Kayo Yasuda

Adaptive responses to oxidative damage in three mutants of Caenorhabditis elegans (age-1, mev-1 and daf-16) that affect life span.

Coenzyme Q10 can prolong C. elegans lifespan by lowering oxidative stress.

A mutation in the SDHC gene of complex II increases oxidative stress, resulting in apoptosis and tumorigenesis.

Direct measurement of oxygen consumption rate on the nematode Caenorhabditis elegans by using an optical technique.

Age-related changes of mitochondrial structure and function in Caenorhabditis elegans.

The role of mitochondrial superoxide anion (O2(-)) on physiological aging in C57BL/6J mice.

Post-dauer life span of Caenorhabditis elegans dauer larvae can be modified by X-irradiation.

Cell growth of the mouse SDHC mutant cells was suppressed by apoptosis throughout mitochondrial pathway.

Mitochondrial reactive oxygen species generation by the SDHC V69E mutation causes low birth weight and neonatal growth retardation.

Interrelationships between mitochondrial fusion, energy metabolism and oxidative stress during development in Caenorhabditis elegans.

Mitochondrial superoxide anion overproduction in Tet-mev-1 transgenic mice accelerates age-dependent corneal cell dysfunctions.

Oxidative stress induced inflammation initiates functional decline of tear production.

Model animals for the study of oxidative stress from complex II.

Genetically induced oxidative stress in mice causes thrombocytosis, splenomegaly and placental angiodysplasia that leads to recurrent abortion.

Liposome-encapsulated hemoglobin enhances chemotherapy to suppress metastasis in mice.

Ethyl methanesulfonate induces mutations in Caenorhabditis elegans embryos at a high frequency.

Infertility and recurrent miscarriage with complex II deficiency-dependent mitochondrial oxidative stress in animal models.

Endogenous reactive oxygen species cause astrocyte defects and neuronal dysfunctions in the hippocampus: a new model for aging brain.

Impaired p53/CEP-1 is associated with lifespan extension through an age-related imbalance in the energy metabolism of C. elegans.