Abstract
Protective Ability of Vitamin E Against Acetylsalicylic Acid-Induced Glutathione Depletion, Acetylcholinesterase and (Na+,K+)-ATPase Activities, and Erythrocyte Osmotic Fragility
Highlights
Non-steroidal anti-inflammatory drugs (NSAIDs) such as acetylsalicylic acid have been demonstrated to induce gastrointestinal erosions and ulcer leading to gastrointestinal mucosal injury and gastric bleeding [1,2,3]
We evaluated the protective ability of α-tocopheryl acetate (Vitamin E, Vit E) against Acetylsalicylic acid (ASA)-induced glutathione depletion, reduction in acetylcholinesterase (AChE) activity, Na+,K+-ATPase activity and erythrocyte osmotic fragility in the red blood cells isolated from male albino rats
Co-treatment of the red blood cells with ASA and vitamin E provided greater than 96% protection
Summary
Non-steroidal anti-inflammatory drugs (NSAIDs) such as acetylsalicylic acid (aspirin, ASA) have been demonstrated to induce gastrointestinal erosions and ulcer leading to gastrointestinal mucosal injury and gastric bleeding [1,2,3]. Parmar et al (2017) have demonstrated that ASA significantly inhibited acetylcholinesterase (AChE) activity in an in vitro mechanistic investigation and indicated that a low dose ASA therapeutic strategy may serve subjects suffering from Alzheimer’s disease [6] In this investigation, we evaluated the efficacy of vitamin E in ASA-induced effects on red blood cells. As it is well documented that hemoglobin assists red blood cells to carry oxygen and perform the routine biochemical and pathophysiological functions, and any disruption in this pathogenesis will cause anemia In this investigation, we extensively conducted erythrocyte osmotic fragility (% Hemolysis) following treatment with ASA and evaluated the protective ability of vitamin E in this pathophysiology. Our investigation was very important because ASA is extensively used worldwide and sometimes ASA is consumed in high dose, so the present investigation is important to evaluate whether co-administration of vitamin E may provide some protection against ASA-induced cellular injury
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