title: Effects of glucose concentration on redox status in rat primary cortical neurons under hypoxia.
abstract: Reduced supply of glucose involves in many pathological conditions such as stroke and contributes to ischemic injuries. In contrast, hyperglycemia has also been regarded as an important factor in causing and exaggerating stroke damage. Although the molecular mechanism(s) of imbalanced glucose-induced cellular injuries under low oxygen conditions are not clear, oxidative stress has been implicated in both hypo- and hypeglycemic damage. Redox status is critical for the regulation of cellular signaling and cell survival. The effects of glucose levels on redox status are not well understood in neurons under hypoxia. The purpose of this study was to determine the effects of glucose concentration on the redox status of rat primary neurons under hypoxia. The cellular redox status was determined from GSH/GSSG ratios, and oxidation of 2,3-dichlorofluorscein diacetate was used to assess levels of reactive oxygen species (ROS). We found that glucose levels were critical in regulating redox state in these neurons under hypoxia. The results showed that under hypoxic conditions: (1) there was an optimal glucose concentration (25mM) at which neurons maintained a reducing environment and showed the lowest levels of ROS and cell death; (2) in the concentration range of 0-25mM, the presence of glucose increased cellular GSH/GSSG ratio and reduced ROS and cell death; and (3) over-supply of glucose (25-100mM) elevated ROS levels, produced an oxidizing environment, and increased cell death. These results suggest that cellular redox status regulated by glucose may play an important role in glucose-mediated cellular responses in hypoxia.
authors.affiliation: Center of Biomedical Research Excellence and College of Pharmacy, University of New Mexico Health Sciences Center, Albuquerque, NM 87131-0001, USA. hshi@salud.unm.edu
authors.forename: Honglian
authors.initials: H
authors.lastname: Shi
authors.forename: Ke Jian
authors.initials: KJ
authors.lastname: Liu
mesh_terms: D000818:Animals; D015687:Cell Hypoxia / Q000187:drug effects*; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology*; D004305:Dose-Response Relationship, Drug; D004622:Embryo, Mammalian; D005947:Glucose / Q000494:pharmacology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D009474:Neurons / Q000187:drug effects*; D010084:Oxidation-Reduction; D010100:Oxygen / Q000494:pharmacology; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D013997:Time Factors
chemical_list: D017382:Reactive Oxygen Species; D007770:L-Lactate Dehydrogenase; D005947:Glucose; D010100:Oxygen