Amelioration of ochratoxin-A induced cytotoxicity by prophylactic treatment of N-Acetyl-L-Tryptophan in human embryonic kidney cells.
Apoptosis
/ drug effects
Cell Cycle
/ drug effects
Cell Survival
/ drug effects
Dose-Response Relationship, Drug
HEK293 Cells
Humans
Kidney
/ drug effects
Membrane Potential, Mitochondrial
/ drug effects
Molecular Docking Simulation
Ochratoxins
/ toxicity
Oxidative Stress
/ drug effects
Tryptophan
/ administration & dosage
Cytotoxicity
HEK-293 cells
Mitochondrial damage
N-Acetyl-L-Tryptophan
Ochratoxin-A
Oxidative stress
Journal
Toxicology
ISSN: 1879-3185
Titre abrégé: Toxicology
Pays: Ireland
ID NLM: 0361055
Informations de publication
Date de publication:
15 01 2020
15 01 2020
Historique:
received:
19
07
2019
revised:
19
09
2019
accepted:
23
10
2019
pubmed:
5
11
2019
medline:
18
8
2020
entrez:
4
11
2019
Statut:
ppublish
Résumé
Ochratoxin A (OTA) is known to induce nephro-toxicity via induction of cellular redox homeostasis perturbation, mitochondrial hyperpolarisation and depolarization, protein synthesis inhibition leading to apoptosis. In the present study, protective efficacy of N-Acetyl-L-Tryptophan (NAT) against OTA induced toxicity was evaluated using Human Embryonic Kidney (HEK-293) cells. Cells were treated with NAT (0-200 μg/ml) before OTA treatment (0-20 μg/ml) and protective efficacy of NAT was evaluated using MTT and SRB assay. OTA-induced intracellular ROS generation and its inhibition by NAT (2.5 μg/ml) pre-treatment was evaluated using 2',7'-dichlorodihydrofluorescein diacetate (H
Identifiants
pubmed: 31678613
pii: S0300-483X(19)30281-1
doi: 10.1016/j.tox.2019.152324
pii:
doi:
Substances chimiques
Ochratoxins
0
ochratoxin A
1779SX6LUY
N-acetyltryptophan
4460NBV53F
Tryptophan
8DUH1N11BX
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
152324Informations de copyright
Copyright © 2019 Elsevier B.V. All rights reserved.