Abstract
γ-l-glutamyl-S-[2-[[[3,4-dihydro-2,5,7,8-tetramethyl-2-(4,8,12-trimethyltridecyl)-2H-1-benzopyran-6-yl]oxy]carbonyl]-3-[[2-(1H-indol-3-yl)ethyl]amino]-3-oxopropyl]-l-cysteinylglycine sodium salt (ESeroS-GS) is a water-soluble derivative of α-tocopherol (vitamin E). We reported previously that ESeroS-GS can act as an anti-inflammatory agent and can induce cell death in breast cancer cells. However, the potential antioxidant capacities of ESeroS-GS remain elusive. Here, we measured its scavenging effects on free radicals and evaluated its protective effects on neuronal cells against oxidative stress. The results indicated that ESeroS-GS effectively scavenged both 2,2’-azinobis(3-ethylbenzothiazoline)-6-sulfonate free radicals (ABTS•+) and 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radicals, and attenuated H2O2-induced neuronal cell death. H2O2 treatment induced lysosomal membrane permeabilization rapidly, and caused the redistribution of lysosomal proteases, which were responsible for the neuronal cell death. ESeroS-GS abolished the interaction between tBid and the lysosomal membranes, blocked the translocation of tBid to the lysosomal membranes, decreased its oligomerization within the membrane circumstances, prevented the lysosomal membrane permeabilization, and thus attenuated the neuronal cell death. These data suggest that ESeroS-GS protected the neuronal cells from oxidative stress by stabilizing lysosomal membranes, and thus might act as a novel neuroprotector for neuronal diseases associated with oxidative stress.
Highlights
In our body, a number of biochemical reactions involve the generation of reactive oxygen species (ROS)
These data suggest that ESeroS-GS protected the neuronal cells from oxidative stress by stabilizing lysosomal membranes, and might act as a novel neuroprotector for neuronal diseases associated with oxidative stress
We reported here that ESeroS-GS effectively scavenged free radicals and protected neuronal cells from oxidative stress-induced cell death by stabilizing lysosomes
Summary
A number of biochemical reactions involve the generation of reactive oxygen species (ROS). The major sources of endogenous ROS are mitochondria. Leakage of electrons during oxidative phosphorylation causes, depending on the animal species and rate of respiration, the conversion of. Under certain pathological conditions, when ROS are not effectively eliminated by the antioxidant defense system, the dynamic balance between the generation and diminution of ROS is broken. Excessive ROS can attack lipids, carbohydrates, proteins and DNA, resulting in oxidative stress. Several lines of evidence link ROS to the onset of a variety of pathologic events, such as coronary heart disease [2], cancer [3], type 2 diabetes [4], and the degenerative diseases associated with aging [5,6]
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