Targeted overexpression of mitochondrial catalase prevents radiation-induced cognitive dysfunction.

ABSTRACT:

Aims

Radiation-induced disruption of mitochondrial function can elevate oxidative stress and contribute to the metabolic perturbations believed to compromise the functionality of the central nervous system. To clarify the role of mitochondrial oxidative stress in mediating the adverse effects of radiation in the brain, we analyzed transgenic (mitochondrial catalase [MCAT]) mice that overexpress human catalase localized to the mitochondria.

Results

Compared with wild-type (WT) controls, overexpression of the MCAT transgene significantly decreased cognitive dysfunction after proton irradiation. Significant improvements in behavioral performance found on novel object recognition and object recognition in place tasks were associated with a preservation of neuronal morphology. Wh

SUBMITTER: Parihar VK 

PROVIDER: S-EPMC4270160 | biostudies-literature | 2015 Jan

REPOSITORIES: biostudies-literature