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Inconsistency between manganese superoxide dismutase expression and its activity involved in the degeneration of
H-M Qiu1, J-X Yang1, Q-S Jiang1
1Key Laboratory of Biochemistry and Molecular Pharmacology, Department of Pharmacology, School of Pharmacy, Chongqing Medical University, Yuzhong, Chongqing, China.
Abstract:
Manganese (Mn) superoxide dismutase (SOD) is mainly located in mitochondrial matrix and is responsible for scavenging about 80% free radicals from oxidative and phospharylative process in mitochondria. It was reported that the insufficiency of Mn SOD expression or activity was connected to the development of neurodegenerative diseases. In this article, we investigated the time course related to the changes of Mn SOD expression and its activity from mouse brain as well as the recognition dysfunction in chronic aluminum (Al) overloading mice. Aluminum gluconate solution (equal to Al 400 mg/kg) was given to mice once a day, 6 days per week for 12 weeks via intragastric gavage. The learning and memory function, malondialdehyde (MDA) level as well as expression and activity of Mn SOD in cortex were determined. It was found that function of passive learning and memory and spatial recognition decreased, MDA level and Mn SOD expression increased during the period of chronic Al loading, but the Mn SOD activity rose from the 4th week and then decreased from the 8th week in cortex in Al overloading mice compared with the control. The results indicated that the inconsistency between Mn SOD expression and its activity might contribute to the development of recognition dysfunction induced by chronic Al overload.
Insights
Chronic aluminum exposure impairs learning and memory in mice. While manganese superoxide dismutase (Mn SOD) expression increased, its activity fluctuated, suggesting a link to cognitive decline.
Area of Science:
- Biochemistry
- Neuroscience
- Toxicology
Background:
- Manganese superoxide dismutase (Mn SOD) is crucial for mitigating mitochondrial oxidative stress.
- Reduced Mn SOD function is implicated in neurodegenerative disease development.
- Chronic aluminum (Al) exposure is a potential risk factor for cognitive impairment.
Purpose of the Study:
- To investigate the temporal changes in Mn SOD expression and activity in the mouse brain during chronic aluminum overload.
- To assess the impact of chronic aluminum exposure on learning, memory, and recognition dysfunction.
- To explore the relationship between Mn SOD alterations and cognitive deficits induced by aluminum.
Main Methods:
- Mice were administered aluminum gluconate (400 mg/kg/day) for 12 weeks.
- Learning and memory functions were evaluated using passive avoidance and spatial recognition tests.
- Malondialdehyde (MDA) levels, Mn SOD expression, and Mn SOD activity in the cortex were measured over time.
Main Results:
- Chronic aluminum exposure led to decreased passive learning, memory, and spatial recognition.
- Malondialdehyde levels and Mn SOD expression in the cortex increased with aluminum loading.
- Mn SOD activity initially rose (from week 4) then declined (from week 8) in aluminum-overloaded mice.
Conclusions:
- An inconsistency between elevated Mn SOD expression and altered Mn SOD activity was observed during chronic aluminum overload.
- This discordance may play a significant role in the development of recognition dysfunction caused by chronic aluminum exposure.
- Findings highlight the complex interplay between oxidative stress, Mn SOD function, and aluminum-induced neurotoxicity.
