Objective: Early life stress (ELS) increases the vulnerability to developing psychopathological disorders in adulthood that are accompanied by brain inflammatory processes. However, it is not known how a combined double hit (stress and immune) at an early age affects the response of the neuroimmune system. Here we investigated the effect of periodic maternal separation (MS) followed by administration of lipopolysaccharide (LPS) on glial cells in the CA3 region and hilus of the hippocampus and on cytokine release on postnatal day (PN) 15. Methods: Male rat pups were subjected to MS (3 h/day, PN1-14). MS and control pups received a single LPS injection (1 mg/kg of body weight) on PN14. They were subjected to an open field test 1 h later. The pups were sacrificed 90 min after LPS injection (PN14) or on PN15 for cytokine or immunohistological analyses, respectively. Results: LPS reduced the locomotion and induced high corticosterone levels in treated pups. MS or LPS reduced microglial density and activated microglial cells in the hippocampal CA3 and hilus regions. Microglial activation was highest in MS-LPS pups. The astrocyte density was mildly reduced by MS or LPS in the CA3 region and hilus, but the reduction was maximal in MS-LPS pups. LPS increased the secretion of plasmatic interleukin (IL)-1β, tumor necrosis factor-α, and IL-6, and of hippocampal IL-1β protein, but these were attenuated in MS-LPS pups. Conclusion: Although MS and LPS activate neuroimmune cells, stress attenuates the hippocampal and peripheral cytokine response to LPS through an as-yet unidentified adaptive mechanism. These results provide information regarding the neurobiology of stress and inflammation.

Reactive oxygen species (ROS) are usually produced by the living cell and have different functions in its normal activity. However, if they are produced excessively, or if the system that keeps them in controlled levels is deficient or insufficient, a phenomenon known as oxidative stress is produced. This is related to the aging process and the onset and development of several diseases as well as their complications such as endothelial dysfunction in cardiovascular disease concomitant with the oxidation of low density lipoproteins and aggravated by smoking, the appearance of advanced glycosylation end products in diabetes mellitus. In neurodegenerative disorders such as Alzheimer's disease, neuron plasma membrane malfunction is caused by phospholipids peroxidation, leading to cell death.Cancer develops from genetic mutations resulting from DNA damage.Taking this into account, several antioxidant properties have been studied in different foods, beverages and spices, including their relationship with the prevention of degenerative diseases. Antioxidants obtained through diet can act in different ways: first, preventing the excess of free radicals, thus avoiding oxidative damage to the cell. Secondly, after damage has occurred, antioxidants can control free radical levels preventing further damage thereby alleviating some symptoms caused by oxidative stress. In this review, some basic concepts of reactive oxygen species, oxidative stress and antioxidants are analyzed, as well as some of the direct and indirect methods used to assess the antioxidant capacity of foods. Some of the food highly consumed by the Mexican population has antioxidant capacity and it is herein summarized.

No abstract

No abstract

No abstract