Posgrado en Ciencias Biológicas y de la Salud, Universidad Autónoma Metropolitana, Unidad Iztapalapa, México D.F., Mexico; APREXBIO S.A.S. de C.V., Laboratorio de Primatología, Ciudad de México, México D.F., Mexico; Biología Integral para Vertebrados (BIOINVERT®), Unidad de Experimentación Animal, Estado de México, Mexico; Centro de Investigación, Proyecto CAMINA A.C. Unidad de Primates No Humanos, Ciudad de México, México D.F., Mexico; Laboratorio de Bioenergética y envejecimiento celular, Depto. de Ciencias de la Salud, Universidad Autónoma Metropolitana, Unidad Iztapalapa, México D.F., Mexico.
Laboratorio de Bioenergética y envejecimiento celular, Depto. de Ciencias de la Salud, Universidad Autónoma Metropolitana, Unidad Iztapalapa, México D.F., Mexico.
Exp Gerontol. 2018 Jan;101:80-94. doi: 10.1016/j.exger.2017.11.003. Epub 2017 Nov 13.
Synapses loss during aging has been related to decreased neuronal excitability and reduced electrophysiological activity in the nervous system, as well as to increased brain damage. Those physiological and biochemical alterations have been related to the oxidative stress increase associated with old age. The main substrate of lipid peroxidation (LPX) in the central and peripheral nervous systems are the myelin sheaths, and their damage generates a delayed nerve conduction velocity. However, studies in which the neural conduction velocity is related to changes in the redox state are still lacking. Therefore, our aim was to correlate the sensory neural pathways delay in healthy geriatric Rhesus monkeys (Macaca mulatta) with the oxidative stress associated with physiological aging. Twenty-four monkeys were divided into four groups according to age and gender. Auditory, visual, and somatosensory evoked potentials were obtained. Superoxide dismutase, catalase, and glutathione peroxidase enzymatic activity, as well as LPX, were determined from blood samples. Our results showed significant differences between the older and younger age groups in all neural generators of the different sensory pathways evaluated, along with an increase in LPX and the antioxidant enzymatic activities. It suggests that, even though the enzymatic activity was found to be higher in older monkeys, probably as a compensatory effect, it was not enough to avoid LPX damage and the declined electric activity associated with age.
衰老过程中的突触损失与神经元兴奋性降低和神经系统电生理活性降低有关，还与大脑损伤增加有关。这些生理和生化变化与衰老相关的氧化应激增加有关。中枢和外周神经系统中脂质过氧化 (LPX) 的主要底物是髓鞘，其损伤会导致神经传导速度延迟。然而，关于神经传导速度与氧化还原状态变化相关的研究仍然缺乏。因此，我们的目的是将健康老年恒河猴（Macaca mulatta）的感觉神经通路延迟与与生理衰老相关的氧化应激相关联。24 只猴子根据年龄和性别分为四组。获得听觉、视觉和体感诱发电位。从血液样本中测定超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶的酶活性以及 LPX。我们的结果表明，在所评估的不同感觉通路的所有神经发生器中，年龄较大的组与年龄较小的组之间存在显著差异，同时 LPX 增加以及抗氧化酶活性增加。这表明，尽管在老年猴子中发现酶活性更高，可能是一种代偿性效应，但这还不足以避免与年龄相关的 LPX 损伤和电活动下降。
