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Published on: July 3, 2015
Rubratoxin B elicits antioxidative and DNA repair responses in mouse brain
1University of South Florida, Tampa, FL 33612, USA.
Abstract:
Rubratoxin B (RB) is a mycotoxin with potential neurotoxic effects that have not yet been characterized. Based on existing evidence that RB interferes with mitochondrial electron transport to produce oxidative stress in peripheral tissues, we hypothesized that RB would produce oxidative damage to macromolecules in specific brain regions. Parameters of oxidative DNA damage and repair, lipid peroxidation, and superoxide dismutase (SOD) activity were measured across six mouse brain regions 24 h after administration of a single dose of RB. Lipid peroxidation and oxidative DNA damage were either unchanged or decreased in all brain regions in RB-treated mice compared with vehicle-treated mice. Concomitant with these decreased indices of oxidative macromolecular damage, SOD activity was significantly increased in all brain regions. Oxyguanosine glycosylase activity (OGG1), a key enzyme in the repair of oxidized DNA, was significantly increased in three brain regions--cerebellum (CB), caudate/putamen (CP), and cortex (CX)--but not in the hippocampus (HP), midbrain (MB), and pons/medulla (PM). The RB-enhanced OGG1 catalytic activity in these brain regions was not due to increased OGG1 protein expression, but was a result of enhanced catalytic activity of the enzyme. In conclusion, specific brain regions responded to an acute dose of RB by significantly altering SOD and OGG1 activities to maintain the degree of oxidative DNA damage equal to, or less than, that of normal steady-state levels.
Insights
Rubratoxin B (RB) did not increase oxidative damage in mouse brains. Instead, antioxidant enzyme activity increased, suggesting a protective response to this mycotoxin.
Area of Science:
- Neuroscience
- Toxicology
- Biochemistry
Background:
- Rubratoxin B (RB) is a mycotoxin suspected of neurotoxicity.
- RB is known to induce oxidative stress in peripheral tissues by interfering with mitochondrial electron transport.
Purpose of the Study:
- To investigate the neurotoxic potential of RB by examining oxidative damage to macromolecules in specific mouse brain regions.
- To determine if RB administration leads to oxidative DNA damage, lipid peroxidation, and alterations in antioxidant enzyme activity.
Main Methods:
- Mice were administered a single dose of RB.
- Oxidative DNA damage, lipid peroxidation, and superoxide dismutase (SOD) activity were measured in six brain regions 24 hours post-administration.
- Oxyguanosine glycosylase (OGG1) activity and protein expression were also assessed.
Main Results:
- RB did not increase lipid peroxidation or oxidative DNA damage in any brain region.
- SOD activity significantly increased in all measured brain regions.
- OGG1 catalytic activity, but not protein expression, significantly increased in the cerebellum, caudate/putamen, and cortex.
Conclusions:
- Acute exposure to RB does not cause oxidative macromolecular damage in the mouse brain.
- Specific brain regions exhibit increased SOD and OGG1 activities in response to RB, indicating a protective mechanism against oxidative stress.
- The observed changes in enzyme activity help maintain oxidative DNA damage levels at or below normal steady-state levels.
