Ameliorating Effect of Fish Oil on Acrylamide Induced Oxidative Stress and Neuronal Apoptosis in Cerebral Cortex

Abstract

Acrylamide (ACR) is a known industrial toxic chemical that produce neurotoxicity characterized by progressive neuronal degeneration. This study was designed to investigate the protective effect of fish oil on ACR-induced neuronal damage in Wistar rats. ACR enhances the production of reactive oxygen species and potentially affects brain. ACR administered rats showed increased levels of lipid peroxidative product, protein carbonyl content, hydroxyl radical and hydroperoxide which were significantly modulated by the supplementation of fish oil. The activities of enzymic antioxidants and levels of reduced glutathione were markedly lowered in ACR-induced rats; fish oil treatment augmented these antioxidant levels in cortex. Free radicals generated during ACR administration reduced the activities of membrane adenosine triphosphatases and acetylcholine esterase. Fish oil enhanced the activities of these enzymes near normal level. Histological observation represented the protective role of fish oil in ACR-induced neuronal damage. Fish oil reduced the ACR-induced apoptosis through the modulation in expressions of B-cell lymphoma 2 (Bcl2)-associated X protein and Bcl2-associated death promoter. Further, fish oil increases the expression of heat shock protein 27 (Hsp27) in ACR-induced rats. This study provides evidence for the neuroprotective effect of fish oil on ACR-induced neurotoxicity by reducing oxidative stress and apoptosis with modulation in the expression of Hsp27.

The effect of lipoic acid on acrylamide-induced neuropathy in rats with reference to biochemical, hematological, and behavioral alterations

“…In contrast, the brain antioxidant enzymes; GST, GPx, and GR activities and GSH content significantly decreased in the ACR-treated rats when compared with the control group (Table 4). These results are inconsistent with those of Lakshmi et al (2012) who reported that the ACR-intoxicated rats exhibited an increase in the LPO, protein carbonyl, hydroxyl radical, and hydroperoxide levels with subsequent decrease in the activities of enzymatic antioxidants, and the level of GSH. ACR promotes the generation of reactive oxygen species (ROS) and the depletion of antioxidants, leading to neurodegeneration (Zhu et al, 2008).…”

“…These results were in agreement with Lakshmi et al (2012) who reported that the activity of AChE was decreased in the ACR-induced rats. Free radical formation by ACR may upset the prooxidant/antioxidant balance within the brain, which could be one of the reasons for the decrease in the AChE activity (Tsakiris et al, 2000).…”

Morphological evaluation of the protective role of dark soy sauce against acrylamide induced neurotoxicity in albino rats

“…The current study was designed to investigate the ameliorating effect of DSS on ACR induced neurotoxicity and neuronal degeneration in trigeminal ganglia -as a part of peripheral nervous system -and cerebellar cortex -as a part of CNS -in rats. The results are explained by previous studies [9,19]. They proved that ACR enhances the production of reactive oxygen species which play a role in the oxidative stress and potentially affect the brain.…”

Determination of acrylamide-induced chick embryo brain glutathione S-transferases expression through enzyme activity and western blot

“…ACR shows its toxic effect on both central nervous system and peripheral nervous system [16]. Both oxidative stress and apoptosis play a key role in ACR-induced toxicity [17][18][19]. ACR-induced lipid peroxidation is the reason forreproductive, and neurotoxic properties [21,22], induces apoptosis in cerebral cortex [19], and efficiently binds to the brain [23].…”

“…Both oxidative stress and apoptosis play a key role in ACR-induced toxicity [17][18][19]. ACR-induced lipid peroxidation is the reason forreproductive, and neurotoxic properties [21,22], induces apoptosis in cerebral cortex [19], and efficiently binds to the brain [23]. In both laboratory animals and humans, ACR neurotoxicity is characterized by ataxia and distal skeletal muscle weakness [24].…”