Reactive oxygen species (ROS) are involved in several cell death processes, including
cerebral ischemic injury. We found that glutamate-induced ROS accumulation and the
associated cell death in mouse hippocampal cell lines were delayed by pharmacological
inhibition of autophagy or lysosomal activity. Glutamate, however, did not stimulate
autophagy, which was assessed by a protein marker, LC3, and neither changes in
organization of mitochondria nor lysosomal membrane permeabilization were observed …