editorial interplay between oxidative stress and metabolism in … · 2019. 7. 30. · trocola et...

EditorialInterplay between Oxidative Stress and Metabolism inSignalling and Disease

Andrés Trostchansky,1 Celia Quijano,1 Hariom Yadav,2

Eric E. Kelley,3 and Adriana Maria Cassina1

1Departamento de Bioquı́mica and Center for Free Radical and Biomedical Research, Facultad de Medicina,Universidad de la República, 11800 Montevideo, Uruguay2NIDDK, NIH, Diabetes, Endocrinology and Obesity Branch, Bethesda, MD 20892, USA3Department of Anesthesiology and Vascular Medicine Institute, School of Medicine, University of Pittsburgh,Pittsburgh, PA 15261, USA

Correspondence should be addressed to Andrés Trostchansky; [email protected]

Received 11 October 2015; Accepted 11 October 2015

Copyright © 2016 Andrés Trostchansky et al. This is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properlycited.

It is well recognized that energy metabolism is linked tothe production of reactive species and critical enzymaticprocesses allied to metabolic pathways can be affected byredox reactions. Both protein and lipid oxidation are involvedin the aging process as well as the onset and progression ofmany age-related diseases. As such, the capacity to identifyspecific targets anddetect subsequent oxidativemodificationsis crucial for the understanding of the molecular basis ofage-related diseases (i.e., diabetes, metabolic syndrome, oratherosclerosis) and for revealing novel treatment strategies.

Formation of mitochondrial reactive oxygen and nitro-gen species (ROS and RNS, resp.) has been extensively stud-ied in the literature. Moreover, mitochondrial dysfunction isobserved in many pathological conditions in addition to anincrease in ROS and RNS production. Thus, the initiationand progression of diseases whose pathogenesis involvesmitochondrial dysfunction may be modulated by decreasingmitochondrial oxidant formation. However, mitochondriaare not the only source of reactive species in cells; for example,catabolism of biomolecules can be a source of oxidant forma-tion with critical intracellular outcomes. For example during𝛽-oxidation of fatty acids, the electron transfer flavoprotein(ETF) produces superoxide (O

2

∙−) and hydrogen peroxide(H2O2) upon reduction with its substrate, medium chain

acyl-CoA dehydrogenase (MCAD). Superoxide and H2O2

can be formed in several metabolic pathways where electron

transfer reactions are involved and can subsequently leadto the formation of highly oxidizing species such as per-oxynitrite and lipid-derived electrophiles. As such, capacityto detoxify reactive species with a battery of antioxidantenzymes is critical in preventing the reactions of oxidantswith cellular components.

In this special issue, we present several examples of theinterplay between oxidative stress and metabolism.

Themanuscript byM. da Cunha and colleagues discussesmitochondria-to-nucleus retrograde signaling in variousorganisms as well as the differences in effector pathways,molecules, and outcomes. Almost 99% of mitochondrialproteins are encoded in the nucleus; however, mitochondrialDNA does encode some key proteins. The correct commu-nication between mitochondria and the nucleus is seminal incoordinatingmitochondrial protein synthesis during biogen-esis whereas potential mitochondrial malfunction can influ-ence in this communication.Mitochondrial role in apoptosis,addressed by J. A. Ronchi et al., describes Ca2+-dependentopening of mitochondrial membrane permeability transitionpore (PTP) and ROS generation. In their manuscript, theauthors propose that PTP opening is a relevant processof mitochondrial Ca2+ signaling when a redox imbalanceis present. The NADPH/NADP+ ratio was also analyzedin terms of mitochondrial ROS formation in hypercholes-terolemic mice after supplementation with citrate or by

Hindawi Publishing CorporationOxidative Medicine and Cellular LongevityVolume 2016, Article ID 3274296, 2 pageshttp://dx.doi.org/10.1155/2016/3274296

2 Oxidative Medicine and Cellular Longevity

inhibition of the NADPH consuming anabolic cholesterolsynthesis pathway. Overall, the authors showed a positivecorrelation of the atherosclerotic lesion with mitochondrialROS formation in liver.

TheNAD-dependent protein deacetylases sirtuins (SIRT)regulate metabolic enzymes maintaining cellular homeosta-sis. L. Santos et al. present a thorough revision on how sirtuinsare regulated at the expression level and/or by proteasomaldegradation depending on the degree of oxidative stress.Finally, the authors discuss how SIRT3 may be regulated byoxidant species generated in the mitochondrial matrix.

Santos J. and colleagues addressed nutrient signalingpathways related to caloric restriction (in particular, howaging and caloric restriction interact by overlapping theactivation of insulin-derived pathways). Meanwhile, R. Mas-trocola et al. analyzed metabolic disorders and its relationwith high fat diet. In their original article S. Kun et al. explorehow hydroxyl radical- or metabolic-derived Phe or Tyrderivatives alter the gluconeogenic pathway in nondiabeticseptic patients and propose that these species may serve asindicators for insulin-based therapies in these patients.

The aim of this special issue was to increase our knowl-edge of the role of metabolism and oxidative stress in cellsignaling and disease, particularly about themolecularmech-anisms participating in these processes as well as their role inhuman diseases and cell physiology.

Acknowledgment

We would like to thank all the reviewers that contributedduring the peer-review process.

Andrés TrostchanskyCelia QuijanoHariom YadavEric E. Kelley

Adriana Maria Cassina

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