Open AccessNovel interactions between mitochondrial superoxide dismutases and the electron transport chain
Author(s) -
Suthammarak Wichit,
Somerlot Benjamin H.,
Opheim Elyce,
Sedensky Margaret,
Morgan Philip G.
Publication year - 2013
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/acel.12144
Subject(s) - reactive oxygen species , superoxide dismutase , electron transport chain , biology , mitochondrion , mitochondrial ros , microbiology and biotechnology , superoxide , mediator , mutant , function (biology) , biophysics , biochemistry , oxidative stress , enzyme , gene
Summary The processes that control aging remain poorly understood. We have exploited mutants in the nematode, C aenorhabditis elegans , that compromise mitochondrial function and scavenging of reactive oxygen species ( ROS ) to understand their relation to lifespan. We discovered unanticipated roles and interactions of the mitochondrial superoxide dismutases (mt SOD s): SOD ‐2 and SOD ‐3. Both SOD s localize to mitochondrial supercomplex I: III : IV . Loss of SOD ‐2 specifically (i) decreases the activities of complexes I and II , complexes III and IV remain normal; (ii) increases the lifespan of animals with a complex I defect, but not the lifespan of animals with a complex II defect, and kills an animal with a complex III defect; (iii) induces a presumed pro‐inflammatory response. Knockdown of a molecule that may be a pro‐inflammatory mediator very markedly extends lifespan and health of certain mitochondrial mutants. The relationship between the electron transport chain, ROS , and lifespan is complex, and defects in mitochondrial function have specific interactions with ROS scavenging mechanisms. We conclude that mt SOD s are embedded within the supercomplex I: III : IV and stabilize or locally protect it from reactive oxygen species ( ROS ) damage . The results call for a change in the usual paradigm for the interaction of electron transport chain function, ROS release, scavenging, and compensatory responses.