Glutathione in Cancer Cell Death

Cancers

Angel L. Ortega²  Salvador Mena¹ 

[1] Green Molecular SL, Pol. Ind. La Coma-Parc Cientific, 46190 Paterna, Valencia, Spain; E-Mail:;Department of Physiology, Faculty of Medicine and Odontology, University of Valencia, 17 Av. Blasco Ibanez, 46010 Valencia, Spain; E-Mail:

关键词: glutathione;    cancer;    cell death;    apoptosis;    necrosis;    autophagy;   

DOI  :  10.3390/cancers3011285

来源: mdpi

【 摘 要 】

Glutathione (L-γ-glutamyl-L-cysteinyl-glycine; GSH) in cancer cells is particularly relevant in the regulation of carcinogenic mechanisms; sensitivity against cytotoxic drugs, ionizing radiations, and some cytokines; DNA synthesis; and cell proliferation and death. The intracellular thiol redox state (controlled by GSH) is one of the endogenous effectors involved in regulating the mitochondrial permeability transition pore complex and, in consequence, thiol oxidation can be a causal factor in the mitochondrion-based mechanism that leads to cell death. Nevertheless GSH depletion is a common feature not only of apoptosis but also of other types of cell death. Indeed rates of GSH synthesis and fluxes regulate its levels in cellular compartments, and potentially influence switches among different mechanisms of death. How changes in gene expression, post-translational modifications of proteins, and signaling cascades are implicated will be discussed. Furthermore, this review will finally analyze whether GSH depletion may facilitate cancer cell death under in vivo conditions, and how this can be applied to cancer therapy.

【 授权许可】

CC BY   
© 2011 by the authors; licensee MDPI, Basel, Switzerland.