Mitochondrial manganese superoxide dismutase knock-down increases oxidative stress and caspase-3 activity in the white shrimp Litopenaeus vannamei exposed to high temperature, hypoxia, and reoxygenation

2021 ◽  
Vol 252 ◽  
pp. 110826
Author(s):  
Ricardo González-Ruiz ◽  
Alma B. Peregrino-Uriarte ◽  
Elisa M. Valenzuela-Soto ◽  
Francisco J. Cinco-Moroyoqui ◽  
Miguel A. Martínez-Téllez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
High Temperature ◽  
Litopenaeus Vannamei ◽  
Manganese Superoxide Dismutase ◽  
Caspase 3 ◽  
White Shrimp ◽  
Knock Down ◽  
Manganese Superoxide

scholarly journals Role of reduced manganese superoxide dismutase in ischemia-reperfusion injury: a possible trigger for autophagy and mitochondrial biogenesis?

2013 ◽  
Vol 304 (3) ◽  
pp. F257-F267 ◽  
Author(s):  
Nirmala Parajuli ◽  
Lee Ann MacMillan-Crow
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Renal Function ◽  
Mitochondrial Biogenesis ◽  
Renal Damage ◽  
Manganese Superoxide Dismutase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Manganese Superoxide ◽  
Oxidant Production

Excessive generation of superoxide and mitochondrial dysfunction has been described as being important events during ischemia-reperfusion (I/R) injury. Our laboratory has demonstrated that manganese superoxide dismutase (MnSOD), a major mitochondrial antioxidant that eliminates superoxide, is inactivated during renal transplantation and renal I/R and precedes development of renal failure. We hypothesized that MnSOD knockdown in the kidney augments renal damage during renal I/R. Using newly characterized kidney-specific MnSOD knockout (KO) mice the extent of renal damage and oxidant production after I/R was evaluated. These KO mice (without I/R) exhibited low expression and activity of MnSOD in the distal nephrons, had altered renal morphology, increased oxidant production, but surprisingly showed no alteration in renal function. After I/R the MnSOD KO mice showed similar levels of injury to the distal nephrons when compared with wild-type mice. Moreover, renal function, MnSOD activity, and tubular cell death were not significantly altered between the two genotypes after I/R. Interestingly, MnSOD KO alone increased autophagosome formation, mitochondrial biogenesis, and DNA replication/repair within the distal nephrons. These findings suggest that the chronic oxidative stress as a result of MnSOD knockdown induced multiple coordinated cell survival signals including autophagy and mitochondrial biogenesis, which protected the kidney against the acute oxidative stress following I/R.

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