Vieyra-Reyes Patricia, Millán-Aldaco Diana, Palomero-Rivero Marcela, Jiménez-Garcés Clementina, Hernández-González Margarita, Caballero-Villarraso Javier
Laboratorio de Neurofisiología de la Conducta. Facultad de Medicina, Universidad Autónoma del Estado de México, 50120, Toluca, Estado de México, Mexico.
División de Neurociencias, Departamento de Neuropatología Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, 04510, México DF, Mexico.
J Physiol Biochem. 2017 Feb;73(1):99-110. doi: 10.1007/s13105-016-0529-x. Epub 2016 Oct 24.
Iron is a trace element and a structural part of antioxidant enzymes, and its requirements vary according to age and gender. We hypothesized that iron deficiency (ID) leads to an increase in free radicals which mainly affect the brain, and the severity of damage would therefore be dependent on age and gender. Two groups of Wistar rats were evaluated evolutionarily: 100 rats (50 males; 50 females) with ID diet and 100 rats (50 males; 50 females) with standard diet. Both groups were offspring from mothers who were previously under the same dietary intervention. The ages studied roughly correspond to stages of human development: birth (0 postnatal day "PND" in rats), childhood (21 PND), early adolescence (42 PND), late adolescence (56 PND), and adulthood (70 PND). The following biomarkers in the brain, blood, and liver were analyzed: lipid peroxidation products (LPO), protein carbonyl content and activity of the antioxidant enzymes, superoxide dismutase, catalase, and glutathione peroxidase. It was demonstrated that ID subjects are born with high levels of LPO in the brain and low antioxidant activity, the damage being more severe in males. After birth, antioxidant defense focuses on the central level (brain) in ID females and on the peripheral level (blood and liver) in ID males. In two critical stages of development, birth and late adolescence, antioxidant protection is insufficient to counteract oxidative damage in ID subjects. Moreover, we observed that the variability of results in the literature on oxidative stress and ID comes from gender and age of the subjects under study. With this, we can establish patterns and exact moments to carry out studies or treatments.
铁是一种微量元素,是抗氧化酶的结构组成部分,其需求量因年龄和性别而异。我们推测缺铁会导致自由基增加,而自由基主要影响大脑,因此损伤的严重程度将取决于年龄和性别。对两组Wistar大鼠进行了长期评估:100只大鼠(50只雄性;50只雌性)采用缺铁饮食,100只大鼠(50只雄性;50只雌性)采用标准饮食。两组大鼠均为先前接受相同饮食干预的母鼠的后代。所研究的年龄大致对应于人类发育阶段:出生(大鼠出生后0天“PND”)、儿童期(21 PND)、青春期早期(42 PND)、青春期晚期(56 PND)和成年期(70 PND)。分析了大脑、血液和肝脏中的以下生物标志物:脂质过氧化产物(LPO)、蛋白质羰基含量以及抗氧化酶超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶的活性。结果表明,缺铁的实验对象出生时大脑中的LPO水平较高,抗氧化活性较低,雄性的损伤更严重。出生后,缺铁雌性的抗氧化防御集中在中枢水平(大脑),而缺铁雄性的抗氧化防御集中在外周水平(血液和肝脏)。在发育的两个关键阶段,即出生和青春期晚期,抗氧化保护不足以抵消缺铁实验对象的氧化损伤。此外,我们观察到关于氧化应激和缺铁的文献中结果的差异来自所研究对象的性别和年龄。据此,我们可以确定开展研究或治疗的模式和确切时机。