Edyta Kapusta

Acrylamide Influence on Activity of Acetylcholinesterase, Thiol Groups, and Malondialdehyde Content in the Brain of Swiss Mice

Acrylamide is a neurotoxin inhibiting neurotransmission in peripheral nerves. Less is known about acrylamide influence on the central nervous system. Here we measured acrylamide influence on the acetylcholinesterase activity in brain stem, hemispheres, and cerebellum of mice (males, Swiss strain) in relation to the thiol groups and malondialdehyde concentration. Acrylamide was injected intraperitoneally (20 and 40 mg/kg, i.e. 0.52 and 1.04 mg per animal). The brain structures were taken 24, 48, and 192 h after the injection. Acetylcholinesterase activity was significantly lower (p < 0.001 to p < 0.05) in all the structures. It was accompanied by the statistically significant (p < 0.001 to p < 0.05) increase in malondialdehyde concentrations in most of the studied structures time periods and ACR doses. –SH groups concentrations were significantly depleted in the right hemisphere (p < 0.01) after 24 h and in brain stem (p < 0.05) after 48 h. We suggest that neurotoxicity of acrylamide in brain is related to acetylcholinesterase inhibition and redox imbalance.

Antioxidative effects of α-lipoic acid in the brain, liver and kidneys in selected mouse organs exposed to zymosan.

This study investigated the role of exogenous α-lipoic acid (ALA) in the inflammation caused by zymosan application. Seventy-two adult male white mice were divided into twelve groups: three control groups, three Zymosan groups, three ALA groups and three groups being the combination of Zymosan and ALA. In the experimental groups, the animals were decapitated after 3, 6 and 24 hours after the injection. The activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were determined in the brain, liver and kidneys of the mice. After the injection of Zymosan, it was found that the activity of SOD, CAT and GSH-Px in the brain, liver and kidneys of mice was significantly lower in all time periods. The administration of ALA resulted in an opposite effect, namely, it increased the activity of the enzymes studied in the selected organs of mice. The Zymosan and ALA combination significantly inhibited the decrease in the activity of the enzymes compared with the values obtained in the groups of animals which received Zymosan only. The results of our study, using the Zymosan-induced inflammation, clearly indicate that ALA is an anti-inflammatory agent.

Effect of N-methyl-D-aspartic acid on activity of superoxide dismutase, catalase, glutathione peroxidase and reduced glutathione level in selected organs of the mouse.

One of the major classes of ionotropic glutamate receptors is the class of N-methyl-D-aspartate receptors (NMDARs). Receptor activation recruits, via calcium signal transduction mechanisms which play important roles in oxidative metabolism, mitochondrial free radical production and occurrence of other mitochondrial factors which potentially contribute to excitotoxicity and neuronal death. In the present study, the effects of stimulation of NMDARs by applying N-methyl-D-aspartic acid (NMDA) in the brain, liver, kidneys and pancreas on change of the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSHPx) and in the amount of reduced glutathione (GSH) in blood, brain, liver and kidneys has been investigated. Statistically significant decrease of the activity of SOD, CAT and GSHPx and in the amount of reduced glutathione (GSH) was found in the examined organs after administration of NMDA, an agonist of NMDA receptors, demonstrating that NMDA administration compromises the antioxidant status in the investigated organs of the mouse.

Influence of the kainic acid on antioxidant status in the brain, liver and kidneys of the mouse

The effect of acute exposure of intraperitoneal injection of kainic acid (KA) on the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSHPx), amount of reduced glutathione (GSH) and content of ascorbic acid (ASC) has been studied in brain, liver and kidneys of male mice. Animals (n = 144) were treated KA with one dose, i.e. 12 mg/kg body weight or saline solution. The influence of KA on the tested parameters after 2, 4, 6 and 24 hours was estimated. After the injection of KA it has been found that the activity of SOD, GSHPx and CAT is very clearly reduced in the brain and to a lesser extent in liver and kidneys. Simultaneously a decrease in the activity of antioxidant enzymes in the brain, liver and kidneys was accompanied by a decrease of the amount of GSH and ASC. A decrease in the activity of SOD, CAT, GSHPx (after 2 and 4 h) and amount of GSH and ASC in the brain, liver and kidneys suggests that oxidative stress plays important role in the pathogenesis of KA in mice. The obtained results suggest that KA not only is toxic to the brain but also for the liver and kidneys of mice.

The Effect of Subacute Exposure to Acrylamideon Femoral Bone Microstructurein Laboratory Mice

Acrylamide, a substituted unsaturated hydrocarbon, is often found in fried potatoes, flour, baby food, coffee, and olives. It is one of the most commonly consumed neurotoxins by humans. To date, its effect on bone structure has not been investigated in experimental animals. The aim of our manuscript was to analyze the impact of subacute exposure to acrylamide on the microscopic compact and trabecular bone tissue structures in laboratory mice. Adult male mice were divided into two groups. Animals from the experimental group (group E, n = 4) were treated perorally with two doses of acrylamide (1 mg/kg b.w.) during 24 hours. The group without administration of AA served as a control (group C, n = 4). Three hours after the second dose of AA (after 27 hours), mice were killed and their femurs were used for microscopic analysis. Our results demonstrate that subacute exposure to acrylamide causes an absence of the primary vascular radial bone tissue in pars posterior of the endosteal border. Mice from E group had more intact secondary osteons in pars medialis of the middle part of compact bone. Also, a few resorption lacunae were found in pars anterior of periosteal borders in these mice. Subacute exposure to AA significantly decreased the size of the primary osteon vascular canals (P<0.05) in compact bone tissue. In trabecular bone tissue, the values for bone volume, trabecular number, and bone surface were significantly increased in mice from the E group. In contrast, the value for trabecular separation was significantly decreased in these mice.