Abstract
The aims of this study were to investigate the influences of sweet grass on chronic ethanol-induced oxidative stress in the rat brain. Chronic ethanol intoxication decreased activities and antioxidant levels resulting in enhanced lipid peroxidation. Administration of sweet grass solution to ethanol-intoxicated rats partially normalized the activity activities of Cu,Zn-superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase, as well as levels of reduced glutathione and vitamins C, E, and A. Sweet grass also protected unsaturated fatty acids (arachidonic and docosahexaenoic) from oxidations and decreased levels of lipid peroxidation products: 4-hydroxynonenal, isoprostanes, and neuroprostanes. The present in vivo study confirms previous in vitro data demonstrating the bioactivity of sweet grass and suggests a possible role for sweet grass in human health protection from deleterious consequences associated with oxidative stress formation.
Highlights
Cells in the nervous systems of animals, including humans, are vulnerable to oxidative damage from reactive oxygen species (ROS)
The activity of antioxidant enzymes in the brain was altered by chronic ethanol intoxication (Table 1)
After administration of sweet grass to ethanol intoxicated rats, activities of superoxide dismutase and GSSG-R were similar to the values observed in the brain of control animals
Summary
Cells in the nervous systems of animals, including humans, are vulnerable to oxidative damage from reactive oxygen species (ROS). Reasons for this vulnerability include a high concentration of readily oxidizable substrates (especially membrane phospholipid polyunsaturated fatty acids), a high ratio of membrane surface area to cytoplasmic volume, and an extended axonal morphology that is prone to peripheral injury. Bielawska : many brain mechanisms promote ROS generation (Joseph et al 2005). If mild oxidative stress occurs, normal tissues often respond by bolstering antioxidant defense, severe or persistent oxidative stress can cause cellular component injury, cellular degeneration, and, brain cell death (Venkataraman et al 2010)
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