Nervous necrosis virus induced oxidative imbalance and host associated antioxidant response in Asian seabass brain.

Abstract

Nervous necrosis virus induced oxidative stress and associated antioxidative response in the brain of Asian seabass were evaluated in the present study. The infection resulted in an increasing level of nitric oxide pro- duction induced by the expression of inducible nitric oxide synthase. The activity of NRF2 was increased and up- regulated the expression of ARE stimulatory genes including heme oxygenase-1 (HO-1), NAD(P)H quinone oxidoreductase-1 (NQO-1), superoxide dismutase (SOD) and catalase (CAT). The antioxidant enzyme SOD and CAT activity were diminished following infection even though the gene expression was upregulated. The activity of glutathione metabolism markers GPx, GR and GST were affected by the NNV infection. Expression of ERK-1 was up-regulated whereas AMPK down-regulated. Our results suggest that NNV influence the homeostasis of the cell by oxidative stress and affects the antioxidative responses by perturbing the glutathione metabolism and antioxidant enzyme activity.