Download Free Oxidation In Vivo And In Vitro Book in PDF and EPUB Free Download. You can read online Oxidation In Vivo And In Vitro and write the review.

This book introduces a novel approach to comprehending and assessing oxidative stress and antioxidant activity as fundamental components in both health and disease. It explores the advantages and peculiarities of innovative electrochemical methods for estimating and monitoring these processes. Recognizing the electrochemical nature of oxidative stress, the book advocates for electrochemical methods as the preferred means of determination. A central focus of the book is the presentation of a new electrochemical method for evaluating oxidative stress and antioxidant activity: potentiometric determination. The book presents results of antioxidant activity analyses for both healthy individuals and patients with diverse pathologies. Additionally, the book discusses the prospective advantages of employing potentiometry as a monitoring tool in areas such as diet, sports, and wellness. Further considerations extend to the future applications of oxidative stress monitoring, encompassing wearable devices, sensors, non-invasive assessments, and telemedicine. In short, this book establishes the method's credibility as a diagnostic criterion for studying oxidative stress across laboratory settings, bedside applications, and everyday life.
Free radicals and other reactive oxygen species are constantly formed in the human body and have been implicated in human diseases such as cancer, atherosclerosis, rheumatoid arthritis, Parkinson's disease, and malaria. This observation has raised the possibility that antioxidants could act as prophylactic agents. However, it remains to be fully established whether oxidative stress makes a significant contribution to the pathology of a given disease or whether it is an epiphenomenon. Indeed, development of specific assays applicable to humans would greatly contribute to our understanding of the role played by free radicals and their modulation by antioxidants in normal physiology and in human diseases. This book addresses the key methodological questions.
This book is based on the papers presented at the "Fourth International Congress on Oxygen Radicals (4-ICOR)," held June 27 - July 3, 1987, at the University of California, La Jolla. The chapters deal with the phenomena associated with highly reactive oxygen species (hydroxy, peroxy, alkoxy, aroxy, and superoxide radicals, as well as singlet oxygen) and their peroxidation products (hydrogen peroxide, hydroperoxides, peroxides, and epoxides) as they relate to the fields of chemistry, food technology, nutrition, biology, pharmacology, and medicine. The kinetics, energetics, and mechanistic aspects of the reactions of these species and the interrelationship of oxygen radicals (or any other free radicals) and peroxidized products have been emphasized. Special attention is focused on the mechanisms of the generation of free radicals and peroxy products in biosystems and on the adverse effects of these radicals and products in humans. The topics span the continuum from the simple chemistry of model systems to the complex considerations of clinical medicine. The book also explores the mechanisms of agents that protect against free radicals and peroxy products in vitro and in vivo. These agents include antioxidants used in materials, food antioxidants, physiological antioxidants, and antioxienzymes (SOD, glutathione peroxidase, and catalases). The use of these inhibitors to prevent damage to organs being prepared for transplantation, thereby maintaining the quality of transplanted organs and/or extending their "shelf-life," also is examined.
This book discusses the importance of oxidative stress, related biomarkers, and its diagnostic methods including bio-analytical and advanced detection systems. Oxidative stress is associated with diminished capacity of a biological system to overcome the overproduction of reactive oxygen species. Since oxidative stress has been suggested as a causative factor in many diseases, its prevention is vital, and there is an urgent need for oxidative stress monitoring using in vitro and in vivo models. Interdisciplinary approaches have lead to the development of various oxidative stress monitoring models for real-world clinical and biomedical applications. The development of such methods requires a broad understanding of biology, chemistry, molecular biology, immunology and microbiology. As such, the book is a valuable resource for students, researchers and clinicians interested in the fundamental as well as applied aspects of oxidative stress associated diseases.
Introduction: It is important to understand oxidative degradation of joint bearing materials to predict in vivo wear, cracking, and delamination due to stress and cycles of use [1]. Traditionally, oxidative degradation is thought to occur when free radicals in the polymer react with oxidative species on the shelf or in vivo. Pre-implantation oxidation of free-radical containing materials was eliminated with gamma-barrier sterilization and oxygen-impermeable packaging, but oxidation has been shown to increase exponentially with time in vivo. Retrieval studies have revealed a threshold ketone oxidation index of 1.0-1.5 (KOI, 1715 cm-1 peak normalized to the 1368 cm-1 peak) for maintaining mechanical integrity of polyethylene. Many bearings are shown to reach this level before 12 years in vivo [1]. Device manufacturers have tackled this problem by removing free-radicals with post irradiation thermal-treatments [2] or by adding radical stabilizing antioxidants [3]. Because the current ASTM artificial aging method (F2003) states u201cthis practice is not intended to simulate any change that may occur in UHMWPE following implantationu201d, studying long-term stability of these materials is limited to retrieval studies with small sample sets, short in vivo times, and uncontrollable surgeon- and patient-specific variables. The current objective is to map a more gentle (relative to ASTM F2003) in vitro artificial aging of gamma barrier devices to published in vivo oxidation trendlines, and to use this aging system to predict stability of an antioxidant material.Methods and Materials: Five rectangular prisms (5 x 5 x 8 cm) were cut from GUR 1020 resin stock materials prepared as follows: u201cVirginu201d non-cross- linked (TVI = -0.001), u201cAntioxidantu201d PHBP-containing, 85 kGY u03b3-irradiation, EtO (TVI = 0.031); u201cRemeltedu201d 75 kGy u03b3-irradiation, melted in argon, gas plasma treated (TVI = 0.024); u201cGVF-Lowu201d conventional UHMWPE, gamma vacuum foil (GVF) (Mean TVI = 0.014); u201cGVF-Highu201d conventional UHMWPE, GVF (TVI = 0.016). The blocks were artificially aged in a pressure vessel under 45 PSI (3 atm) O2 at 63oC for 10 weeks, with sampling at intermediate timepoints. Oxidation at 0, 4, and 6 weeks are reported as the maximum KOI measured from test coupons collected at each time point. Uniaxial tensile testing was conducted with an Intron 5544 load frame with a 2-kN load cell, pneumatic sample grips, and a video extensometer on ~200 micron thick dogbone specimens stamped from thin sections microtomed from the longitudinal sides of the prisms at each time point (ASTM spec D638). Oxidation profile and trend line data for retrievals presented in Figures 1 and 2 come from an IRB-approved retrieval database, queried for all u03b3-barrier sterilized tibial components. In total, 216 retrievals were analyzed, with in vivo duration ranging from 0 to 190 months and an average duration of 54 months. Literature- based retrieval maximum oxidation and mechanical data [1] were shown for comparison in Figure 3.Results: The oxidation profile of the in vitro-aged GVF materials showed a sub-surface oxidation peak after 6 weeks (Figure 1). The oxidation profile of a tibial bearing retrieval implanted for 6.8 years is shown for comparison. KOI measured in the GVF materials increased exponentially with time (Figure 2) Oxidation rate data from retrieved u03b3-barrier knee retrievals is shown for comparison. To achieve clinically relevant oxidation in GVF-Low and GVF-High (KOI 1.0-1.5), the aging process presented in this study takes approximately 6 weeks (Figure 2). Remelted, Antioxidant, and Virgin are chemically stable for at least 6 weeks in vitro (Figure 1, 2). Increasing KOI negatively correlated with Ultimate Tensile Strength (UTS) (Figure 3).Discussion: In vitro oxidation of GVF materials yielded oxidation profiles similar to those observed in gamma-sterilized retrievals, as characterized by the subsurface oxidation peak and identity of chemical species. While the oxidation peaks appear at approximately the same depth, the breadth of the peak is greater in the artificially aged samples, likely owing to increased oxygen diffusivity in the high-pressure/high-temperature environment. In vivo aging can be mapped to an accelerated aging process by a conversion factor of ~1.2 years in vivo to 1 week in vitro. The effects of this oxidation on UTS and other tensile properties were analogous to those observed in retrieval studies (Figure 3). The relative chemical inertness of virgin, remelted, and antioxidant materials in the absence an initiator (e.g. stress, lipids, etc.) is consistent with a free-radical mediated oxidation mechanism but does not suggest an explanation for in vivo oxidation of remelted highly cross-linked polyethylene [3]. Antioxidant material appears stable to this aging method for 6 weeks.References: [1]JOA Vol. 22 No. 5 2007. [2]JBMR-B 106.1 (2018): 353-359. [3]JBJS-A. 2010;92:2409-18.Abstract Significance: In vivo oxidation is mimicked in oxidation profile and oxidation rate by an in vitro aging environment. This technique has promisein evaluation of materials against the free-radical oxidation pathway. Future work must be done to assess other (e.g. lipid-related) pathways.
Four indices of lipid peroxidation were studied in rat brain, lung, and plasma to determine if these would be useful markers of progressive oxidative damage. Conjugated dienes, thiobarbituric acid reactive substances, and water and lipid soluble fluorescent products were measured following IN vitro and in vivo O2 exposures. For in vitro studies, homogenized tissues were oxidized non-enzymatically in increasing amounts of O2. For in vivo studies, rats were exposed to normobaric or hyperbaric O2 for a range of times and pressures. In vitro, all 4 indices increased with PO2 of exposure: brain> lung> plasma. In vivo exposures resulted in lower levels than those achieved in vitro. Hyperbaric exposure produced higher levels than normobaric exposures, but fairly long duration and/or high P02 exposures were required for increases in tissues. On the other hand, plasma thiobarbituric acid reactive substances increased after only 6 h of normobaric 02 exposure and remained elevated. Brain lipid peroxidation was detected following normobaric 02, giving evidence of non-pulmonary oxidation. These results show that there is a relationship between severity of O2 exposure and level of lipid peroxidation, but suggest that other markers should also be investigated for earlier changes.