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Both inorganic and organic selenium supplements can decrease brain monoamine oxidase B enzyme activity in adult rats
Ya-Li Tang1, Shih-Wei Wang, Shyh-Mirn Lin
1Department of Food and Nutrition, Chung Hwa University of Medical Technology, no. 89, Wenhwa 1st Street, Tainan County 717, Taiwan.
Abstract:
It has been observed that the levels of brain monoamine oxidase B (MAO-B) increase during ageing. MAO catalyses the oxidative deamination of neurotransmitters, in which the by-product H2O2 is subsequently generated. Se exists naturally in inorganic and organic forms and is considered to play a key role in antioxidation functioning. The objective of the present study was to investigate two chemical forms of Se compounds for their inhibition effect on rat brain MAO-B. The total antioxidant capacity and lipid peroxidation of rats were also examined. The rats (age 7 weeks) were divided into four groups: the control group, tocopherol group (T group, positive control), selenite group (SE group, representing the inorganic Se group) and seleno-yeast group (SY group, representing the organic Se group). The rats were fed for 11 weeks with normal diets and 12 weeks with test diets. The serum total antioxidant capacity of the SE and SY groups was significantly higher than that in the control and T groups. In rat brains and livers, the lipid peroxidation levels were significantly decreased in the T, SE and SY groups. MAO-B activity showed a significant decrease in the T, SE and SY groups in rat brains but no significant change could be noted in the rat livers. In conclusion, the present study indicates that inorganic or organic Se supplementation can decrease the brain MAO-B enzyme activity in adult rats and can be accomplished by the effect of the Se antioxidation capability.
Insights
Selenium supplementation, in both inorganic and organic forms, effectively reduces brain monoamine oxidase B (MAO-B) activity in adult rats. This effect is linked to selenium's antioxidant properties, offering potential neuroprotective benefits.
Area of Science:
- Biochemistry
- Neuroscience
- Nutritional Science
Background:
- Brain monoamine oxidase B (MAO-B) activity increases with age, contributing to neurotransmitter imbalance and oxidative stress.
- Hydrogen peroxide (H2O2), a byproduct of MAO activity, exacerbates oxidative damage.
- Selenium (Se) is a vital antioxidant, existing in both inorganic and organic forms, with potential roles in mitigating age-related neurological changes.
Purpose of the Study:
- To investigate the inhibitory effects of inorganic (selenite) and organic (selenoyeast) selenium compounds on rat brain MAO-B activity.
- To evaluate the impact of selenium supplementation on overall antioxidant capacity and lipid peroxidation in rats.
- To explore the relationship between selenium's antioxidant function and its effect on MAO-B activity.
Main Methods:
- Adult rats were divided into four groups: control, tocopherol (positive control), selenite (inorganic Se), and selenoyeast (organic Se).
- Animals received normal diets for 11 weeks followed by test diets for 12 weeks.
- Measurements included serum total antioxidant capacity, lipid peroxidation levels in brain and liver, and MAO-B enzyme activity in brain and liver tissues.
Main Results:
- Serum total antioxidant capacity was significantly elevated in both selenite and selenoyeast groups compared to control and tocopherol groups.
- Lipid peroxidation levels were significantly reduced in the brains and livers of rats supplemented with tocopherol, selenite, or selenoyeast.
- MAO-B activity in the brain significantly decreased in the tocopherol, selenite, and selenoyeast groups, with no significant changes observed in the liver.
Conclusions:
- Both inorganic and organic selenium supplementation can effectively decrease brain MAO-B enzyme activity in adult rats.
- The observed reduction in MAO-B activity is likely mediated by selenium's inherent antioxidant capabilities.
- Selenium supplementation demonstrates potential as a strategy to manage age-related increases in MAO-B activity and associated oxidative stress.