Oxidative stress, DNA damage and apoptosis induced by tebuconazole in the kidney of male Wistar rat.
Animals
Apoptosis
/ drug effects
DNA Damage
/ drug effects
Dose-Response Relationship, Drug
Fungicides, Industrial
/ toxicity
Gene Expression Regulation
Glutathione
/ metabolism
Glutathione Disulfide
/ metabolism
Glutathione Reductase
/ metabolism
Kidney
/ drug effects
Male
Oxidation-Reduction
Oxidative Stress
/ drug effects
Rats
Rats, Wistar
Triazoles
/ toxicity
Apoptosis
Nephrotoxicity
Oxidative stress
Rats
Tebuconazole
Journal
Chemico-biological interactions
ISSN: 1872-7786
Titre abrégé: Chem Biol Interact
Pays: Ireland
ID NLM: 0227276
Informations de publication
Date de publication:
01 Oct 2020
01 Oct 2020
Historique:
received:
21
08
2019
revised:
03
04
2020
accepted:
22
04
2020
pubmed:
1
8
2020
medline:
21
10
2020
entrez:
1
8
2020
Statut:
ppublish
Résumé
Tebuconazole (TEB) is a broad-spectrum conazole fungicide that has been used in agriculture in the control of foliar and soil-borne diseases of many crops. The present study has investigated the adverse effects of subchronic exposure to TEB on the kidney of male rats. Animals were divided into four equal groups and treated with TEB at increasing doses 0.9, 9 and 27 mg/kg body weight for 28 consecutive days. The results showed that TEB induced oxidative stress in the kidney demonstrated by an increase in malondialdehyde (MDA), protein carbonyl (PC), advanced oxidation protein product (AOPP) levels and DNA damage, as compared to the controls. Furthermore, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities were increased in the renal tissue of treated rats. Moreover, significant decrease in reduced glutathione (GSH) content in TEB-treated rats was observed, while oxidized glutathione (GSSG) levels were increased, thus a marked fall in GSH/GSSG ratio was registered in the kidney. Glutathione reductase (GR) activity showed a significant increase after TEB exposure. Moreover, TEB down-regulated the expression of Bcl2 and up-regulated the expression of Bax and caspase 3, which triggered apoptosis via the Bax/Bcl2 and caspase pathway. Also, TEB administration resulted in altered biochemical indicators of renal function and varying lesions in the overall histo-architecture of renal tissues. Taken together, our findings brought into light the renal toxicity induced by TEB, which was found to be significant at low doses.
Identifiants
pubmed: 32735800
pii: S0009-2797(19)31436-X
doi: 10.1016/j.cbi.2020.109114
pii:
doi:
Substances chimiques
Fungicides, Industrial
0
Triazoles
0
tebuconazole
401ATW8TRW
Glutathione Reductase
EC 1.8.1.7
Glutathione
GAN16C9B8O
Glutathione Disulfide
ULW86O013H
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
109114Informations de copyright
Copyright © 2020 Elsevier B.V. All rights reserved.