性在所有区域受衰老和饮食限制的影响很小。同样,AL大鼠大脑中谷胱甘肽(GSH)过氧化物酶活性随年龄增加,而饮食限制在24个月时抑制了该活性。这些数据进一步支持了大脑对氧化应激的易感性具有区域特异性这一证据。