Carmen García-Ruiz

TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.

TL;DR: It is suggested that mitochondria are a target of ceramide produced in the signaling of TNF whose effect on mitochondrial electron transport chain leads to overproduction of hydrogen peroxide and consequently this phenomena may account for the generation of reactive oxygen species during TNF cytotoxicity.

TL;DR: It is suggested that GSH protects mitochondria against the endogenous oxidative stress produced at the ubiquinone site of the electron transport chain and potentiates oxidant-induced loss of mitochondrial functions.

TL;DR: Limiting the mitochondrial GSH pool represents a critical contributory factor that sensitizes alcoholic hepatocytes to the prooxidant effects of cytokines and prooxids generated by oxidative metabolism of ethanol, and S-adenosyl-L-methionine prevents development of the ethanol-induced defect.

TL;DR: Mitochondrial GSH depletion by ethanol feeding preceded the onset of functional changes in mitochondria, suggesting that mitochondrial GSH is critical in maintaining a functionally competent organelle and that the greater depletion of mitochondria byanol feeding in PV cells could contribute to the pathogenesis of alcoholic liver disease.