Abstract
ABSTRACTPurpose:Reactive oxygen species (ROS), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) have been shown in the pathogenesis of acrylamide neurotoxicity. Hippophae rhamnoides L. extract (HRE) has a cytoprotective effect by stabilizing the production of ROS, IL-1β and TNF-α. The objective of the article was to investigate the effect of HRE on acrylamide-induced brain damage in rats biochemically and histopathologically.Methods:To the HRE+acrylamide only (ACR) group (n=6) of the animals, HRE was administered orally at a dose of 50 mg / kg into the stomach by gavage. The same volume of solvent (olive oil) was administered orally to the ACR (n=6) and healthy (HG) (n=6) groups. One hour after HRE administration, acrylamide was given orally at a dose of 20 mg/kg to HRE+ACR and ACR groups in the same way. This procedure was repeated once a day for 30 days. At the end of this period, brain tissues extracted from animals killed with 50 mg/kg thiopental anesthesia were examined biochemically and histopathologically.Results:It has been shown that HRE prevents the increase of malondialdehyde (MDA), myeloperoxidase (MPO), IL-1β and TNF-α with acrylamide and the decrease of total glutathione (tGSH) and glutathione reductase (GSHRd) levels in brain tissue.Conclusions:HRE may be useful in the treatment of acrylamide-induced neurotoxicity.
Highlights
Acrylamide (2-propenamid) is an active compound investigated among heat-induced food contaminants[1]
When the acrylamide only (ACR) group was compared with HG group, a significant increase in MDA levels and MPO activities were noted in brain tissues (p < 0.05)
This study investigated the effect of Hippophae rhamnoides L. extract (HRE) on acrylamideinduced oxidative stress-related neurotoxicity in brain tissue
Summary
Acrylamide (2-propenamid) is an active compound investigated among heat-induced food contaminants[1]. Several studies have reported that various food substances contain differing levels of acrylamide. High levels of acrylamide have been reported in fried and roasted food in particular[2,3]. Acrylamide has been documented to exhibit genotoxic, carcinogenic, neurotoxic, reproductive, and developmental effects[4]. Tabeshpour et al.[7] showed that acrylamide leads to oxidative brain damage by increasing malondialdehyde (MDA) production in brain tissue and reducing endogenous glutathione (GSH) production. Goudarzi et al.[8] showed that acrylamide exhibits neurotoxic effects by increasing the production of both oxidants and proinflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α)
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