Reactive oxygen species: the unavoidable environmental insult

Advances in Bioscience and Biotechnology, 2012

Redox degenerative reactions of the biological system inevitably produce reactive oxygen species (ROS) and their derivatives. Oxidative stress is the result of an imbalance in pro-oxidant/antioxidant homeostasis that leads to the generation of toxic reactive oxygen species (ROS), such as hydrogen peroxide, organic hydro peroxides, nitric oxide, superoxide and hydroxyl radicals etc. Information are accumulating steadily, supporting the general importance of oxidative damage of tissue and cellular components as a primary or secondary causative factor in many different human diseases and aging processes. Many of the recent landmarks in scientific research have shown that in human beings, oxidative stress has been implicated in the progression of major health problems by inactivating the metabolic enzymes and damaging important cellular components, oxidizing the nucleic acids, leading to cardiovascular diseases, eye disorders, joint disorders, neurological diseases (Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis), atherosclerosis, lung and kidney disorders, liver and pancreatic diseases, cancer, ageing, disease of the reproductive system including the male and female infertility etc. The advent of a growing number of in vitro and in vivo models for evaluating the human disease pathology is aiding scientists in deciphering the detailed mechanisms of the point of intersection of the oxidative stress with other cellular components or events in the growing roadmap leading to different human disorders. The toxic effect of reactive oxygen and nitrogen species in human is balanced by the antioxidant action of non-enzymatic antioxidants, as well as by antioxidant enzymes. Such antioxidant defences are extremely important as they represent the direct removal of free radicals (prooxidants), thus providing maximal protection for biological sites. These systems not only assert with the problem of oxidative damage, but also play a crucial role in wellness, health maintenance, and prevention of chronic and degenerative diseases. In this review we have tried to generate a gross picture on the critical role of ROS in deteriorating human health and the importance of antioxidative defense system in ameliorating the toxicity of ROS.

JOURNAL OF ADVANCES IN BIOTECHNOLOGY

A free radical is any molecule capable of independent existence that contains one or more free electrons. These free radicals fall under the broader category of reactive oxygen species (ROS). ROS such as O2- , H2O2, NO-, OH-, HOCl, ONOO- are toxic to cells. ROS act largely by driving several important molecular pathways that play important roles in pathologic processes including neurodegeneration. injury, atherosclerosis, and inflammatory responses and ischemia-reperfusion. ROS, as in various radicals ions leads to mitochondrial dysfunction and consequently other cell organelles damage either through environmental effect or through genetic or metabolic disorders. Reactive molecular species also disturbs other metabolic pathways in a manner that cell’s normal functionality gets disrupted. Though diseases caused by reactive oxygen species are many, this review has covered its effect on major diseases. The present review paper will provide the detail of mechanism of ROS and its effec...

Journal of Neuroscience and Neurological Disorders, 2019

The biological changes caused by oxidative stress (OS) are known to be involved in the etiology of neurodegenerative disorders, including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease. The brain is particularly vulnerable to OS due to its high lipid content and extensive consumption of oxygen. OS processes, particularly the excessive production of reactive oxygen species (ROS), play a critical role in how neurodegenerative disorders develop. This is evidenced by in vivo studies investigating various biomolecules related to OS, such as products of lipid and DNA oxidation. Accordingly, ROS can also cause oxidativerelated damage in neurodegenerative disorders, including dopamine auto-oxidation, mitochondrial dysfunction, glial cell activation, α-synuclein aggregation, excessive free iron, and changes in calcium signaling. Furthermore, excessive levels of cellular oxidants reduce antioxidant defenses, which in turn propagate the cycle of OS. As such, it is increasingly important to determine the linkage between a high intake of antioxidants through dietary interventions and a lower risk of developing neurodegenerative diseases. Indeed, in addition to modulating the immune system, optimal nutritional status is capable of changing various processes of neuroinfl ammation known to be involved in the pathogenesis of neurodegeneration. Accordingly, a better understanding of the role ROS plays in the etiology of neurodegeneration is needed, along with the identifi cation of dietary interventions that may lead to improved therapeutic strategies for both the treatment and prevention of neurodegenerative disorders. Therefore, this review presents a comprehensive summary of the role of ROS in the pathogenesis of neurodegenerative disorders. In addition, nutrients believed to be useful for mitigating and counteracting ROS are discussed.

Journal of Controversies in Biomedical Research, 2015

The production of intracellular reactive oxygen species and reactive nitrogen species has long been proposed as leading to the random deleterious modification of macromolecules (i.e., nucleic acids, proteins) with an associated progressive development of the age associated systemic diseases (e.g., diabetes, Parkinson's disease) as well as contributing to the ageing process. Superoxide anion (hydrogen peroxide) and nitric oxide (peroxynitrite) comprise regulated intracellular second messenger pro-oxidant systems, with specific sub-cellular locales of production and are essential for the normal function of the metabolome and cellular electro-physiology. We have posited that the formation of superoxide anion and its metabolic product hydrogen peroxide, and nitric oxide, do not conditionally lead to random damage of macromolecular species such as nucleic acids or proteins. Under normal physiological conditions their production is intrinsically regulated that is very much consistent with their second messenger purpose of function. We further propose that the concept of an orally administered small molecule antioxidant as a therapy to abrogate free radical activity (to control oxidative stress) is a chimera. As such we consider that free radicals are not a major overwhelming player in the development of the chronic diseases or the ageing process.

Journal of the American Oil Chemists' Society, 1998

Free radicals and other reactive oxygen species (ROS) are constantly formed in the human body. Free-radical mechanisms have been implicated in the pathology of several human diseases, including cancer, atherosclerosis, malaria, and rheumatoid arthritis and neurodegenerative diseases. For example, the superoxide radical (O 2 • -) and hydrogen peroxide (H 2 O 2 ) are known to be generated in the brain and nervous system in vivo, and several areas of the human brain are rich in iron, which appears to be easily mobilizable in a form that can stimulate free-radical reactions. Antioxidant defenses to remove O 2 • - and H 2 O 2 exist. Superoxide dismutases (SOD) remove O 2 • -by greatly accelerating its conversion to H 2 O 2 . Catalases in peroxisomes convert H 2 O 2 into water and O 2 and help to dispose of H 2 O 2 generated by the action of the oxidase enzymes that are located in these organelles. Other important H 2 O 2 -removing enzymes in human cells are the glutathione peroxidases. When produced in excess, ROS can cause tissue injury. However, tissue injury can itself cause ROS generation (e.g., by causing activation of phagocytes or releasing transition metal ions from damaged cells), which may (or may not, depending on the situation) contribute to a worsening of the injury. Assessment of oxidative damage to biomolecules by means of emerging technologies based on products of oxidative damage to DNA (e.g., 8-hydroxydeoxyguanosine), lipids (e.g., isoprostanes), and proteins (altered amino acids) would not only advance our understanding of the underlying mechanisms but also facilitate supplementation and intervention studies designed and conducted to test antioxidant efficacy in human health and disease.

Pathology International, 1999

radicals associated with the oxygen atom or their equivalents and have stronger reactivity with other molecules than with molecular oxygen (O 2 ). Reactive oxygen species usually indicate the following four species: (i) superoxide anion (O 2 Ϫ );

2010

Oxidative stress is a phenomenon associated with pathogenetic mechanisms of several diseases including atherosclerosis, neurodegenerative diseases, such as Alzheimer's and Parkinson's disease, cancer, diabetes mellitus, inflammatory diseases, as well as psychological diseases or aging processes. Oxidative stress is defined as an imbalance between production of free radicals and reactive metabolites, so-called oxidants, and their elimination by protective mechanisms, referred to as antioxidative systems. This imbalance leads to damage of important biomolecules and organs with potential impact on the whole organism. Oxidative and antioxidative processes are associated with electron transfer influencing the redox state of cells and the organism. The changed redox state stimulates or inhibits activities of various signal proteins, resulting in a changed ability of signal pathways to influence the fate of cells. At present, the opinion that oxidative stress is not always harmful,...

International Journal of Molecular Sciences, 2021

Living species are continuously subjected to all extrinsic forms of reactive oxidants and others that are produced endogenously. There is extensive literature on the generation and effects of reactive oxygen species (ROS) in biological processes, both in terms of alteration and their role in cellular signaling and regulatory pathways. Cells produce ROS as a controlled physiological process, but increasing ROS becomes pathological and leads to oxidative stress and disease. The induction of oxidative stress is an imbalance between the production of radical species and the antioxidant defense systems, which can cause damage to cellular biomolecules, including lipids, proteins and DNA. Cellular and biochemical experiments have been complemented in various ways to explain the biological chemistry of ROS oxidants. However, it is often unclear how this translates into chemical reactions involving redox changes. This review addresses this question and includes a robust mechanistic explanati...

Oxygen is one of the most important and indispensable elements, since life molecules on Earth can, under certain situations, produce from it constantly in the human body toxic molecules, called free radicals and/or other reactive oxygen species (ROS). ROS play a dual role in biological systems, since they can be either harmful or beneficial to living systems. These highly reactive species capable of wide spread, indiscriminate oxidation and peroxidation of proteins, lipids and DNA which can lead to significant cellular damage and even tissue and/or organ failure. However, it is well known fact, that many of the ROS-mediated responses actually protect the cells against oxidative stress. On the other hand, over-production of ROS has the potential to cause damage. In addition currently some increasing evidence appeared showing that oxidative stress is associated with the pathogenesis of number diseases, like neurodegenerative disorders, cardiovascular diseases, neuropsychiatric disorde...

Oxidative Stress and Diseases, 2012