Longer period of oral administration of aspartame on cytokine response in Wistar albino rats

Choudhary, Arbind Kumar; Devi, Rathinasamy Sheela

doi:10.1016/j.endonu.2014.11.004

Cited by 20 publications

(13 citation statements)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The data of the present study indicated a significant increase in the expression of IL-6 and TNF-a in ASP group and a correlation co exists between IL-6 and TNF and the severity as well as toxicity of ASP metabolite, methanol or formaldehyde may be the causative factors behind the changes observed (Choudhary and Devi, 2015). These results suggest that both cytokines had toxic effects on myelin, Schwann cells, and endothelial cells, increased vascular permeability, and broke down the BBB and blood-nerve barrier (BNB) (Misawa et al, 2001).…”

Section: Discussionmentioning

confidence: 66%

“…This study indicated that the cytokines bind to the luminal side of the blood vessels and do not enter the brain but instead induce production of PGE 2 that can enter the brain and forward the signal. Additionally it has been proven that COX-2, which is critical for PGE 2 production, is activated in the brain vasculature in response to ASP metabolites as mentioned by Choudhary and Devi (2015).…”

Section: Discussionmentioning

confidence: 96%

“…Atrophy of the hippocampus and other limbic structures has been shown to take place in humans suffering from chronic depression (Hwang et al, 2006). BDNF has been implicated as a specific growth and differentiation factor in the development of serotonergic neurons (Choudhary and Devi, 2015). BDNF has a pleiotropic profile, preserving cell viability and function, preventing neuronal degeneration during stress, and acting as an antidepressant (Lu et al, 2013), with actions occurring through the stimulation of the tropomyosin-related kinase B (TrkB) receptor (Feng et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

“…Aspartate is a highly excitatory neurotransmitter and phenylalanine is a precursor of catecholamines in the brain, increased levels of these molecules could change the basic activity level of the brain to an unhealthy state (Nosti-Palacios et al, 2014). The methanol metabolized from ASP is converted to formaldehyde and then formic acid (Choudhary and Devi, 2015). Besides, ASP ingestion is implicated in neurological problems and chronic exposure of aspartame resulted in detectable methanol in blood (Simintzi et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

“…It is found in more than 6000 products including carbonated and powdered soft drinks, hot chocolate, chewing gum, candy, desserts, yogurt, and tabletop sweeteners, as well as some pharmaceutical products like vitamins and sugar-free cough drops. Artificial sweeteners, such as ASP, are therefore often included in the diet of diabetic patients because these compounds sweeten foods without adding calories or raising blood glucose levels (Choudhary and Devi, 2015). In the European Union, it is codified as E951.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Anti-neuroinflammatory and antioxidant effects of N-acetyl cysteine in long-term consumption of artificial sweetener aspartame in the rat cerebral cortex

Saleh

2015

The Journal of Basic & Applied Zoology

View full text Add to dashboard Cite

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 E 2 (PGE 2 ) production with selective attenuation in expression of proinflammatory cytokines of interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-a) 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. ª 2015 The Egyptian German Society for Zoology. Production and hosting by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

show abstract

Section: Discussionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 96%