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trans,trans-2,4-decadienal induces mitochondrial dysfunction and oxidative stress
Carlos A O Sigolo1, Paolo Di Mascio, Alicia J Kowaltowski
1Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, Av. Prof. Lineu Prestes 748, CEP 05508-900, São Paulo, Brazil.
Journal of Bioenergetics and Biomembranes
|March 28, 2008
Summary
Reactive aldehydes like trans,trans-2,4-decadienal (DDE) from lipid peroxidation cause mitochondrial dysfunction. DDE treatment led to increased oxygen consumption, swelling, and loss of membrane potential in isolated rat liver mitochondria.
Area of Science:
- Biochemistry
- Cell Biology
- Toxicology
Background:
- Lipid peroxidation generates reactive aldehydes.
- Cytochrome c forms adducts with trans,trans-2,4-decadienal (DDE).
- Previous work identified specific modification sites on cytochrome c by DDE.
Purpose of the Study:
- To investigate the effects of DDE on isolated rat liver mitochondria.
- To determine if DDE induces mitochondrial dysfunction.
Main Methods:
- Isolated rat liver mitochondria were treated with DDE.
- Mitochondrial oxygen consumption was measured.
- Mitochondrial swelling was assessed using light scattering and transmission electron microscopy.
- Inner mitochondrial membrane potential was monitored using safranin O fluorescence.
- Lipid peroxidation was quantified by malondialdehyde (MDA) formation.
Main Results:
- DDE treatment increased mitochondrial oxygen consumption.
- DDE induced significant mitochondrial swelling.
- Loss of inner mitochondrial membrane potential was observed.
- DDE exposure elevated lipid peroxidation levels (MDA formation) in mitochondria.
Conclusions:
- Reactive aldehydes, such as DDE, contribute to mitochondrial dysfunction.
- DDE directly impairs mitochondrial integrity and function.
- These findings highlight the detrimental impact of lipid peroxidation byproducts on cellular energy production.
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