Upregulation of Antioxidant Gene Expressions and Enzyme Activity Against Acrylamide-Induced Neurotoxicity in Mice after Grape Seed Extract Treatment

Sarah Albogami

doi:10.2174/1874070702014010023

Abstract

Background: The risk of occupational exposure to acrylamide is high and long-term acrylamide exposure can cause neurotoxicity. Thus, therapeutic agents that can protect against acrylamide-induced neurotoxicity are needed. Objective: To investigate whether Grape Seed Extract (GSE) protects against acrylamide-induced neurotoxicity in mice. Methods: Mice were divided into saline, GSE, acrylamide, GSE followed by acrylamide, acrylamide followed by GSE, and simultaneous acrylamide and GSE treatment groups. Gene expression and antioxidant enzyme levels were then determined using RT-PCR and biochemical assays. Results: Gpx1 (P < 0.05), Prdx3 (P < 0.01), SOD1 (P < 0.05), and CAT (P < 0.05) significantly upregulated in GSE-treated mice, compared to those in untreated controls. In contrast, Gpx1 (P < 0.05), Prdx3 (P < 0.05), SOD1 (P < 0.05), and CAT (P < 0.05) significantly downregulated in acrylamide-treated mice compared to those in untreated controls. Results of the treatment with GSE before exposure to acrylamide or simultaneously with acrylamide indicated that GSE restored Gpx1, Prdx3, SOD1, and CAT expression to similar levels as those in the control group. GSE treatment after exposure to acrylamide did not exert any neuroprotective effects against acrylamide, as revealed by significant downregulation of Gpx1 (P < 0.05), Prdx3 (P < 0.01), SOD1 (P < 0.05), and CAT (P < 0.05) compared to that in untreated controls. Animals treated with grape seed before acrylamide treatment showed no significant change in LPO activities and a significant increase in GSH levels, compared to those in untreated controls. Conclusion: GSE exerted neuroprotective effects against acrylamide-induced neurotoxicity. Acrylamide caused oxidative stress 20 days post-exposure. However, grape seed treatment before exposure to acrylamide restored all test parameters to levels similar to control values.

Highlights

Acrylamide (C3H5NO), known as prop-2-enamide or acrylic amide, has a relative molecular mass of 71.08 Da [1 - 4]
Animals treated with grape seed after acrylamide treatment (Group III) showed an evident increase in the Lipid Peroxidation (LPO) activities (P < 0.05) and a significant decrease in the GSH levels (P < 0.05) in brain tissues, relative to those in the untreated controls (Group I)
Animals treated with grape seed before acrylamide treatment (Group IV) showed no significant change in the LPO

Summary

Introduction

Acrylamide (C3H5NO), known as prop-2-enamide or acrylic amide, has a relative molecular mass of 71.08 Da [1 - 4]. Acrylamide can act as an effective neurotoxin (nerve toxin) in humans and animals [5 - 7]. Sarah Albogami and/or attenuation of acrylamide in the polluted water, is an effective way to avoid such pollution. Long-term acrylamide exposure can cause neurotoxicity, which is characterized by skeletal muscle weakness, ataxia, numbness of the hands and feet, gait abnormalities, and cognitive deficits [12]. Toxicological studies imply that acrylamide vapors can irritate the skin and eyes and cause paralysis of the cerebrospinal system [13 - 15]. Studies conducted with laboratory animals, including guinea pigs, rodents, rabbits, dogs, and cats, have indicated that daily exposure to acrylamide (0.5–50 mg/kg per day) causes neurological changes similar to those observed during neurotoxicity in humans [16]. The risk of occupational exposure to acrylamide is high and long-term acrylamide exposure can cause neurotoxicity. Therapeutic agents that can protect against acrylamide-induced neurotoxicity are needed

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Discussion

Conclusion