Evaluation of Chromosomal Instability in Diabetic Rats Treated with Naringin

We used the bone marrow DNA strand breaks, micronucleus formations, spermatocyte chromosomal aberrations, and sperm characteristic assays to investigate the chromosomal instability in somatic and germinal cells of diabetic rats treated with multiple doses of naringin. The obtained results revealed t...

Full description

Bibliographic Details
Main Authors: Saleh A. Bakheet, Sabry M. Attia
Format: Article
Language:English
Published: Hindawi Limited 2011-01-01
Series:Oxidative Medicine and Cellular Longevity
Online Access:http://dx.doi.org/10.1155/2011/365292
id doaj-1fc5c27bee274c36936a59652e54c7a1
record_format Article
spelling doaj-1fc5c27bee274c36936a59652e54c7a12020-11-25T00:11:25ZengHindawi LimitedOxidative Medicine and Cellular Longevity1942-09001942-09942011-01-01201110.1155/2011/365292365292Evaluation of Chromosomal Instability in Diabetic Rats Treated with NaringinSaleh A. Bakheet0Sabry M. Attia1Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, P.O. 2457, Riyadh 11451, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, P.O. 2457, Riyadh 11451, Saudi ArabiaWe used the bone marrow DNA strand breaks, micronucleus formations, spermatocyte chromosomal aberrations, and sperm characteristic assays to investigate the chromosomal instability in somatic and germinal cells of diabetic rats treated with multiple doses of naringin. The obtained results revealed that naringin was neither cytotoxic nor genotoxic for the rats at all tested doses. Moreover, naringin significantly reduced the diabetes-induced chromosomal instability in somatic and germinal cells in a dose-dependent manner. In addition, diabetes induced marked biochemical alterations characteristic of oxidative stress including enhanced lipid peroxidation, accumulation of oxidized glutathione, reduction in reduced glutathione, and accumulation of intracellular reactive oxygen species. Treatment with naringin ameliorated these biochemical markers dose-dependently. In conclusion, naringin confers an appealing protective effect against diabetes-induced chromosomal instability towards rat somatic and germinal cells which might be explained partially via diminishing the de novo free radical generation induced by hyperglycemia. Thus, naringin might be a good candidate to reduce genotoxic risk associated with hyperglycemia and may provide decreases in the development of secondary malignancy and abnormal reproductive outcomes risks, which seems especially important for diabetic patients.http://dx.doi.org/10.1155/2011/365292
collection DOAJ
language English
format Article
sources DOAJ
author Saleh A. Bakheet
Sabry M. Attia
spellingShingle Saleh A. Bakheet
Sabry M. Attia
Evaluation of Chromosomal Instability in Diabetic Rats Treated with Naringin
Oxidative Medicine and Cellular Longevity
author_facet Saleh A. Bakheet
Sabry M. Attia
author_sort Saleh A. Bakheet
title Evaluation of Chromosomal Instability in Diabetic Rats Treated with Naringin
title_short Evaluation of Chromosomal Instability in Diabetic Rats Treated with Naringin
title_full Evaluation of Chromosomal Instability in Diabetic Rats Treated with Naringin
title_fullStr Evaluation of Chromosomal Instability in Diabetic Rats Treated with Naringin
title_full_unstemmed Evaluation of Chromosomal Instability in Diabetic Rats Treated with Naringin
title_sort evaluation of chromosomal instability in diabetic rats treated with naringin
publisher Hindawi Limited
series Oxidative Medicine and Cellular Longevity
issn 1942-0900
1942-0994
publishDate 2011-01-01
description We used the bone marrow DNA strand breaks, micronucleus formations, spermatocyte chromosomal aberrations, and sperm characteristic assays to investigate the chromosomal instability in somatic and germinal cells of diabetic rats treated with multiple doses of naringin. The obtained results revealed that naringin was neither cytotoxic nor genotoxic for the rats at all tested doses. Moreover, naringin significantly reduced the diabetes-induced chromosomal instability in somatic and germinal cells in a dose-dependent manner. In addition, diabetes induced marked biochemical alterations characteristic of oxidative stress including enhanced lipid peroxidation, accumulation of oxidized glutathione, reduction in reduced glutathione, and accumulation of intracellular reactive oxygen species. Treatment with naringin ameliorated these biochemical markers dose-dependently. In conclusion, naringin confers an appealing protective effect against diabetes-induced chromosomal instability towards rat somatic and germinal cells which might be explained partially via diminishing the de novo free radical generation induced by hyperglycemia. Thus, naringin might be a good candidate to reduce genotoxic risk associated with hyperglycemia and may provide decreases in the development of secondary malignancy and abnormal reproductive outcomes risks, which seems especially important for diabetic patients.
url http://dx.doi.org/10.1155/2011/365292
work_keys_str_mv AT salehabakheet evaluationofchromosomalinstabilityindiabeticratstreatedwithnaringin
AT sabrymattia evaluationofchromosomalinstabilityindiabeticratstreatedwithnaringin
_version_ 1725404101672435712