Literature Review On Oxidative Stress

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Title: Mastering the Art of Crafting a Literature Review on Oxidative Stress

Embarking on the journey of composing a literature review on oxidative stress can be a daunting task
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investigation. When it comes to a complex topic like oxidative stress, the challenge intensifies.

Oxidative stress, the imbalance between free radicals and antioxidants in the body, is a multifaceted
phenomenon with implications across various disciplines, including biology, medicine, and
environmental science. Navigating through the extensive literature surrounding oxidative stress
demands not only expertise in these fields but also a keen eye for critical analysis.

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articles, and extracting relevant data to construct a coherent narrative. Moreover, synthesizing
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Antioxidant Functionalized Nanoparticles: A Combat against Oxidative Stress. Increasing evi- dence
suggests that the speci al physicochemical proper- ties of these nanomaterials pose potential risk to
human health. Cencioni C, Spallotta F, Martelli F, Valente S, Mai A, Zeiher AM, Gaetano C. On the
other hand, synthetic polymeric NPs have emerged as the promising nano-drug delivery system, as
they can encapsulate the therapeutic agent and progressively release the therapeutic compound at the
target site. In scientific and clinical research they were mostly utilized to assess involvement of
oxidative stress in a certain type of disease, but were usually considered too much unspecific to give
specific clues regarding diagnosis or therapy 97. Hence, the epigenetic machinery may represent an
oxidative stress sensor that orchestrates the progressive homeostasis impairment typical of ageing,
thus shaping the cellular senescence often observed during cardiovascular, respiratory and nervous
system degeneration. 5. Youth Fountain: Struggle with ROS Lifespan is often correlated to metabolic
rate. Consumption of vegetables and plant-derived foods and beverages has positive effect on the
prevention of age associated diseases like coronary heart disease and atherosclerosis as well as for
longevity 51. Humans have a complex antioxidant protection system, which functions interactively
and synergistically to neutralize free radicals and knowledge as presented in this review will be
important in the management of oxidative stress and its associated diseases. Many clinical trials in
which individuals received one or more synthetic antioxidants failed to obtain beneficial results.
Albeit that several exceptions exist, it is often observed that the faster the metabolism, the higher the
ROS production and, thus, the shorter the lifespan. In vivo redox cycling with oxygen can occur
giving rise to OS through generation of ROS. That cellular perturbation may persist despite the
return of normoglycemia, the so-called memory effect. The primary cellular target of OS can vary;
DNA is an important early target of damage ( Gueteens et al., 2002 ). Oxidative Lipid Damage
Although lipid peroxidation (LP) affects many cellular components, the primary action sites involve
membrane associated polyunsaturated fatty acids (PUFA). Hence, these compounds could be used in
amalgamation with biogenic derived nanoparticles (NPs) for better antioxidant potential. Oxidative
Stress and Epigenetic Regulation in Ageing and Age-Related Diseases. To browse Academia.edu and
the wider internet faster and more securely, please take a few seconds to upgrade your browser.
Rises in calcium interfere with mitochondrial function (including neural), increasing formation of
superoxide which can react with nitric oxide (NO) to form the potent oxidant peroxyni- trite (ONOO
- ), accompanied by lipid peroxidation. At normal levels, they are controlled by antioxidant defenses,
but in disease their levels increase, causing oxidative damage to biomolecules. The section following
that discusses the role of nano-antioxidants; antioxidant functionalized nanoparticles and challenges
associate with them. 2. Synergism between ROS and Age-Related Diseases The overproductions of
ROS have been found to be associated with numerous chronic diseases like cancer, cardiovascular,
neurodegenerative and respiratory ailments. Some of the early glycosylation products on long-lived
proteins (e.g., vessel wall collagen) continue to undergo complex series of chemical rearrangement to
form AGEs, once formed, AGE-protein adducts are stable and virtually irreversible. Many studies
have demonstrated serum lipid abnormalities in children with T1DM as well as an association
between elevated HbA1c and dyslipidemia. ISPRS International Journal of Geo-Information (IJGI).
Previous Article in Special Issue Preventive or Potential Therapeutic Value of Nutraceuticals against
Ionizing Radiation-Induced Oxidative Stress in Exposed Subjects and Frequent Fliers. Keywords:
Health; Organ Toxicity; Oxidative Stress; Reactive Oxygen Species; Electron Transfer 1. Consult a
doctor for medical advice, treatment or diagnosis. Another way to understand the antioxidant is that
it is a stable molecule, which donates an electron to unwanted free radical species and neutralizes it,
and curbs its ability to cause damage. Product Identifiers Publisher Humana Press ISBN-10
1617793965 ISBN-13 9781617793967 eBay Product ID (ePID) 109021569 Product Key Features
Author Kenneth J. You are covered by the eBay Money Back Guarantee opens in a new tab or
window if you receive an item that is not as described in the listing. Free radicals are molecules or
atoms containing an unpaired electron 1. Recent evidence emerging from different studies discussed
below shows that such possibilities exist.
For more information on the journal statistics, click here. In summary, ageing presents specific
epigenetic markers, which, taken altogether, could define the ageing epigenome. Under OS
conditions, mitochondria release various pro-apoptoic factors. In order to maintain proper cell
signaling, it is likely that a number of radical scavenging enzymes maintain a threshold level of ROS
inside the cell. Journal of Pharmaceutical and BioTech Industry (JPBI). Harmful effects of chronic
oxidative stress include faster aging, DNA mutations, epigenetic changes that in worst cases
cumulate with development and progression of many diseases including malignant alterations and
cellular death 41. That cellular perturbation may persist despite the return of normoglycemia, the so-
called memory effect. Furthermore, ageing is characterized by specific histone modifications ( Table
1 ). The cells of all present aerobic organisms produce the majority of chemical energy by consuming
oxygen in their mitochondria. The size and shape of AuNPs are greatly influenced by the quantity of
protein, as extracellular proteins significantly increases the shelf life of nanoparticles by acting as a
capping agent, and thereby conferring them with stability. As part of these preventive measures, there
is indirect evidence for the importance of glycemic control in improving lipid profile in children with
T1DM. Additionally, peroxynitrite and nitroxidative stress have also been implicated in various
aspects of nitrooxidative cellular damage since peroxynitrite also yields secondary one-electron
oxidants 59. Accessibility, User Agreement, Privacy, Payments Terms of Use, Cookies, CA Privacy
Notice, Your Privacy Choices and AdChoice. Peroxynitrite: biochemistry, pathophysiology and
development of therapeutics. Starting antioxidant therapy as one of the corner stones of treatment
early after diagnosis of type 1DM may give a future hope in preventing diabetic microvascular
disease. The major enzymes that convert ROS to less reactive molecules are superoxide dismutase,
catalase and glutathione peroxidase ( Zhu et al., 2008 ). Fig. 6: Mechanisms of oxidative stress-
induced cell damage ( Agarwal et al., 2005 ) In healthy individuals, antioxidants form the body's
primary defense against ROS. The basic theme involves continuing and autocatalytic generation of
hydroxyl radicals by way of the Fenton reaction in- volving poorly liganded iron. 3. PULMONARY
TOXICITY The pulmonary system is one of the main targets for toxicity. Aerobic organisms have
integrated antioxidant systems, which include enzymatic and non-enzymatic antioxidant that are
usually effective in blocking harmful effects of reactive oxygen species. Hammond, Mark S.
LeDoux, Ronald F. Pfeiffer, The University of Memphis, Tennessee, USA, and others). You consent
to our cookies if you continue to use our website. Ok. Both endogenous and exogenous factors can
contribute to free-radical formation. Besides, glucose in the blood increases after consuming a meal,
and for this reason, work instead of resting should be performed in order to maintain an appropriate
electron flow and avoid electron leaks. Increased oxidative stress with age may be in part due to a
decline in the levels of the endogenous cellular antioxidants, among them also coenzyme Q10
declines significantly with age 73. Free-radical modified lipids 20 and lipid-derived free radicals
may play an important role in the development of atherosclerosis. Recommendations for achieving
the appropriate metabolic control and management of dyslipidemia are the most beneficial in
preventing the OS and improving endothelial function. See all condition definitions opens in a new
window or tab Book Title Oxidative Stress: Biological Aspects Author Gilmour, Nick (Editor)
Language English ISBN 9781632395054 Item description from the seller Seller assumes all
responsibility for this listing. Diverse mechanisms have been proposed for these agents. Lotito SB,
Frei B. Consumption of flavonoid-rich foods and increased plasma antioxidant capacity in humans:
cause, consequence, or epiphenomenon. ROS can be from endogenous or exogenous sources and
they are produced from molecular oxygen as a result of normal cellular metabolism, they are divided
into free radicals and non-radicals. You ran into a security check to verify the validity of your request.
This included 11,324 Italian men and women who had survived a myocardial infarction (heart
attack) within the 3 previous months. You ran into a security check to verify the validity of your
request. Oxidative stress causes High levels of reactive oxygen species (ROS), compared to
antioxidant defenses, are considered to play a major role in diverse chronic age-related diseases and
aging. Ex- perimental Biology and Medicine, 232, 592-606. In addition, further analyses revealed
that p66ShcA is transcriptionally repressed by SIRT1, as confirmed by the evidence that p66Shc
increases following SIRT1 inhibition. Furthermore, they are very important participants in the
regulation of smooth muscle tone and bacterial function of phagocytes ( Droge, 2002 ). An important
issue is that these findings appear even in patients with short non-complicated diabetes course and
this provides a direct evidence for the beneficial and early effect of tight metabolic control and
antioxidant therapy in prevention of MVCs. Hyperglycemia can directly cause increased ROS
generation. Gene polymorphisms, which condition endogenous antioxidant deficiencies, would be
the exception to such advice. Nutritional, dietary and postprandial oxidative stress. Free radical-
mediated reactions can cause structural alterations in DNA (e.g., nicking, base-pair mutations,
rearrangement, deletions, insertions and sequence amplification). An- other source of brain ROS is
NA DPH oxidase enzymes. Antioxidant Functionalized Nanoparticles: A Combat against Oxidative
Stress. People who eat fruits and vegetables, which happen to be good sources of antioxidants and
other phytochemicals, have a lower risk of heart disease and some neurological diseases 46 and there
is evidence that some types of vegetables and fruits in general, protect against a number of cancers
47 as epidemiological studies revealed, without providing the answer whether any specific bioactive
molecules within fruit and vegetable have a special contribution on lower incidence. Although
generally considered as harmful by-products of oxygen metabolism, ROS also have important
physiological functions in signal transduction and immunological response 24. To understand the
process leading to age-associated alterations is, therefore, of the highest relevance for the
development of new treatments for age-associated diseases, such as cancer, diabetes, Alzheimer and
cardiovascular accidents. As mentioned above, NO is fundamental for endothelial function.
Mitochondria are thus the main site of intracellular oxygen consumption and the main source of
ROS formation 57. Oxidative stress is a determinant of ageing, and p66ShcA knockout results in
oxidative stress resistance and low levels of apoptosis. Emotional stress increases catecholamine
metabolism, which increases oxidative stress by increasing the production of free radicals. Foods rich
in antioxidants include all fresh and seasonal fruit and vegetables (peppers, apples, onions, pineapple,
dark leafy vegetables, flaxseeds, walnuts, pumpkin seeds, and olives), olive oil, and fish.
INTRODUCTION Abundant literature exists on involvement of reactive oxygen species (ROS) and
oxidative stress (OS) on hu- man health. All these pathological modifications contribute to the
pathogenesis of vascular dysfunction. The basic theme involves continuing and autocatalytic
generation of hydroxyl radicals by way of the Fenton reaction in- volving poorly liganded iron. 3.
PULMONARY TOXICITY The pulmonary system is one of the main targets for toxicity.
Cytotoxicity of uranium, has been in the spotlight in recent decades. Their formation is considered as
a pathobiochemical mechanism involved in the initiation or progression phase of various diseases
such as atherosclerosis, ischemic heart diseases, diabetes, and initiation of carcinogenesis or liver
diseases. In addition to these materials, selenium nanoparticles (SeNPs) are also attracting
researchers, owing to their enhanced properties like semi-conduction, photoelectrical,
photoconduction, catalytic etc., and their potential in optical and electronic instruments. Other
epigenetic molecules are now under evaluation for their potentially positive effect in age-associated
diseases. Aldehydes are generated during numerous physiological processes. In conclusion, the
authors established that methylation imprinting hits both gene expression and susceptibility to
oxidative DNA damage in the late stages of Alzheimer’s disease.

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