Possibly it's because the reactive oxygen species (ROS) may have some physiological roles in the normal body functioning, for example in the maintenance of the DNA protection and repair mechanisms and too much antioxidant turns them off. So the ROS may have an "optimal level" that is needed.
Some literature about these roles:
Physiological levels of reactive oxygen species are required to maintain genomic stability in stem cellsStem Cells. 2010 Jul;28(7):1178-85. doi: 10.1002/stem.438.
Li TS, Marbán E.
The Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA.
http://www.ncbi.nlm....pubmed/20506176Abstract
Stem cell cytogenetic abnormalities constitute a roadblock to regenerative therapies. We investigated the possibility that reactive oxygen species (ROSs) influence genomic stability in cardiac and embryonic stem cells. Karyotypic abnormalities in primary human cardiac stem cells were suppressed by culture in physiological (5%) oxygen, but addition of antioxidants to the medium unexpectedly increased aneuploidy. Intracellular ROS levels were moderately decreased in physiological oxygen, but dramatically decreased by the addition of high-dose antioxidants. Quantification of DNA damage in cardiac stem cells and in human embryonic stem cells revealed a biphasic dose-dependence: antioxidants suppressed DNA damage at low concentrations, but potentiated such damage at higher concentrations. High-dose antioxidants decreased cellular levels of ATM (ataxia-telangiectasia mutated) and other DNA repair enzymes, providing a potential mechanistic basis for the observed effects. These results indicate that physiological levels of intracellular ROS are required to activate the DNA repair pathway for maintaining genomic stability in stem cells. The concept of an "oxidative optimum" for genomic stability has broad implications for stem cell biology and carcinogenesis.
Physiological regulation of cardiac contractility by endogenous reactive oxygen speciesActa Physiol (Oxf). 2012 May;205(1):26-40. doi: 10.1111/j.1748-1716.2012.02391.x.
Perjés A, Kubin AM, Kónyi A, Szabados S, Cziráki A, Skoumal R, Ruskoaho H, Szokodi I.
Heart Institute, Medical School, University of Pécs, Hungary.
http://www.ncbi.nlm....pubmed/22463609Abstract
Increased production of reactive oxygen species (ROS) has been linked to the pathogenesis of congestive heart failure. However, emerging evidence suggests the involvement of ROS in the regulation of various physiological cellular processes in the myocardium. In this review, we summarize the latest findings regarding the role of ROS in the acute regulation of cardiac contractility. We discuss ROS-dependent modulation of the inotropic responses to G protein-coupled receptor agonists (e.g. β-adrenergic receptor agonists and endothelin-1), the potential cellular sources of ROS (e.g. NAD(P)H oxidases and mitochondria) and the proposed end-targets and signalling pathways by which ROS affect contractility. Accumulating new data supports the fundamental role of endogenously generated ROS to regulate cardiac function under physiological conditions.
and
Role of reactive oxygen species in the regulation of cardiac contractilityJ Mol Cell Cardiol. 2011 May;50(5):884-93. doi: 10.1016/j.yjmcc.2011.02.005. Epub 2011 Feb 21.
Kubin AM, Skoumal R, Tavi P, Kónyi A, Perjés A, Leskinen H, Ruskoaho H, Szokodi I.
Institute of Biomedicine, Department of Pharmacology and Toxicology, Biocenter Oulu, University of Oulu, Finland.
http://www.ncbi.nlm....pubmed/21320508and
Physiological roles of mitochondrial reactive oxygen speciesMol Cell. 2012 Oct 26;48(2):158-67. doi: 10.1016/j.molcel.2012.09.025.
Sena LA, Chandel NS.
Department of Medicine, Division of Pulmonary and Critical Care Medicine, Northwestern University
Feinberg School of Medicine, Chicago, USA.
http://www.ncbi.nlm....pubmed/23102266Abstract
Historically, mitochondrial reactive oxygen species (mROS) were thought to exclusively cause cellular damage and lack a physiological function. Accumulation of ROS and oxidative damage have been linked to multiple pathologies, including neurodegenerative diseases, diabetes, cancer, and premature aging. Thus, mROS were originally envisioned as a necessary evil of oxidative metabolism, a product of an imperfect system. Yet few biological systems possess such flagrant imperfections, thanks to the persistent optimization of evolution, and it appears that oxidative metabolism is no different. More and more evidence suggests that mROS are critical for healthy cell function. In this Review, we discuss this evidence following some background on the generation and regulation of mROS.
The role of mitochondrial DNA mutations and free radicals in disease and ageingJ Intern Med. 2013 Jun;273(6):529-43. doi: 10.1111/joim.12055. Epub 2013 Mar 7.
Lagouge M, Larsson NG.
Department of Mitochondrial Biology, Max Planck Institute for Biology of Ageing, Cologne, Germany.
http://www.ncbi.nlm....pubmed/23432181Abstract
Considerable efforts have been made to understand the role of oxidative stress in age-related diseases and ageing. The mitochondrial free radical theory of ageing, which proposes that damage to mitochondrial DNA (mtDNA) and other macromolecules caused by the production of reactive oxygen species (ROS) during cellular respiration drives ageing, has for a long time been the central hypothesis in the field. However, in contrast with this theory, evidence from an increasing number of experimental studies has suggested that mtDNA mutations may be generated by replication errors rather than by accumulated oxidative damage. Furthermore, interventions to modulate ROS levels in humans and animal models have not produced consistent results in terms of delaying disease progression and extending lifespan. A number of recent experimental findings strongly question the mitochondrial free radical theory of ageing, leading to the emergence of new theories of how age-associated mitochondrial dysfunction may lead to ageing. These new hypotheses are mainly based on the underlying notion that, despite their deleterious role, ROS are essential signalling molecules that mediate stress responses in general and the stress response to age-dependent damage in particular. This novel view of ROS roles has a clear impact on the interpretation of studies in which antioxidants have been used to treat human age-related diseases commonly linked to oxidative stress.
