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Antioxidant changes in the hypertrophied heart due to energy metabolic disorder
1Internal Medicine II and First Department of Pathology, Nagoya University School of Medicine, Japan.
Insights
Juvenile visceral steatosis (JVS) mice show altered antioxidant capacity during heart hypertrophy. While initially increased, antioxidant levels change as hypertrophy progresses, suggesting oxidative stress may contribute to this condition.
Area of Science:
- Cardiovascular Biology
- Oxidative Stress Research
- Metabolic Disorders
Background:
- Oxidative stress is linked to heart hypertrophy and failure.
- Pressure-overload hypertrophy increases antioxidant capacity.
- Antioxidant changes in metabolic disorder-induced hypertrophy are unstudied.
Purpose of the Study:
- To investigate antioxidant capacity changes in juvenile visceral steatosis (JVS) mice.
- To examine the role of oxidative stress in JVS-induced heart hypertrophy.
Main Methods:
- Assessed antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase, catalase) in JVS mice at 4 and 8 weeks.
- Measured lipid peroxidation and vitamin E levels in JVS mouse hearts.
- Administered long-term vitamin E and 2-mercaptopropionyl glycine treatments.
Main Results:
- JVS mice exhibited higher superoxide dismutase activity at 4 weeks, but not at 8 weeks.
- Glutathione peroxidase activity was lower in 8-week-old JVS mice.
- Lipid peroxidation decreased initially then rose towards control levels; vitamin E increased in JVS hearts. Vitamin E treatment partially mitigated hypertrophy.
Conclusions:
- Heart hypertrophy in JVS mice involves altered antioxidant capacity, similar to other models.
- Oxidative stress may play a role in the pathogenesis of JVS-induced heart hypertrophy.
- Further research is needed to elucidate the precise mechanisms.
Abstract:
Oxidative stress has been implicated in the pathogenesis of both heart hypertrophy and heart failure. Hypertrophied heart, in response to pressure overload, is associated with an increase in antioxidant capacity and a decrease in oxidative stress. However, in the hypertrophied heart due to energy metabolic disorder, antioxidant capacity has not been investigated. Antioxidant changes in juvenile visceral steatosis (JVS) mice, a model of heart hypertrophy due to disorder of fatty-acid oxidation, were examined at 4 weeks (developing hypertrophy stage) and 8 weeks of age (established hypertrophy stage). Superoxide dismutase activity in the JVS mice was higher than that in control mice at 4 weeks of age and was not different from that in the control mice at 8 weeks of age. Glutathione peroxidase activity in the JVS mice at 8 weeks of age was lower than that in the control mice. Catalase activity showed no significant differences between the control and the JVS mice. Lipid peroxidation in the JVS mice was significantly reduced at 4 weeks of age and increased toward control levels at 8 weeks of age. The levels of vitamin E in the heart were increased in the JVS mice at 8 weeks of age. To determine whether antioxidants affect the pathogenesis of hypertrophy in this model, long-term treatments of vitamin E and 2-mercaptopropionyl glycine were performed. Vitamin E treatment partially reduced the heart hypertrophy in these mice. The present study shows that heart hypertrophy in the JVS mice is accompanied with increased antioxidant capacity as indicated in other animal models of heart hypertrophy. The precise mechanism of heart hypertrophy in JVS mice is still unknown, but oxidative stress may play a role in the pathogenesis of heart hypertrophy.