Effects of Acrylamide on the Nervous Tissue Antioxidant System and Sciatic Nerve Electrophysiology in the Rat

Abstract

To investigate the time-dependent effects of acrylamide (ACR) on the antioxidative status in rat nerve tissues, adult male Wistar rats were given ACR (40 mg/kg, i.p., 3 times/week) for 2, 4, 6 and 10 weeks, respectively. The time-dependent changes of the lipid peroxidation (malondialdehyde, MDA) and antioxidative status (glutathione, GSH; glutathione peroxidase, GSH-Px; glutathione reductase, GR; superoxide dismutase, SOD and anti-reactive oxygen species, anti-ROS) in nerve tissues were investigated. The electrophysiology indices (nerve conduction velocity, NCV; compound action potential duration, CAPD; compound action potential amplitude, CAPA; compound action potential latency, CAPL) in the sciatic nerve were determined using BL-420E Biologic Function Determining System. The results showed that MDA levels increased significantly (P < 0.05) in nerve tissues, while GSH levels markedly decreased (P < 0.05) in a time-dependent manner. SOD activity (in the spinal cord and sciatic nerve) and GR activity (in the sciatic nerve) increased significantly after 4 weeks ACR treatment (P < 0.01), but then decreased (P < 0.05). The anti-ROS activity in the sciatic nerve was markedly decreased at the end of week 6 and 10 (P < 0.01). The above indices changed most in the sciatic nerve. The levels of GSH, MDA and anti-ROS in rat sciatic nerve were in high correlation (P < 0.05, |r| > 0.80) with the electrophysiology indices according to the exposure time. Thus, ACR-induced neurotoxicity may be associated with the enhancement of lipid peroxidation and reduction of the antioxidative capacity. Depletion of neural GSH level might be one of the primary events in ACR-induced neuropathy.

The protective effect of N-acetylcysteine against acrylamide toxicity in liver and small and large intestine tissues

“…However, the changes in antioxidant structures following exposure to ACR have not been clarifi ed yet. In a study about the effects of ACR on nerve tissues and antioxidant system, it was observed that while MDA level signifi cantly increased, GSH level signifi cantly decreased (15). Smoking is one of the most striking risk factors for lipid peroxidation.…”

Procyanidin B2 and a cocoa polyphenolic extract inhibit acrylamide-induced apoptosis in human Caco-2 cells by preventing oxidative stress and activation of JNK pathway

“…Exposure to AA induces a significant reduction in GSH concentration in different cells [7][8][9] and contributed to the onset of oxidative stress conditions, which can adversely affect cell function and potentially lead to cell damage and death [10]. However, while previous studies have documented the link between AA-induced oxidative stress and cytotoxicity in several tissues [3][4][5], to date the potential impact of AA on the integrity of gastrointestinal tract, the primary organ in contact with food, is poorly understood.…”

Alzheimer’s Disease Pathogenesis: The Denied Access Model

“…One group examined the time-dependent effects acrylamide had on the antioxidative stress in rat nerve tissues. With increased concentrations injected into rats over a few weeks, decreases were found in both CAP duration and CAP amplitude [116]. Furthermore, they found that acrylamide may be associated with an increase in lipid peroxidation and reduction of the anti-oxidative capacity.…”