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Hybridization increases mitochondrial production of reactive oxygen species in sunfish
Author(s) -
Du Sherry N. N.,
Khajali Fariborz,
Dawson Neal J.,
Scott Graham R.
Publication year - 2017
Publication title -
evolution
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.84
H-Index - 199
eISSN - 1558-5646
pISSN - 0014-3820
DOI - 10.1111/evo.13254
Subject(s) - biology , reactive oxygen species , oxidative phosphorylation , mitochondrion , oxidative stress , mitochondrial ros , electron transport chain , respirometry , lipid peroxidation , microbiology and biotechnology , biochemistry , biophysics
Mitochondrial dysfunction and oxidative stress have been suggested to be possible mechanisms underlying hybrid breakdown, as a result of mito‐nuclear incompatibilities in respiratory complexes of the electron transport system. However, it remains unclear whether hybridization increases the production of reactive oxygen species (ROS) by mitochondria. We used high‐resolution respirometry and fluorometry on isolated liver mitochondria to examine mitochondrial physiology and ROS emission in naturally occurring hybrids of pumpkinseed ( Lepomis gibbosus ) and bluegill ( L. macrochirus ). ROS emission was greater in hybrids than in both parent species when respiration was supported by complex I (but not complex II) substrates, and was associated with increases in lipid peroxidation. However, respiratory capacities for oxidative phosphorylation, phosphorylation efficiency, and O 2 kinetics in hybrids were intermediate between those in parental species. Flux control ratios of capacities for electron transport (measured in uncoupled mitochondria) relative to oxidative phosphorylation suggested that the limiting influence of the phosphorylation system is reduced in hybrids. This likely helped offset impairments in electron transport capacity and complex III activity, but contributed to augmenting ROS production. Therefore, hybridization can increase mitochondrial ROS production, in support of previous suggestions that mitochondrial dysfunction can induce oxidative stress and thus contribute to hybrid breakdown.