Alicia J. Kowaltowski

Thiol enzymes protecting mitochondria against oxidative damage.

Mechanisms by which opening the mitochondrial ATP- sensitive K(+) channel protects the ischemic heart.

Effect of Bcl-2 overexpression on mitochondrial structure and function.

Opening of mitochondrial K+ channels increases ischemic ATP levels by preventing hydrolysis.

Mitochondrial ATP-sensitive K+ channel opening decreases reactive oxygen species generation.

Ischemic preconditioning inhibits mitochondrial respiration, increases H2O2 release, and enhances K+ transport.

H(2)O(2) generation in Saccharomyces cerevisiae respiratory pet mutants: effect of cytochrome c.

ATP-sensitive K+ channels in renal mitochondria.

Glutathione and thioredoxin peroxidases mediate susceptibility of yeast mitochondria to Ca(2+)-induced damage.

Binding, aggregation and photochemical properties of methylene blue in mitochondrial suspensions.

A highly active ATP-insensitive K+ import pathway in plant mitochondria.

Mitochondrial permeability transition in neuronal damage promoted by Ca2+ and respiratory chain complex II inhibition.

Higher respiratory activity decreases mitochondrial reactive oxygen release and increases life span in Saccharomyces cerevisiae.

Phosphate increases mitochondrial reactive oxygen species release.

Bcl-2 family proteins regulate mitochondrial reactive oxygen production and protect against oxidative stress.

Redox mechanisms of cytoprotection by Bcl-2.

Mitochondrial ATP-sensitive K+ channels prevent oxidative stress, permeability transition and cell death.

Letter regarding article by Argaud et al, "postconditioning inhibits mitochondrial permeability transition".

Tissue protection mediated by mitochondrial K+ channels.

Ischemic preconditioning requires increases in reactive oxygen release independent of mitochondrial K+ channel activity.

Mitochondrial Ca2+ transport, permeability transition and oxidative stress in cell death: implications in cardiotoxicity, neurodegeneration and dyslipidemias.

Diazoxide protects against methylmalonate-induced neuronal toxicity.

Hyperlipidemic mice present enhanced catabolism and higher mitochondrial ATP-sensitive K+ channel activity.

Inhibition of specific electron transport pathways leads to oxidative stress and decreased Candida albicans proliferation.

Dihydrolipoyl dehydrogenase as a source of reactive oxygen species inhibited by caloric restriction and involved in Saccharomyces cerevisiae aging.

Pharmacological and physiological stimuli do not promote Ca(2+)-sensitive K+ channel activity in isolated heart mitochondria.

Mitochondrial ATP-sensitive K+ channels are redox-sensitive pathways that control reactive oxygen species production.

Interaction of cationic meso-porphyrins with liposomes, mitochondria and erythrocytes.

Mitochondrial energy metabolism and redox state in dyslipidemias.

Ischemic preconditioning enhances fatty acid-dependent mitochondrial uncoupling.

Redox properties of the adenoside triphosphate-sensitive K+ channel in brain mitochondria.

trans,trans-2,4-decadienal induces mitochondrial dysfunction and oxidative stress.

Nicorandil protects cardiac mitochondria against permeability transition induced by ischemia-reperfusion.

Mild mitochondrial uncoupling in mice affects energy metabolism, redox balance and longevity.

Increased aerobic metabolism is essential for the beneficial effects of caloric restriction on yeast life span.

Tissue-, substrate-, and site-specific characteristics of mitochondrial reactive oxygen species generation.

Cross-talk between mitochondria and NADPH oxidase: effects of mild mitochondrial dysfunction on angiotensin II-mediated increase in Nox isoform expression and activity in vascular smooth muscle cells.

Mitochondria and reactive oxygen species.

Mitochondrial bioenergetics and redox state are unaltered in Trypanosoma cruzi isolates with compromised mitochondrial complex I subunit genes.

Mitochondrial ATP-sensitive K(+) channels as redox signals to liver mitochondria in response to hypertriglyceridemia.

Mitochondrial ion transport pathways: role in metabolic diseases.

Effects of a high fat diet on liver mitochondria: increased ATP-sensitive K+ channel activity and reactive oxygen species generation.

Yeast as a model to study mitochondrial mechanisms in ageing.

Commonly adopted caloric restriction protocols often involve malnutrition.

Potent cardioprotective effect of the 4-anilinoquinazoline derivative PD153035: involvement of mitochondrial K(ATP) channel activation.

Saccharomyces cerevisiae coq10 null mutants are responsive to antimycin A.

Redox regulation of the mitochondrial K(ATP) channel in cardioprotection.

Mitochondrial energy metabolism in neurodegeneration associated with methylmalonic acidemia.

Mild mitochondrial uncoupling as a therapeutic strategy.

Mild mitochondrial uncoupling and calorie restriction increase fasting eNOS, akt and mitochondrial biogenesis.

Major determinants of photoinduced cell death: Subcellular localization versus photosensitization efficiency.

Aging and calorie restriction modulate yeast redox state, oxidized protein removal, and the ubiquitin-proteasome system.

Long-term intermittent feeding, but not caloric restriction, leads to redox imbalance, insulin receptor nitration, and glucose intolerance.

Respiratory and TCA cycle activities affect S. cerevisiae lifespan, response to caloric restriction and mtDNA stability.

Neuronal differentiation involves a shift from glucose oxidation to fermentation.

Diguanoside tetraphosphate (Gp₄G) is an epithelial cell and hair growth regulator.

Caloric restriction and redox state: does this diet increase or decrease oxidant production?

Calorie restriction increases cerebral mitochondrial respiratory capacity in a NO•-mediated mechanism: impact on neuronal survival.

Serum from calorie-restricted rats activates vascular cell eNOS through enhanced insulin signaling mediated by adiponectin.

Mitochondrial metabolism in aging: effect of dietary interventions.

Mitochondrial compartmentalization of redox processes.

nde1 deletion improves mitochondrial DNA maintenance in Saccharomyces cerevisiae coenzyme Q mutants.

Bicarbonate modulates oxidative and functional damage in ischemia-reperfusion.

Mitochondria as a source of reactive oxygen and nitrogen species: from molecular mechanisms to human health.

Exercise training restores cardiac protein quality control in heart failure.

Calorie restriction hysteretically primes aging Saccharomyces cerevisiae toward more effective oxidative metabolism.

Deletion of the transcriptional regulator opi1p decreases cardiolipin content and disrupts mitochondrial metabolism in Saccharomyces cerevisiae.

Proline dehydrogenase regulates redox state and respiratory metabolism in Trypanosoma cruzi.

Diet-sensitive sources of reactive oxygen species in liver mitochondria: role of very long chain acyl-CoA dehydrogenases.

Dietary restriction in cerebral bioenergetics and redox state.