ABSTRACT
Taurine, a sulphur - containing amino acid, has been termed a functional nutrient. Its synthetic form is a common ingredient in supplements and energy drinks. There is no information concerning taurine impact on bone microstructure after prolonged supplemental use. Also, differences in bone parameters of mice following taurine exposure are unknown. In this study, a detailed microstructure of compact and trabecular bone tissues of mice subchronically exposed to taurine was determined. Animals (n=12) were segregated into three groups: E1 group - mice received 20 mg/kg b.w. of taurine per day during 8 weeks; E2 group - mice were fed by taurine at a dose of 40 mg/kg b.w. for 8 weeks and a control (C) group. Decreased density of secondary osteons, increased sizes of primary osteon's vascular canals (P<0.05) were observed in taurine - treated animals. Cortical bone thickness, trabecular thickness were decreased (P<0.05) in E1 group, and relative volume of trabecular bone was lower (P<0.05) in E2 group as compared to C group. According to our results, prolonged taurine exposure at the doses used in this study can negatively affect both compact and trabecular bone tissues microstructure.
Subject(s)
Bone Density/drug effects , Femur/drug effects , Femur/pathology , Taurine/administration & dosage , Animals , Bone Density/physiology , Cortical Bone/cytology , Cortical Bone/drug effects , Cortical Bone/physiology , Drug Administration Schedule , Femur/physiology , Mice , Random Allocation , Taurine/toxicityABSTRACT
Our study aimed to investigate subacute exposure to alcohol in relation to bone microstructure of mice. Animals from experimental (E) group drank a solution composed of 15 % ethanol and water for 14 days (one remodeling cycle), while those from control (C) group drank only water. In the compact bone of E group, decreased bone formation and increased porosity were observed which corresponds with lower levels of serum alkaline phosphatase and glutathione. Alcohol significantly increased sizes of primary osteon's vascular canals and decreased those of secondary osteons, Haversian canals. Relative bone volume, bone mineral density (BMD), relative bone volume without marrow cavity were also lower in E group. On the contrary, trabecular bone microstructure did not differ significantly between E and C groups. Liver function test showed higher levels of alanine aminotransferase, aspartate aminotransferase in alcohol-fed mice. Serum calcium, phosphate were significantly lower in E group. According to our study, only changes in compact bone microstructure of mice following one remodeling cycle were observed due to both direct and indirect effects of alcohol.
Subject(s)
Bone Density/drug effects , Bone Density/physiology , Bone Matrix/drug effects , Bone Matrix/diagnostic imaging , Ethanol/administration & dosage , Ethanol/toxicity , Animals , Bone Matrix/physiology , Imaging, Three-Dimensional/methods , Male , MiceABSTRACT
Acrylamide (AA) is one of the most common toxins in foods. Its effect on bone microstructure has not been investigated. The aim of our study was to analyze the impact of acute exposure to AA on femoral bone microstructure in mice. Adult animals were treated perorally with 2 doses of AA (E1 group, 1 mg/kg b.w.) in a 24-h period and with 3 doses of AA (E2 group, 1 mg/kg b.w.) in a 48-h period. Mice exposed to AA had smaller sizes of primary osteon's vascular canals. Secondary osteons were significantly smaller in mice from E2 group; however their increased number (from 38 % to 77 %) was identified in both E1 and E2 groups. In these groups, a higher number of resorption lacunae (from 100 % to 122 %) was also found. The values for bone volume, trabecular number were increased and that for trabecular separation was decreased in mice administered AA. Significantly higher value of bone surface was observed in mice from E1 group whereas trabecular thickness was increased in E2 group. The effect of AA on microstructure of compact and trabecular bone tissues is different. In our study, one dose of AA was used and acute effects of AA were investigated. Therefore, further studies are needed to study mechanisms by which AA acts on bone.
Subject(s)
Acrylamide/toxicity , Cancellous Bone/drug effects , Cortical Bone/drug effects , Femur/drug effects , Food Contamination , Animals , Cancellous Bone/diagnostic imaging , Cancellous Bone/pathology , Cortical Bone/diagnostic imaging , Cortical Bone/pathology , Femur/diagnostic imaging , Femur/pathology , Male , Mice , X-Ray MicrotomographyABSTRACT
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.
Subject(s)
Catalase/metabolism , Excitatory Amino Acid Agonists/pharmacology , Glutathione Peroxidase/metabolism , Glutathione/metabolism , N-Methylaspartate/pharmacology , Receptors, N-Methyl-D-Aspartate/agonists , Superoxide Dismutase/metabolism , Animals , Brain/drug effects , Brain/enzymology , Glutathione/blood , Kidney/drug effects , Kidney/enzymology , Liver/drug effects , Liver/enzymology , Male , Mice , Oxidative Stress/drug effects , Pancreas/drug effects , Pancreas/enzymology , Receptors, N-Methyl-D-Aspartate/metabolism , Time FactorsABSTRACT
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.
Subject(s)
Antioxidants/metabolism , Brain/drug effects , Kainic Acid/toxicity , Kidney/drug effects , Liver/drug effects , Oxidative Stress/drug effects , Animals , Ascorbic Acid/metabolism , Brain/metabolism , Catalase/metabolism , Excitatory Amino Acid Agonists/toxicity , Glutathione/metabolism , Glutathione Peroxidase/metabolism , Injections, Intraperitoneal , Kidney/metabolism , Liver/metabolism , Male , Mice , Oxidative Stress/physiology , Superoxide Dismutase/metabolismABSTRACT
The authors present the results of their research concerning the bacteriostatic or bactericidal function of the secretion of ceruminous glands of the external auditory duct. In accordance with the statements of the other authors, neither bacteriostatic nor bactericidal function of the ear wax was discovered.
