Search NEL Online

Comparative Study 2012; 33(Suppl 3): 60-65 PubMed PMID: 23353845 Citation  Keywords:  Abnormalities, Multiple:chemically induced, Acetone:toxicity, Animals, Dimethyl Sulfoxide:toxicity, Dose-Response Relationship, Drug, Edema:chemically induced, Embryo, Nonmammalian:drug effects, Ethanol:toxicity, Eye Abnormalities:chemically induced, Meth.   

OBJECTIVES: The aim of this study was to determine the effects of 96 hour exposure to selected solvents on the embryonic stages of zebrafish (Danio rerio). We investigated mortality and various types of changes which appeared (oedema, tail and eye defects, weak pigmentation, and deformation of the body). Based on the results, values of NOEC and LOEC for embryos of D. rerio were determined.

METHODS: Embryonal toxicity tests were conducted according to OECD guideline 212. Ethanol and methanol were tested at concentrations of 0.1, 0.5, 1, 1.5, 2%; acetone at concentrations of 0.1, 0.5, 1, 1.25, 1.5%; and dimethylsulfoxide at concentrations of 1, 1.5, 2, 2.5, 3%.

RESULTS: The LOEC values of ethanol and methanol were detected in the 1% concentration. Statistically significant changes (oedema) were reported in 1% ethanol, and oedema, weak pigmentation and deformation of the body were observed in 1% methanol. After exposure to acetone, the most common occurrence of oedema was in the 0.5% concentration (LOEC = 0.5%). The solvent dimethylsulfoxide caused oedema and body deformation at the 2% concentration (LOEC = 2%).

CONCLUSIONS: The NOEC concentrations of the individual solvents were as follows: ethanol and methanol, 0.5%; acetone, 0.1%; and dimethylsulfoxide, 1.5%. These concentrations of individual solvents were higher than the maximum recommended concentration for toxicity tests on fish. For this reason, it can be assumed that the concentration of solvent allowed by the norm does not affect the procedure or results of such tests....

Read abstract  Full text PDF

Journal Article 2011; 32(6): 831-835 PubMed PMID: 22286794 Citation  Keywords:  Animals, Axons:pathology, Blood-Brain Barrier:drug effects, Brain Edema:chemically induced, Female, Male, Mannitol:pharmacology, Methylprednisolone:pharmacology, Myelin Sheath:pathology, Neuroprotective Agents:pharmacology, Rats, Rats, Wistar,.   

OBJECTIVES: In our earlier paper we demonstrated that opening of the blood-brain barrier with an osmotic insult induces brain oedema which represents a factor triggering axonal impairment accompanied with myelin disintegration. The aim of the present study was to find whether methylprednisolone can reduce such axonal impairment in our model of brain oedema.

METHODS: Brain oedema was induced by osmotic blood-brain barrier opening with 20% mannitol applied selectively into the internal carotid. Axonal changes were recognized as signs of myelin disintegration (oedematous vesicles, varicosity, myelin fragmentation) at histological sections stained with Black Gold in hippocampal areas CA1 and CA3 and in the dentate gyrus at time intervals of 30 minutes (acute group) or one week (chronic group) after the blood-brain barrier opening. At the same time intervals methylprednisolone was applied in two different ways - into peritoneal cavity or into the right carotid artery.

RESULTS: Impairment of the axonal integrity (changes of the myelin sheet integrity) was identified in all areas studied in both experimental groups. Whereas in the control group axons were of the uniform diameter, in the experimental groups various forms of myelin disintegration were observed. Methylprednisolone reduced the degree of myelin disintegration in both time intervals with the highest effect in the acute group with the intracarotic administration.

CONCLUSION: Methylprednisolone can effectively reduce myelin changes accompanying brain oedema induced by blood-brain barrier opening with an osmotic insult....

Read abstract  Full text PDF

Journal Article 2010; 31(4): 477-482 PubMed PMID: 20802439 Citation  Keywords:  Analysis of Variance, Animals, Axons:pathology, Blood-Brain Barrier:pathology, Brain Edema:chemically induced, Dentate Gyrus:pathology, Female, Male, Mannitol, Myelin Sheath:pathology, Rats, Rats, Wistar, Time Factors,.   

OBJECTIVES: Clinically very serious condition of ischaemia and brain injury which are often associated with brain oedema is frequently accompanied by the impairment of the structural integrity of axons. We wondered whether the brain oedema (without ischemia brain injury) can induce structural axonal impairment.

METHODS: Brain oedema was induced by osmotic blood-brain barrier opening with 20% mannitol applied selectively into the internal carotid. Axonal changes were recognized as signs of myelin disintegration (oedematous vesicles, varicosity, myelin fragmentation) at histological sections stained with Black Gold in hippocampal areas CA1 and CA3 and in the dentate gyrus and cerebral cortex at time intervals of one hour, one day, three days and one week after the oedema induction.

RESULTS: Impairment of the structural integrity was identified in myelin sheets in all areas studied in all experimental groups. Whereas in the control group axon were of the uniform diameter, in the experimental groups various forms of myelin disintegration were observed. The progression of myelin damage depended on the time elapsed after the oedema induction.

CONCLUSION: Opening the blood-brain barrier with an osmotic insult induces brain oedema which represents a factor triggering axonal impairment accompanied with myelin changes. The development of axonal changes initiated by brain oedema only (without ischemia brain injury) is a novel observation....

Read abstract  Full text PDF

Journal Article 2009; 30(Suppl 1): 22-24 PubMed PMID: 20027138 Citation  Keywords:  Administration, Oral, Animals, Antioxidants:metabolism, Aorta:physiopathology, Arthritis, Experimental:chemically induced, Edema:chemically induced, Freund's Adjuvant, Hexosaminidases:metabolism, Immunologic Factors:administration & dosage, Male, Mycobact.   

OBJECTIVES: The goal of this study was to evaluate the effect of sesame oil on functional damage induced by adjuvant arthritis (AA) and on changes of selected biochemical parameters reflecting oxidative tissue injury.

DESIGN: Mycobacterium butyricum in incomplete Freund's adjuvans was intradermally administered to Lewis male rats. Hind paw edema and endothelium-dependent relaxation of the aorta were determined on day 28. Further, plasmatic levels of TBARS, gamma-glutamyltransferase (GGT) activity in the joint and spleen tissues, level of protein carbonyls and total antioxidant capacity (TAC) in plasma, as well as activity of the lysosomal enzyme N-acetyl-glucosaminidase (NAGA) in serum were assessed. The effect of sesame oil (SO, 1ml/kg, daily oral administration) was evaluated on day 28.

RESULTS: The beneficial effect of sesame oil on markers of oxidative stress accompanying AA was demonstrated by decrease of plasma TBARS and decrease of GGT activity in the joint and spleen tissues. Level of protein carbonyls, TAC in plasma and activity of NAGA in serum and in the kidney were improved, yet not significantly. In the hind paw edema the maximal increase was found on day 28 of AA, and in the same time we observed a significant decrease of aortic endothelium-dependent relaxation. Administration of SO resulted in mild, non-significant decrease of hind paw swelling and in significantly increased acetylcholine-evoked relaxation.

CONCLUSION: We conclude that SO has beneficial effects on oxidative stress induced biochemical changes occurring in AA, moreover it improves endothelium-dependent relaxation of the aorta and tends to decrease hind paw edema....

Read abstract  Full text PDF