Antagonistic Impact of Acrylamide and Ethanol on Biochemical and Morphological Parameters Consistent with Bone Health in Mice.

The aim of present study was to verify antagonistic effect of acrylamide (AA) and ethanol (Et) on bone quality parameters. Adult mice (n = 20) were segregated into four groups following 2 weeks administration of toxins: group E1, which received AA (20 mg/kg body weight daily); group E2, which received 15% Et (1.7 g 100% Et/kg body weight daily); group E12, which received simultaneously both toxins; and a control group. An insignificant impact of individual applications of AA, Et or their simultaneous supplementation on the total body weight of mice and the length and weight of their femoral bones was identified. In group E1, higher levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG), a decreased level of glutathione (GSH) and elevated endocortical bone remodelling were determined. A significantly lower relative volume of cortical bone, bone mineral density (BMD), elevated endocortical bone remodelling and cortical porosity, higher levels of ALT, AST, lower values for total proteins (TP), GSH, alkaline phosphatase (ALP), calcium, and phosphorus were recorded in group E2. In the mice from group E12, the highest endocortical bone remodelling, decreased values for BMD, TP, GSH and ALP and increased levels of ALT and AST were found. Our findings confirmed the antagonistic impact of AA and Et at doses used in this study on biochemical and morphological parameters consistent with bone health in an animal model.

Effect of taurine on ethanol-induced oxidative stress in mouse liver and kidney.

The purpose of this study was to investigate the effect of alcohol exposure on liver and kidney antioxidant systems in taurine exhibition during different time periods. Mice were divided into groups: I - control; II - alcohol (2.5 g/kg b.w.); III - taurine (42.84 mg/kg b.w.); and IV - alcohol + taurine. Treatments were provided for 24 h, 14 days, and 56 days. In the liver and kidney of the alcohol group, antioxidant enzyme (superoxide dismutase, catalase, and glutathione peroxidase) activities, reduced glutathione (GSH), and malondialdehyde (MDA) levels were decreased, as compared to the control group in all time periods. Taurine was found to be effectively inhibiting oxidative action of alcohol and increasing all the tested parameters in the liver (after 24 h) and kidney (after 24 h and 14 days). Moreover, the positive effect of taurine administration on GSH and MDA levels persisted in the kidneys of mice exposed to alcohol for 56 days. In conclusion, alcohol administration led to a significant influence on antioxidant system in the liver and kidney, but simultaneous intake of taurine, along with ethanol, partly attenuated the antioxidant changes in these organs.

Single and simultaneous effects of acrylamide and ethanol on bone microstructure of mice after one remodeling cycle.

BACKGROUND: This study aimed to examine femoral bone microstructure of mice after single and simultaneous administration to acrylamide and ethanol since both substances are often consumed separately and/or together by humans. Interactive effects of these toxins were analysed after one remodeling cycle. METHODS: Twenty clinically healthy adult mice were randomly divided into four groups following 2 weeks administration of toxins: A group - mice were fed with acrylamide (40 mg/kg bw); E group - mice were ethanol-fed (15% ethanol); AE group - mice were simultaneously fed with both toxins, and a C group - control (without acrylamide and/or ethanol supplementation). Generally, 2D and 3D imaging methods were used to determine cortical and trabecular bone tissues microstructure. Biochemical analyses of plasma parameters were also realized using commercially available ELISA tests and spectrophotometrically. RESULTS: Single and simultaneous exposure to acrylamide and ethanol affected only cortical bone microstructure. No significant changes in trabecular bone morphometry were detected among all groups. In mice from the A group, increased endocortical remodeling associated with a higher level of serum calcium and vasoconstriction of primary osteon's vascular canals (POVC) were identified. On the contrary, increased cortical porosity consistent with a decreased relative bone volume, bone mineral density (BMD) and lower levels of alkaline phosphatase (ALP), glutathione (GSH), calcium in plasma and also with vasodilation of POVC were observed in the E group. In the AE group, the highest density of secondary osteons associated with a lower BMD and decreased levels of ALP, GSH were documented. The parameters of POVC and Haversian canals approximated to the C group. In addition, single and simultaneous exposure to both toxins caused liver disease consistent with a higher values of alanine aminotransferase (ALT), aspartate aminotransferase (AST) in plasma of all experimental groups. CONCLUSIONS: Single administration to acrylamide and ethanol had negative effects on cortical bone structure of mice after one remodeling cycle. However, we identified possible antagonistic impact of these toxins on the structure of the cortical bone.

Changes in the microstructure of compact and trabecular bone tissues of mice subchronically exposed to alcohol.

BACKGROUND: Alcohol is one of the most commonly consumed neurotoxins by humans. Its negative effect on bone health is known for a long time. However, its impact on qualitative and quantitative 2D characteristics of the compact bone is still unclear. Therefore, the aim of this study was to investigate in detail the effects of subchronic alcohol exposure on compact and trabecular bone tissues microstructure of laboratory mice using 2D and 3D imaging methods. Ten clinically healthy 12 weeks-old mice (males) were randomly divided into two groups. Animals from experimental group (group E; n = 5) drank a solution composed of 15% ethanol and water (1.7 g 100% ethanol kg-1 b.w. per day) for 8 weeks, while those from control group (group C; n = 5) drank only water. RESULTS: Subchronic exposure to alcohol leads to several changes in qualitative 2D characteristics of the compact bone such as the presence of primary vascular radial bone tissue in pars anterior of endosteal border and a higher number of resorption lacunae (five times more) in the middle part of substantia compacta. Morphometrical 2D evaluations of the compact bone showed significantly increased sizes of primary osteons' vascular canals (p < 0.05) in mice from the experimental group (E group). Sizes of Haversian canals and secondary osteons were not affected by alcohol consumption. In mice from the E group, significantly lower values for relative bone volume and bone mineral density of the compact bone were observed. In the trabecular bone, decreased values for bone volume, trabecular number, trabecular thickness and bone surface (p < 0.05) were documented. CONCLUSIONS: Alcohol decreased not only bone volume and density of the compact bone, but it also reduced trabecular bone volume and leads to trabecular thinning. It caused vasodilation of primary osteons' vascular canals and increased porosity in the compact bone.

Protective effects of melatonin on the activity of SOD, CAT, GSH-Px and GSH content in organs of mice after administration of SNP.

Sodium nitroprusside (SNP) is an antihypertensive drug with proven dose-dependent toxic effects attributed mainly to the production of cyanide but also excesive nitric oxide (NO) and derived reactive species. The present study evaluated whether melatonin administration would have time-dependent protective effect against SNP−induced toxicity. Male Swiss mice were used in this study. Control mice were treated with 0.9% NaCl; the second group was injected with 10 mg melatonin (MEL)/kg body weight (b.w.); the third group was given SNP at the dose of 3,6 mg/kg b.w.; the fourth group received both MEL and SNP at the same doses. In homogenates of brain, liver and kidneys, activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were estimated after 3, 6 and 24 h of drugs administration. The concentration of reduced glutathione (GSH) was also evaluated in the blood, brain, liver and kidneys of mice at the same time intervals. In animals receiving MEL, the highest levels of GSH were observed in all the organs as compared to the control after 3, 6 h. Meanwhile, SNP decreased GSH concentration in the blood, brain, liver and kidneys in all time intervals. Administration of MEL in combination with SNP increased the GSH levels in all organs, as compared to the administration of SNP alone; this effect was observed after 3, 6 and 24 h. The activity of SOD, CAT and GSH-Px in the MEL-treated group increased after 3 h in all the organs, while in liver and kidney the increase was also observed after 6 h. Conversely, the SNP intoxication caused a decrease of the activity of enzymes in the tested organs in all intervals, while administration of MEL + SNP resulted in increased activities of SOD, CAT and GSH-Px in all the organs after 3 h and 6 h. The investigation carried out in the present study provide new data to add to the study of antioxidant properties of MEL and SNP-induced oxidative stress with regard to time-dependent properties in different types of tissues.

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.