• Publications
  • Influence
Life and death: metabolic rate, membrane composition, and life span of animals.
The links between metabolic rate andmaximum life span of mammals and birds as well as the linking role of membrane fatty acid composition in determining the maximum life span are reviewed. Expand
A signalling role for 4‐hydroxy‐2‐nonenal in regulation of mitochondrial uncoupling
The findings indicate that hydroxynonenal is not merely toxic, but may be a biological signal to induce uncoupling through UCPs and ANT and thus decrease mitochondrial ROS production. Expand
Mitochondrial membrane peroxidizability index is inversely related to maximum life span in mammals.
It may be proposed that, during evolution, a low degree of fatty acid unsaturation in liver mitochondria may have been selected in longevous mammals in order to protect the tissues against oxidative damage, while maintaining an appropriate environment for membrane function. Expand
Membrane phospholipids, lipoxidative damage and molecular integrity: a causal role in aging and longevity.
  • R. Pamplona
  • Chemistry, Medicine
  • Biochimica et biophysica acta
  • 1 October 2008
The causal role of ALEs in aging and longevity is inferred from the findings that follow: a) its accumulation with aging in several tissues and species; b) physiological interventions that increase longevity, decrease ALEs content; c) the longer the longevity of a species, the lower is the lipoxidation-derived molecular damage; and finally d) exacerbated levels of ALES are associated with pathological states. Expand
Pathological aspects of lipid peroxidation
Striking evidences implicating LPO in foetal vascular dysfunction occurring in pre-eclampsia, in renal and liver diseases, as well as their role as cause and consequence to cancer development are addressed. Expand
Hyperglycemia and glycation in diabetic complications.
The mechanism of glycation and of AGEs formation and the role of hyperglycemia, A GEs, and oxidative stress in the pathophysiology of diabetic complications are summarized. Expand
Molecular and structural antioxidant defenses against oxidative stress in animals.
The study of inheritance mechanisms of antioxidant mechanisms has clear potential to evaluate the contribution of epigenetic mechanisms to stress response phenotype variation, which can help explain life-history trade-offs. Expand
Mitochondrial DNA Mutations Induce Mitochondrial Dysfunction, Apoptosis and Sarcopenia in Skeletal Muscle of Mitochondrial DNA Mutator Mice
It is demonstrated that mutations in mtDNA can be causal in sarc Openia by affecting the assembly of functional ETC complexes, the lack of which provokes a decrease in oxidative phosphorylation, without an increase in oxidative stress, and ultimately, skeletal muscle apoptosis and sarcopenia. Expand
Proteins in Human Brain Cortex Are Modified by Oxidation, Glycoxidation, and Lipoxidation
An important role for lipid peroxidation-derived protein modifications in Alzheimer disease pathogenesis is supported, and increases in the concentrations of all evaluated markers support this role. Expand
Mitochondrial oxidative stress, aging and caloric restriction: the protein and methionine connection.
Data suggest that lowering of methionine levels is involved in the control of mitochondrial oxidative stress and vertebrate longevity by at least two different mechanisms: decreasing the sensitivity of proteins to oxidative damage, and lowering of the rate of ROS generation at mitochondria. Expand