作者: Vered Gazit , Ron Ben-Abraham , Chaim G. Pick , Izhar Ben-Shlomo , Yeshayahu Katz
DOI: 10.1016/S0091-3057(03)00147-3
关键词: Internal medicine 、 Chemistry 、 Hypoglycemia 、 Lesion 、 Toxicity 、 Hippocampal formation 、 TUNEL assay 、 Neurotoxicity 、 Glutamate receptor 、 Brain damage 、 Endocrinology
摘要: Abstract We investigated whether structural central neural damage and long-term neurobehavioral deficits after l -cysteine ( -Cys) administration in mice is caused by hypoglycemia. Neonatal ICR were injected subcutaneously with -Cys (0.5–1.5 mg/g body weight [BW]) or saline (control). Blood glucose was measured. At 50 days of age, introduced individually into an eight-arm maze for evaluation spatial memory (hippocampal-related behavior). Times visiting all eight arms number entries until completion the visits (maze criteria) The test repeated once daily 5 days. In situ terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay used detection brain damage. As early as 20 min up to 2 h postinjection, animals treated doses higher than 1.2 BW developed hypoglycemia looked ill. Several convulsed. Long-term survivors required more time, a dose-dependent manner, assimilate structure maze, (1.5 BW) exhibited TUNEL-positive changes hippocampal regions. All these reversible coadministration glucose. conclude that injection can cause pronounced associated mice. Since chemically different from other excitatory amino acids (glutamate aspartate), long-reported -Cys-mediated neurotoxicity may be connected its hypoglycemic effect.