Access Restriction

Author Saleh, Afaf Abbass Sayed
Source Directory of Open Access Journals (DOAJ)
Content type Text
Publisher Springer
File Format HTM / HTML
Date Created 2017-01-16
Copyright Year ©2015
Language English
Subject Domain (in LCC) QL1-991
Subject Keyword Cytokine ♦ Aspartame ♦ Free-radical ♦ Inflammation ♦ Science ♦ N-acetyl cysteine ♦ Zoology
Abstract This study specifically focuses to investigate whether N-acetyl cysteine (NAC) has potential ameliorative effects against aspartame-induced brain pathophysiology in rats. Thirty adult male Wistar rats weighing 200–220 g were randomly divided into three groups as follows: the first group was administered with distilled water and served as the control group; the second group was given aspartame at a dose of 75 mg/kg b.wt. and the third group was given both aspartame and N-acetyl cysteine at dose of 75 mg/kg b.wt. and 600 mg/kg b.wt. respectively. Oral administration was done in the morning daily for 90 days. Long term consumption of the artificial sweetener aspartame (ASP) induced large increments in cortical inflammation and oxidative stress. Daily oral NAC administration can significantly reverse brain-derived neurotrophic factor (BDNF) levels, blocked the cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) production with selective attenuation in expression of proinflammatory cytokines of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in the rat cerebral cortex. Also, NAC can significantly replenish and correct intracellular glutathione (GSH) levels, modulate the elevated levels of total nitric oxide (TNO) and lipid peroxidation (LPO). Conclusions: The present results amply support the concept that the brain oxidative stress and inflammation coexist in experimental animals chronically treated with aspartame and they represent two distinct therapeutic targets in ASP toxicity. The present data propose that NAC attenuated ASP neurotoxicity and improved neurological functions, suppressed brain inflammation, and oxidative stress responses and may be a useful strategy for treating ASP-induced neurotoxicity.
ISSN 20909896
Age Range 18 to 22 years ♦ above 22 year
Educational Use Research
Education Level UG and PG ♦ Career/Technical Study
Learning Resource Type Article
Publisher Date 2015-10-01
e-ISSN 20909896
Journal Journal of Basic and Applied Zoology
Volume Number 72
Issue Number C
Page Count 8
Starting Page 73
Ending Page 80

Source: Directory of Open Access Journals (DOAJ)