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The potential neuroprotective effect of allicin and melatonin in acrylamide-induced brain damage in rats

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Abstract

Acrylamide (ACR) is an unsaturated monomer that served various fields; however, it is a potent neurotoxin. The target of the present study is to explore the neuroprotective efficacy of allicin and melatonin on ACR-induced neurotoxicity. Thirty-six male adult rats were non-selectively separated into six groups: placebo, allicin (20 mg/kg b.w daily per os), melatonin (10 mg/kg b.w 3 times/week per os), ACR (50 mg/kg b.w daily per os), ACR-allicin, and ACR-melatonin at the same doses as the preceding groups. The assessment of brain biomarkers, neurotransmitters, antioxidative status, Nrf2 signaling pathway, and histopathological analyses was performed following 21 days. ACR exposure induced brain lipid and DNA oxidative damage as well as reduced the glutathione (GSH) levels. The obvious brain oxidative injuries contributed to distinct brain dysfunction that was assured by alteration of brain neurotransmitters (serotonin, dopamine, acetylcholine, and acetylcholinesterase) and pathological brain lesions. Furthermore, ACR exposure increased hydroxy deoxyguanosine (8-OHdG), tumor necrosis factor-α (TNF-α), and amyloid protein (AB1-42). Finally, the mRNA transcripts of brain Keap-1, Nrf2, and NF-kB were upregulated after ACR intoxication. Interestingly, allicin and melatonin alleviated the ACR-induced brain damage assessed by the normalization of the mentioned analyses. The present study demonstrated the protective role of both allicin and melatonin in ACR-prompted neuropathy by alleviation of redox imbalance and enhancement of neurotransmitters as well as relieving DNA damage and anti-inflammatory effect.

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Data Availability

All data analyzed during the current study are included in this published article.

Abbreviations

Ach:

Acetylcholine

AchE:

Acetylcholine esterase

ACR:

Acrylamide

ANOVA:

Analysis of variance

ARE:

Antioxidant response element

Aβ1-42:

Amyloid protein1-42

BDNF:

Brain-derived neurotrophic factor

DDS:

Diallyl disulfide

DTS:

Diallyl trisulfide

GAPDH:

Glyceraldehyde-3-phosphate dehydrogenase

GSH:

Reduced glutathione

GSSG:

Oxidized glutathione

Keap-1:

Kelch-like ECH-associated protein-1

MDA:

Malondialdehyde

MT:

Melatonin

NF-kB:

Nuclear factor-kappa B

nNOS:

Nitric oxide synthase

Nrf2:

Nuclear factor erythroid 2 like factor

8-OHdG:

8-Hydroxy deoxyguanosine

ROS:

Reactive oxygen species

SAC:

S-Allylcysteine

SE:

Standard error

TNF-α:

Tumor necrosis factor

TTR:

Transthyretin

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H.A.E: funding, investigation, and methodology; N.M.T: idea, design, and supervision; M.A.L: design, validation, writing the manuscript draft, manuscript revision, and editing; M.S.E: data collection and analysis, software, and visualization.

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Correspondence to Mohamed A. Lebda.

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Edres, H.A., Taha, N.M., Lebda, M.A. et al. The potential neuroprotective effect of allicin and melatonin in acrylamide-induced brain damage in rats. Environ Sci Pollut Res 28, 58768–58780 (2021). https://doi.org/10.1007/s11356-021-14800-x

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