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Oxidative Stress Induction by Infectious Pancreatic Necrosis Virus in RTG-2 Cell Line

Oxidative Stress Induction by Infectious Pancreatic Necrosis Virus in RTG-2 Cell Line

Semra Okur Gumusova1, Gul Fatma Yarim2, Cuneyt Tamer1,*, Ayris Salt2 and Gokhan Inat3

1Department of Virology, Faculty of Veterinary Medicine, Ondokuz Mayis University, Samsun, Turkey
2Department of Biochemistry, Faculty of Veterinary Medicine, Ondokuz Mayis University, Samsun, Turkey
3Department of Food Hygiene and Technology, Faculty of Veterinary Medicine, Ondokuz Mayis University, Samsun, Turkey
 
* Corresponding author: cuneyt_tamer@hotmail.com

ABSTRACT

Investigation of the relationship between oxidative stress and cell damage may provide important insight into infection treatment. Previous studies have shown that many viruses induce oxidative cell damage during their replication in mamalian cell culture, but fish viruses has not been well-studied. Infectious pancreatic necrosis (IPN) is caused by infectious pancreatic necrosis virus (IPNV) and it is a viral, fatal and contagious disease of young salmonids and nonsalmonid fish with acute to peracute clinical forms. This study was designed to investigate the relationship between oxidative stress and cell damage due to IPNV in rainbow trout gonad cell line-2 (RTG-2). For this purpose, IPNV was inoculated in RTG-2. Then, media of IPNV infected cell and media of negative control were collected (n=3) for each incubation time (0, 8, 24, 48, 72 and 96 h) and superoxide dismutase (SOD), glutathione peroxidase (GPx) activities and malondialdehyde (MDA) concentrations were measured by the spectrophotometric methods. Data obtained revealed higher MDA levels in IPNV infected cells than negative control medium (p<0.001). However, SOD and GPx levels in IPNV infected cells were lover than negative control cells medium (p<0.001). These results indicate that, cell damage in RTG-2 cell line, that is caused by IPNV is assosiated with oxidative stress.

 

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Pakistan Journal of Zoology

August

Vol. 54, Iss. 4, Pages 1501-2001

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