Alpha-Tocopherol Supplementation Restricts Aluminium- and Ethanol-Induced Oxidative Damage in Rat Brain but Fails to Protect Against Neurobehavioral Damage

Nayak, Prasunpriya; Sharma, Shiv Bhushan; Chowdary, N V S

doi:10.1080/19390211.2018.1451940

Cited by 9 publications

(3 citation statements)

References 29 publications

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“…Maintenance of systemic, organ or regional GSH level by vitamin E, TRF or T3 in presence of oxidative stressor had been reported times and again. [23,32,[37][38][39][40][41][42] Increases in cerebellar GSH level were noticed in the ST3 group (statistically significant) and TT3 group (statistically significant) in comparison to NT3 and PT3 groups of Et-0 phase of current study. However, in presence of Et exposures, TT3 group abled to maintain the level of cerebellar GSH while ST3 group failed to do so.…”

Section: Biochemical Parametermentioning

confidence: 53%

Evaluation of Varied Modalities of Tocotrienol Supplementations to Counter the Cerebellar Oxidative Stress Caused by Low-to-moderate Doses of Ethanol in Rats

Dasari¹,

Nayak²

2019

IJCEP

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Background and Aim: Self-intoxication with Ethanol (Et) is a common problem worldwide. Being a psychoactive drug, neurotoxic effects of Et are well known. Cerebellum is highly vulnerable to Et exposure. Tocotrienols (T3) are relatively rare components of vitamin E and have the potential to prevent the oxidative stress and act as neuroprotective. Varied modalities of T3 supplementations were evaluated to identify the possibilities of countering cerebellar oxidative stress caused by low-to-moderate doses of Et exposure. Methods: Four phase of experiments were carried out with nil (Et-0) and three doses of Et exposures (Et-I, Et-II and Et-III) for 4 weeks. In each phase, 4 groups of Wistar rats were maintained with sham supplementation (NT3), Prior Supplementation (PT3), Simultaneous Supplementation (ST3) and Total Supplementation (TT3) with T3 for 6 weeks. Cerebellar levels of reduced Glutathione (GSH), Lipid Peroxidation (LPO) and activities of catalase, Superoxide Dismutase (SOD), Glutathione Peroxidase (GPx) and Glutathione Reductase (GR) were estimated and Superoxide and Peroxide Handling Capacities (SPHCs) were calculated. Results: All the tested cerebellar oxidative stress parameters and handling capacities were significantly influenced by the modalities of T3 supplementation. However, low-to-moderate doses of Et exposures contributed significantly in alterations of LPO level, GPx activity, GR activity and glutathione-dependent SPHC of cerebellum. Conclusion: Critical evaluation of studied parameters suggest insufficient overall performance of ST3 type of supplementation, whereas, TT3 type of supplementation was the best among the modalities of T3 supplementation. However, excess T3 supplementation may not be beneficial in some cases of oxidative stress parameters and SPHC of cerebellum.

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Section: Biochemical Parametermentioning

confidence: 53%

Evaluation of Varied Modalities of Tocotrienol Supplementations to Counter the Cerebellar Oxidative Stress Caused by Low-to-moderate Doses of Ethanol in Rats

Dasari¹,

Nayak²

2019

IJCEP

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“…This finding agrees with the work of Dwivedi and Tomar (42), which also showed significantly severe hypokinesia both in terms of latency to leave the starting square of the OFT and the number of lines crossed. However, Nayak et al (43) demonstrated the failure of vitamin E to protect against neurodegeneration in rat brains at a given dose, making the rats perform poorly in some motor coordination tasks. There was also a significant increase in the number of lines crossed following the co-administration of both vitamins compared to the reserpine group, and this effect was more profound than that observed following single administrations.…”

Section: Discussionmentioning

confidence: 99%

Co-Administration of Vitamins C and E is Protective against Reserpine-induced Motor Impairment in Mice.

Danboyi¹,

Jimoh²,

lhassan³

et al. 2021

ABMS

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Background: The conventional treatments for Parkinson's disease, the most common movement disorder globally, have not been able to halt its progression hence, newer approaches targeting its pathogenesis are being explored. We investigated the effect of vitamins C and E (in combination) on reserpine-induced motor impairment in mice. Materials and Methods: Twenty-five mice were randomly grouped into five groups of five mice each. All the groups except group I (control), were given an alternate days injection of reserpine 0.1 mg/kg intraperitoneally. Groups III and IV were administered vitamin E 200 mg/kg/day (vitamin E group), and vitamin C 250 mg/kg/day (vitamin C group), respectively while group V (co-administered group) was given both vitamins orally. Group II (reserpine group) received nothing in addition to reserpine. All drugs were given concurrently for 28 days. The neurobehavioral assessment was performed using beam walking and open field tasks. Results were presented as mean±SEM and statistical significance was placed at p < 0.05. Results: There were significant increases in a number of foot slips (3.60±0.68; p = 0.002) and the time spent in reaching the 'safe' platform (36.60±5.78 s; p = 0.0001) in the reserpine group, both of which were markedly reduced in the co-administered group (0.25±0.25 and 3.00±0.41s respectively). The co-administered group demonstrated a marked decrease in transfer latency (10.33±1.45s; p = 0.005) and crossed significantly more lines (56.00±13.53 lines; p = 0.0001) in the open field compared to the reserpine group (214.00±64.16s and 4.3±1.67 lines respectively). Conclusion: Co-administration of vitamins C and E protected against motor impairment induced by reserpine in mice.

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“…The exposure sources for Al include geochemical, industrial, anthropological and uses in daily life. [1,2] Enhancement of Al exposure is caused from various eatables, medications, avoidable deliberate / intentional uses of topically applied cosmetics and hygiene products like deodorants and toothpaste. [3] In addition, some occupational groups are specifically subjected to high level of Al exposures.…”

Section: Introductionmentioning

confidence: 99%

Effects of Acute Aluminium Exposure on Liver Cytoarchitecture of Adolescent Female Wistar Rats

Nayak¹,

Krishna

Sharma

et al. 2022

IJCEP

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Background and Aim: Exposure to aluminium is unavoidable, but there is no useful function of aluminium in our body. There are several reports demonstrating hepatotoxicity of aluminium. The current investigation was planned to evaluate the effects of acute exposure of aluminium to adolescent female Wistar rats. Methods: Adolescent female Wistar rats were intraperitoneally exposed to AlCl 3 at a dose of 5 and 10 mg/Kg bw for 2 weeks. Results: There was no statistically significant change in the growth and size of livers of the exposed animals. However, the current doses of aluminium exposures caused significant reductions in total number of hepatocytes and significant rise in hepatocytes with cytosolic vacuolation. In addition, there were certain other histopathologic changes in the cytoarchitecture of hepatic tissues. Conclusion: In summary, this is the first report showing degenerative changes in liver by low dose of aluminium exposure for 2 weeks in adolescent female rats. This could be used as real-life hepatotoxic model in adolescent rats.

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Alpha-Tocopherol Supplementation Restricts Aluminium- and Ethanol-Induced Oxidative Damage in Rat Brain but Fails to Protect Against Neurobehavioral Damage

Cited by 9 publications

References 29 publications

Evaluation of Varied Modalities of Tocotrienol Supplementations to Counter the Cerebellar Oxidative Stress Caused by Low-to-moderate Doses of Ethanol in Rats

Evaluation of Varied Modalities of Tocotrienol Supplementations to Counter the Cerebellar Oxidative Stress Caused by Low-to-moderate Doses of Ethanol in Rats

Co-Administration of Vitamins C and E is Protective against Reserpine-induced Motor Impairment in Mice.

Effects of Acute Aluminium Exposure on Liver Cytoarchitecture of Adolescent Female Wistar Rats

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