Damage to Nuclear and Mitochondrial DNA in Different Organs in Streptozotocin-Induced Diabetes Models in BALB/c Mice.

Autor: Zhanataev AK; V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia. pharmacol@yandex.ru., Anisina EA; V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia., Kulakova AV; V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia., Lisitsyn AA; V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia., Pligina KL; V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia., Chaika ZV; V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia., Durnev AD; V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia.
Jazyk: angličtina
Zdroj: Bulletin of experimental biology and medicine [Bull Exp Biol Med] 2023 Jan; Vol. 174 (3), pp. 349-353. Date of Electronic Publication: 2023 Feb 01.
DOI: 10.1007/s10517-023-05717-1
Abstrakt: Male BALB/c mice with streptozotocin-induced diabetes mellitus were used to study nuclear DNA (nDNA) and mitochondrial DNA (mtDNA) damage using comet DNA assay and real-time PCR, respectively. In animals receiving single injection of streptozotocin in a dose of 200 mg/kg, severe hyperglycemia was observed on days 10 and 21 of the experiment, while after 5-fold administration of streptozotocin in a dose of 40 mg/kg, it developed on days 14 and 28. DNA damage and the level of atypical DNA comets in the liver increased both on days 10 and 21 after single administration of streptozotocin, and on days 14 and 28 after repeated administrations. The level of atypical DNA comets on day 21 after a single administration of streptozotocin increased in the kidneys, but not in the brain, testes, and pancreas. Real-time PCR revealed mtDNA damage in the liver, kidney, and pancreatic cells of mice with streptozotocin-induced diabetes. Thus, these animal models were found to reproduce pathognomic signs of diabetes, hyperglycemia, and nDNA damage; mtDNA damage was also detected.
(© 2023. Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze: MEDLINE
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