Author
Carol C. Cunningham
Other affiliations: University of Missouri
Bio: Carol C. Cunningham is an academic researcher from Wake Forest University. The author has contributed to research in topics: Mitochondrion & ATP synthase. The author has an hindex of 31, co-authored 65 publications receiving 3221 citations. Previous affiliations of Carol C. Cunningham include University of Missouri.
Topics: Mitochondrion, ATP synthase, Phospholipid, Adenine nucleotide, ATPase
Papers published on a yearly basis
Papers
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TL;DR: In this article, the authors focused on observations which indicate that the ability of ethanol to increase mitochondrial reactive oxygen species production is linked to its metabolism via oxidative processes and/or ethanol-related alterations to the mitochondrial electron transport chain.
280 citations
TL;DR: The bovine heart F0F1-ATPase preparation has been further delipidated and the enzyme appears to have high affinity for cardiolipin exclusively, since PC (a prominent inner membrane lipid), phosphatidyl serine (an acidic phospholipid), and phosphatids were not immobilized (rendered NMR-invisible) when added to the delipidation preparation.
227 citations
TL;DR: Results indicate that the NADH dehydrogenase complex, as well as complex III of mitochondria, are involved in ethanol-related production of reactive oxygen species.
197 citations
TL;DR: The hypothesis that acute and chronic ethanol exposure enhances the mitochondrial generation of ROS in fresh, isolated hepatocytes is tested and exacerbates mitochondrial ROS production, contributing to cell death.
186 citations
TL;DR: It appears that the decreased levels of mitochondria-derived polypeptide components of the oxidative phosphorylation system are primarily responsible for the depression in both the rate and efficiency of ATP synthesis.
Abstract: Chronic ethanol consumption results in a generalized depression in hepatic mitochondrial energy metabolism. Both the rate and efficiency of ATP synthesis via the oxidative phosphorylation system are decreased. Alterations in the activities of several components of the oxidative phosphorylation system contribute to the overall decrease in the capacity for ATP synthesis. There appears to be no alteration in any particular component which is rate-limiting. Although changes in membrane lipids may play a minor role, it appears that the decreased levels of mitochondria-derived polypeptide components of the oxidative phosphorylation system are primarily responsible for the depression in both the rate and efficiency of ATP synthesis. The concentrations of these mitochondrial gene products are lowered due to effects of chronic ethanol consumption on the mitochondrial translational process.
171 citations
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TL;DR: This review summarizes the current state of knowledge of the functions of NOX enzymes in physiology and pathology.
Abstract: For a long time, superoxide generation by an NADPH oxidase was considered as an oddity only found in professional phagocytes. Over the last years, six homologs of the cytochrome subunit of the phag...
5,873 citations
TL;DR: This review describes the main mitochondrial sources of reactive species and the antioxidant defences that evolved to prevent oxidative damage in all the mitochondrial compartments and discusses various physiological and pathological scenarios resulting from an increased steady state concentration of mitochondrial oxidants.
Abstract: The reduction of oxygen to water proceeds via one electron at a time. In the mitochondrial respiratory chain, Complex IV (cytochrome oxidase) retains all partially reduced intermediates until full reduction is achieved. Other redox centres in the electron transport chain, however, may leak electrons to oxygen, partially reducing this molecule to superoxide anion (O2−•). Even though O2−• is not a strong oxidant, it is a precursor of most other reactive oxygen species, and it also becomes involved in the propagation of oxidative chain reactions. Despite the presence of various antioxidant defences, the mitochondrion appears to be the main intracellular source of these oxidants. This review describes the main mitochondrial sources of reactive species and the antioxidant defences that evolved to prevent oxidative damage in all the mitochondrial compartments. We also discuss various physiological and pathological scenarios resulting from an increased steady state concentration of mitochondrial oxidants.
4,282 citations
TL;DR: This review examines how target selectivity and antioxidant effectiveness vary for different oxidants and highlights areas where greater understanding is required on the fate of oxidants generated by cellular NADPH oxidases and on the identification of oxidant sensors in cell signaling.
Abstract: There is a vast literature on the generation and effects of reactive oxygen species in biological systems, both in relation to damage they cause and their involvement in cell regulatory and signaling pathways. The biological chemistry of different oxidants is becoming well understood, but it is often unclear how this translates into cellular mechanisms where redox changes have been demonstrated. This review addresses this gap. It examines how target selectivity and antioxidant effectiveness vary for different oxidants. Kinetic considerations of reactivity are used to assess likely targets in cells and how reactions might be influenced by restricted diffusion and compartmentalization. It also highlights areas where greater understanding is required on the fate of oxidants generated by cellular NADPH oxidases and on the identification of oxidant sensors in cell signaling.
2,011 citations
TL;DR: It is expected that cell cultures of patients with mitochondrial diseases will increasingly be used to address fundamental questions about mtDNA expression, and several key enzymes involved in mtDNA replication, transcription and protein synthesis have now been biochemically identified and some have been cloned.
1,337 citations
TL;DR: The newly introduced concepts of the protonmotive ubiquinone cycle, or Q cycle, and of the cyclic loop 2–3 system, which represent developments of the redox loop concept, are shown to provide a promising basis for the evolution of a satisfactory theory.
1,218 citations