Nitric oxide (NO)-mediated mitochondrial damage plays a critical role in T-2 toxin-induced apoptosis and growth hormone deficiency in rat anterior pituitary GH3 cells

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F62690094%3A18470%2F17%3A50005606" target="_blank" >RIV/62690094:18470/17:50005606 - isvavai.cz</a>

Result on the web

<a href="http://dx.doi.org/10.1016/j.fct.2017.01.017" target="_blank" >http://dx.doi.org/10.1016/j.fct.2017.01.017</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.fct.2017.01.017" target="_blank" >10.1016/j.fct.2017.01.017</a>

Result language

angličtina

Original language name

Nitric oxide (NO)-mediated mitochondrial damage plays a critical role in T-2 toxin-induced apoptosis and growth hormone deficiency in rat anterior pituitary GH3 cells

Original language description

T-2 toxin, a major compound of trichothecenes, induces cell apoptosis and growth hormone (GH) deficiency and causes considerable growth retardation in animals and human cells. However, the mechanism underlying its growth suppression still remains unclear. Recent studies have suggested that ROS induced cell apoptosis and animal feed intake reduction, but there are limited reports on the role of RNS in T-2 toxin-mediated mitochondrial damage, cell apoptosis and growth retardation. Herein, T-2 toxin-induced GH3 cell damage and apoptosis were tested by MTT assay, LDH leakage and flow cytometry, respectively. Intracellular NO and antioxidant enzyme activity, DJm, morphometric changes of mitochondria, the caspase pathway, and inflammatory factors were investigated. Free radical scavengers NAC, SOD and NO scavenger haemoglobin were used to explore the role of oxidative stress and the relationship between NO production and caspase pathway. The results clearly revealed that T-2 toxin caused significant increases in NO generation, cell apoptosis, GH deficiency, increased iNOS activity, upregulation of inflammatory factors and caspase pathway, decreases in DJm and morphosis damage. These data suggest that mitochondria are a primary target of T-2 toxin-induced NO, and NO is a key mediator of T-2 toxininduced cell apoptosis and GH deficiency via the mitochondria-dependent pathway in cells.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

30108 - Toxicology

Project

—

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2017

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Food and chemical toxicology

ISSN

0278-6915

e-ISSN

—

Volume of the periodical

102

Issue of the periodical within the volume

April

Country of publishing house

GB - UNITED KINGDOM

Number of pages

13

Pages from-to

11-23

UT code for WoS article

000397689200002

EID of the result in the Scopus database

2-s2.0-85010851197