Neuroprotective Dipeptide Noopept Prevents DNA Damage in Mice with Modeled Prediabetes

In experiments on BALB/c mice, prediabetes was modeled by administration of streptozotocin in a dose of 130 mg/kg. DNA damage was assessed by the method of DNA comets. Noopept (0.5 mg/kg intraperitoneally) was administered for 14 days before and for 6, 13, or 14 days after streptozotocin administrat...

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Bibliographic Details
Published in:Bulletin of experimental biology and medicine 2019-12, Vol.168 (2), p.233-237
Main Authors: Ostrovskaya, R. U., Yagubova, S. S., Zhanataev, A. K., Anisina, E. A., Gudasheva, T. A., Durnev, A. D.
Format: Article
Language:English
Subjects:
Analysis
Animal experimentation
Animals
Biomedical and Life Sciences
Biomedicine
Blood Glucose - analysis
Cell Biology
Diabetes Mellitus, Experimental - pathology
Dipeptides - pharmacology
DNA
DNA damage
DNA Damage - drug effects
Hyperglycemia - pathology
Insulin-Secreting Cells - pathology
Internal Medicine
Kidney - pathology
Laboratory Medicine
Liver
Liver - pathology
Male
Malondialdehyde - blood
Mice
Mice, Inbred BALB C
Neuroprotective Agents - pharmacology
Pathology
Pharmacology and Toxicology
Prediabetic state
Prediabetic State - genetics
Streptozocin
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Summary:In experiments on BALB/c mice, prediabetes was modeled by administration of streptozotocin in a dose of 130 mg/kg. DNA damage was assessed by the method of DNA comets. Noopept (0.5 mg/kg intraperitoneally) was administered for 14 days before and for 6, 13, or 14 days after streptozotocin administration. Despite moderate hyperglycemia and increased malondialdehyde level, the intensity of DNA damage in cells of the pancreas, liver, and kidneys significantly surpassed the control values. Noopept normalized these parameters due to its pronounced antigenotoxic effect. For both the damaging effect of streptozotocin and the normalizing effect of Noopept, DNA changes manifested mainly in terms of atypical DNA comets. Our findings confirm the role of DNA damage in the pathogenesis of diabetes. They indicate the possibility of pharmacological protection of pancreatic β cells with the neuroprotective drug and provide an important argument in favor of the hypothesis about the similarity of the mechanisms of formation of the resistance of neurons and β cells to the cytotoxic influences.
ISSN:0007-4888
1573-8221
DOI:10.1007/s10517-019-04681-z