Neurobehavioral changes and activation of neurodegenerative apoptosis on long-term consumption of aspartame in the rat brain

Ashok, Iyyasamy; Wankhar, Dapkupar; Wankhar, Wankupar; Sheeladevi, Rathinasamy

doi:10.1016/j.jnim.2015.09.001

Cited by 27 publications

(34 citation statements)

References 58 publications

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“…Thereby, consumption of ASP leads to induction of apoptosis by downregulation of antiapoptotic and upregulation of apoptotic mediators, which ensued as a result of mRNA and DNA damages. In line with our study, other researchers reported downregulation of antiapoptotic and upregulation of apoptotic mediators in the different organs of experimental animals following long‐term intake of ASP 6,8,49,53,54 …”

Section: Discussionsupporting

confidence: 93%

“…In line with our study, other researchers reported downregulation of antiapoptotic and upregulation of apoptotic mediators in the different organs of experimental animals following long-term intake of ASP. 6,8,49,53,54 The decrease in concentration of FSH, LH and testosterone in the serum (at 80 and 160 mg/kg) could be related to direct and/or indirect negative effects of ASP consumption and subsequent OS induction on the pituitary-gonadal axis. The ultrastructural investigations in the juvenile rats and rabbits revealed that the chronic administration of ASP altered the structure of gonadotropic cells of the anterior pituitary gland.…”

Section: Discussionmentioning

confidence: 99%

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Insight into the mechanism of aspartame‐induced toxicity in male reproductive system following long‐term consumption in mice model

Anbara

Sheibani

Razi

et al. 2020

Environmental Toxicology

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Aspartame is one of the most common consumed artificial sweeteners utilized in many food products and beverages. It has been indicated that long‐term consumption of aspartame leads to reproductive toxicity but its mechanism is not well‐clear. In this study we investigated mechanism of aspartame‐induced reproductive toxicity in male mice. For this purpose, 36 NMRI mature male mice received three doses of 40, 80, and 160 mg/kg body weight of aspartame, respectively per day by gavage for 90 days and also a control group was considered which received 0.5 mL of normal saline as the same route. The results revealed that long‐term administration of aspartame at high doses significantly (P < .05) reduced gonadosomatic index, serum concentration of pituitary‐testicular axis hormones (FSH, LH, and testosterone). It also decreased sperm parameters and total antioxidant capacity, antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase), while it caused increase in nitric oxide and malondialdehyde levels in testis tissue and sperm samples. Also, it decreased attenuated testicular histomorphometric indices (tubular differentiation index, spermiogenesis index, and repopulation index), and steroidogenic foci, while increased mRNA damages and apoptosis rate, downregulated antiapoptotic (Bcl‐2) and upregulated proapoptotic (P53, BAX, and caspase‐3) mediators respectively in testis. These findings indicated that consumption of aspartame for a long period results in male reproductive toxicity by decrease in serum concentration of pituitary‐testis axis hormones and induction of oxidative stress and apoptosis in testis.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Insight into the mechanism of aspartame‐induced toxicity in male reproductive system following long‐term consumption in mice model

Anbara

Sheibani

Razi

et al. 2020

Environmental Toxicology

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“…A study reported that aspartame produced a biphasic modulation of internal calcium that was associated with up-regulation of calcium in resting neurons and down-regulation in activated neurons52. In another report, aspartame-treated animals showed an increase in the expression of apoptotic genes and consequently, enhanced neuronal cell death53. These results suggest that aspartame plays distinct roles in neuronal functions compared to the roles played by sugar in the brain.…”

Section: Discussionmentioning

confidence: 86%

Long-term consumption of sugar-sweetened beverage during the growth period promotes social aggression in adult mice with proinflammatory responses in the brain

Choi

Park

Kim

et al. 2017

Sci Rep

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Overconsumption of sugar-sweetened beverages (SSBs) is known to be a key contributor to the obesity epidemic; however, its effects on behavioral changes are yet to be fully studied. In the present study, we examined the long-term effects of SSB on social aggression in mice. Three-week-old weaned mice started to drink either a 30 w/v% sucrose solution (S30), plain water (CT), or an aspartame solution with sweetness equivalent to the sucrose solution (A30) and continued to drink until they were 11-week-old adults. Aggressive behaviors were assessed by the resident-intruder test. We found that SSB significantly promoted social aggression, accompanied by heightened serum corticosterone and reduced body weight. To understand the underlying mechanism, we performed transcriptome analyses of brain. The profiles of mice on S30 were dramatically different from those on CT or A30. Transcriptional networks related to immunological function were significantly dysregulated by SSB. FACS analysis of mice on S30 revealed increased numbers of inflammatory cells in peripheral blood. Interestingly, the artificial sweetener failed to mimic the effects of sugar on social aggression and inflammatory responses. These results demonstrate that SSB promotes aggressive behaviors and provide evidence that sugar reduction strategies may be useful in efforts to prevent social aggression.

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“…People with low levels of serotonin are often compelled to consume more sugar in a bid to increase serotonin production and this often results in a sugar addiction [108], which in turn can lead to insulin resistance (high levels of insulin cause receptors for insulin to shut down by means of 'down-regulation) [109]. Aspartame consumption in both higher doses [16] and safety doses [110,111] were shown to induce oxidative stress in the hypothalamus, leading to neuronal death (apoptosis). The glucose regulatory role of the hypothalamus would thus be impaired.…”

Section: Neurotransmitter Alterations Within Brain To Insulin Resistancementioning

confidence: 99%

“…Aspartame induces excess free radical production, in particular, reactive oxygen species (ROS) and reactive nitrogen species (RNS). These free radicals result in systemic oxidative stress [23] such as in blood cells [50,89,[115][116][117], brain cells [16,110,111,118,119], liver and kidney cells [20,22,120], heart cells [83,84] and immune organs [15,[121][122][123] (Figure 5). Systemic oxidative stress is associated with insulin resistance [124].…”

Section: Oxidative Stress To Insulin Resistancementioning

confidence: 99%

Aspartame: Should Individuals with Type II Diabetes be Taking it?

Choudhary

2018

CDR

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Neurobehavioral changes and activation of neurodegenerative apoptosis on long-term consumption of aspartame in the rat brain

Cited by 27 publications

References 58 publications

Insight into the mechanism of aspartame‐induced toxicity in male reproductive system following long‐term consumption in mice model

Insight into the mechanism of aspartame‐induced toxicity in male reproductive system following long‐term consumption in mice model

Long-term consumption of sugar-sweetened beverage during the growth period promotes social aggression in adult mice with proinflammatory responses in the brain

Aspartame: Should Individuals with Type II Diabetes be Taking it?

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