Advanced

Aminoguanidin-kezeles pozitiv hatasa a peroxinitrit-termelodesre es szivhipertrofiara streptozotocinnal indukalt diabeteses patkanyokban

Stadler, Krisztian; Jenei, Veronica LU ; Somogyi, Aniko and Jakus, Judit (2004) In Orvosi Hetilap 145(49). p.2491-2496
Abstract
The effect and possible mechanisms of action of aminoguanidine (a preferential iNOS inhibitor) has been studied on cardiovascular damages and overproduction of reactive nitrogen species in streptozotocin-induced diabetic rats. MATERIALS AND METHODS: 40 rats were divided into five groups (control and diabetic, with or without aminoguanidine treatment, diabetic with insulin treatment) and oxidative stress parameters were examined. Tissue nitric oxide levels were determined by EPR spectroscopy, while peroxynitrite generation by a chemiluminescence method. Cardiac hypertrophy, blood metabolic parameters (blood glucose, HbA1c, fructosamine), as well as tissue protein carbonyl levels were also determined. RESULTS: Diabetic animals showed... (More)
The effect and possible mechanisms of action of aminoguanidine (a preferential iNOS inhibitor) has been studied on cardiovascular damages and overproduction of reactive nitrogen species in streptozotocin-induced diabetic rats. MATERIALS AND METHODS: 40 rats were divided into five groups (control and diabetic, with or without aminoguanidine treatment, diabetic with insulin treatment) and oxidative stress parameters were examined. Tissue nitric oxide levels were determined by EPR spectroscopy, while peroxynitrite generation by a chemiluminescence method. Cardiac hypertrophy, blood metabolic parameters (blood glucose, HbA1c, fructosamine), as well as tissue protein carbonyl levels were also determined. RESULTS: Diabetic animals showed increased nitric oxide and peroxynitrite generation in the aorta along with a significant hypertrophy and protein carbonylation of the cardiac tissue. Both aminoguanidine and insulin treatment suppressed high levels of nitric oxide and peroxynitrite in the vasculature, but only aminoguanidine was able to prevent hypertrophic alterations and to reduce protein carbonylation in the heart. CONCLUSIONS: The results show that (1) aminoguanidine reduces nitric oxide production and prevents cardiac hypertrophy, (2) insulin therapy improves carbohydrate metabolism, reduces nitrosative stress but has no effect on cardiac hypertrophy. Cardiac hypertrophy in diabetes is strongly correlated with non-enzymatic glycation. Aminoguanidine prevented hypertrophy by blocking the formation of advanced glycation end products rather than via other mechanisms. (Less)
Please use this url to cite or link to this publication:
author
organization
alternative title
Aminoguanidine prevents peroxynitrite production and cardiac hypertrophy in streptozotocin-induced diabetic rats
publishing date
type
Contribution to journal
publication status
published
subject
in
Orvosi Hetilap
volume
145
issue
49
pages
2491 - 2496
publisher
Akademiai Kiado
external identifiers
  • pmid:15633737
  • scopus:13744253074
ISSN
0030-6002
language
Other
LU publication?
yes
id
0e778a08-61eb-40c6-8bb7-63d177bd0371 (old id 1130053)
date added to LUP
2008-06-18 13:40:51
date last changed
2017-01-29 04:10:01
@article{0e778a08-61eb-40c6-8bb7-63d177bd0371,
  abstract     = {The effect and possible mechanisms of action of aminoguanidine (a preferential iNOS inhibitor) has been studied on cardiovascular damages and overproduction of reactive nitrogen species in streptozotocin-induced diabetic rats. MATERIALS AND METHODS: 40 rats were divided into five groups (control and diabetic, with or without aminoguanidine treatment, diabetic with insulin treatment) and oxidative stress parameters were examined. Tissue nitric oxide levels were determined by EPR spectroscopy, while peroxynitrite generation by a chemiluminescence method. Cardiac hypertrophy, blood metabolic parameters (blood glucose, HbA1c, fructosamine), as well as tissue protein carbonyl levels were also determined. RESULTS: Diabetic animals showed increased nitric oxide and peroxynitrite generation in the aorta along with a significant hypertrophy and protein carbonylation of the cardiac tissue. Both aminoguanidine and insulin treatment suppressed high levels of nitric oxide and peroxynitrite in the vasculature, but only aminoguanidine was able to prevent hypertrophic alterations and to reduce protein carbonylation in the heart. CONCLUSIONS: The results show that (1) aminoguanidine reduces nitric oxide production and prevents cardiac hypertrophy, (2) insulin therapy improves carbohydrate metabolism, reduces nitrosative stress but has no effect on cardiac hypertrophy. Cardiac hypertrophy in diabetes is strongly correlated with non-enzymatic glycation. Aminoguanidine prevented hypertrophy by blocking the formation of advanced glycation end products rather than via other mechanisms.},
  author       = {Stadler, Krisztian and Jenei, Veronica and Somogyi, Aniko and Jakus, Judit},
  issn         = {0030-6002},
  language     = {mis},
  number       = {49},
  pages        = {2491--2496},
  publisher    = {Akademiai Kiado},
  series       = {Orvosi Hetilap},
  title        = {Aminoguanidin-kezeles pozitiv hatasa a peroxinitrit-termelodesre es szivhipertrofiara streptozotocinnal indukalt diabeteses patkanyokban},
  volume       = {145},
  year         = {2004},
}