Oxidation-reduction and reactive oxygen species homeostasis in mutant plants with respiratory chain complex I dysfunction
Autor: | Izabela M. Juszczuk, Bożena Szal, Anna M. Rychter |
---|---|
Rok vydání: | 2011 |
Předmět: |
chemistry.chemical_classification
Alternative oxidase Reactive oxygen species Physiology Superoxide Respiratory chain Cellular homeostasis Plant Science Biology Mitochondrion medicine.disease_cause chemistry.chemical_compound chemistry Biochemistry Electron Transport Complex I medicine Oxidative stress |
Zdroj: | Plant, Cell & Environment. 35:296-307 |
ISSN: | 0140-7791 |
Popis: | Mutations in a mitochondrial or nuclear gene encoding respiratory chain complex I subunits lead to decreased or a total absence of complex I activity. Plant mutants with altered or lost complex I activity adapt their respiratory metabolism by inducing alternative pathways of the respiratory chain and changing energy metabolism. Apparently, complex I is a crucial component of the oxidation-reduction (redox) regulatory system in photosynthetic cells, and alternative NAD(P)H dehydrogenases of the mitochondrial electron transport chain (mtETC) cannot fully compensate for its impairment. In most cases, dysfunction of complex I is associated with lowered or unchanged hydrogen peroxide (H(2)O(2)) concentrations, but increased superoxide (O(2)(-)) levels. Higher production of reactive oxygen species (ROS) by mitochondria in the mosaic (MSC16) cucumber mutant may be related to retrograde signalling. Different effects of complex I dysfunction on H(2)O(2) and O(2)(-) levels in described mutants might result from diverse regulation of processes involved in H(2)O(2) and O(2)(-) production. Often, dysfunction of complex I did not lead to oxidative stress, but increased the capacity of the antioxidative system and enhanced stress tolerance. The new cellular homeostasis in mutants with dysfunction of complex I allows growth and development, reflecting the plasticity of plant metabolism. |
Databáze: | OpenAIRE |
Externí odkaz: |