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Trace Minerals
Published in Luke R. Bucci, Nutrition Applied to Injury Rehabilitation and Sports Medicine, 2020
Cytochrome c oxidase is the terminal enzyme in oxidative phosphorylation, consuming oxygen and generating ATP, thus being vital for production of cellular energy.900 Ceruloplasmin is also an acute phase reactant that catalyzes oxidation of ferrous ions to ferric ions and, in so doing, possesses weak antioxidant properties.901
Muscle Pain and Aging
Published in Robert M. Bennett, The Clinical Neurobiology of Fibromyalgia and Myofascial Pain, 2020
The activity of various marker enzymes has also been measured in skeletal muscle from individuals of different ages to quantify the effect of aging on the metabolic capacity of the muscle. A decrease in the activity of cytochrome oxidase appears to be involved in the age-related increases in the production of mitochondria-derived oxidants (38). A functional consequence of oxidant damage is increased membrane rigidity, which can lead to a decline in receptor-mediated signaling.
Miscellaneous poisons
Published in Jason Payne-James, Richard Jones, Simpson's Forensic Medicine, 2019
Jason Payne-James, Richard Jones
Cyanide ions prevent cells from utilising oxygen; they inhibit the enzyme cytochrome c oxidase. High concentrations of cyanide lead to cardiac arrest within minutes of exposure. Exposure to lower levels of cyanide over a long period (e.g., after use of cassava roots as a primary food source, which is a relatively common occurrence in tropical Africa) results in increased blood cyanide levels, which can cause weakness and a variety of symptoms including permanent paralysis. Cigarette smoking also increases blood cyanide concentrations, although most of the time the increase is asymptomatic and blood concentrations are modest. In non-smokers, the average blood cyanide concentration is less than 0.01 micromol μ mol/L, rising fourfold after smoking. In chronic smokers, concentrations may be 10 times higher.
Evaluation of aqueous dimethyl trisulfide as an antidote to a highly lethal cyanide poisoning in a large swine model
Published in Clinical Toxicology, 2022
Tara B. Hendry-Hofer, Carter C. Severance, Subrata Bhadra, Patrick C. Ng, Kirsten Soules, Dennean S. Lippner, Diane M. Hildenberger, Melissa O. Rhoomes, Jessica N. Winborn, Brian A. Logue, Gary A. Rockwood, Vikhyat S. Bebarta
Cyanide is a readily available, highly lethal chemical agent with over 5 billion pounds produced annually worldwide [1]. Exposure can occur via ingestion, inhalation, or dermal absorption. Cyanide acts as a metabolic poison by binding cytochrome c oxidase and inhibiting cellular respiration. Lactic acidosis, hypotension, apnea, and cardiac arrest are hallmark symptoms of toxicity [2–4]. Intentional poisonings, such as the potassium cyanide mailings that occurred in Japan in 2019 [5], as well as the industrial accident that occurred in that same year resulting in the release of cyanide into Lake Michigan [6] demonstrate the ongoing risk of a mass cyanide exposure that could result in multiple casualties. While cyanide remains a high threat to civilian and military personnel, there currently are no FDA-approved antidotes that are capable of rapid administration by first responders at a scale adequate for a mass casualty incident.
Conjugated linoleic acid protects brain mitochondrial function in acrolein induced male rats
Published in Toxicology Mechanisms and Methods, 2021
Birsen Aydın, Cansu Güler Şahin, Vedat Şekeroğlu, Zülal Atlı Şekeroğlu
Mitochondrial dysfunction and ROS production play a role in the basis of many neurological and neurodegenerative diseases (Trushina and McMurray 2007; Migliore and Coppedè 2009; Kausar et al. 2018). It has been stated that neurodegenerative diseases are directly related to increases in oxidative stress, oxidized proteins and mitochondrial dysfunction (Naoi et al. 2005). Decreases in cytochrome c oxidase activity and ATP level and increases in free radicals have been found in Alzheimer's disease (Cardoso et al. 2004). A very strong relationship has also been found between Parkinson's disease and mitochondrial dysfunction (Morais and De Strooper 2010). We observed in our study AC induced oxidative stress and mitochondrial dysfunction in rat brain. AC decreased GSH, Mn-SOD and GPx levels, whereas it increased LP and PC formation. ICDH, α-CGDH, complex I and complex IV activities, and ATP levels were suppressed with the effect of AC. The results of the present study also clearly demonstrate that CLA exhibited protective activities against AC-induced toxicity in rat brain as evidenced by GSH, GPx, MnSOD, PC, LP, ICDH, α-CGDH, complex I, complex IV, and ATP levels. Therefore, CLA can play a beneficial role in reducing and improving oxidative stress and mitochondrial dysfunction in the brain in many neurological and neurodegenerative diseases.
Pro-apoptotic properties and mitochondrial functionality in platelet-like-particles generated from low Aspirin-incubated Meg-01 cells
Published in Platelets, 2021
Gala Freixer, Khaoula Zekri-Nechar, José J. Zamorano-León, Carlos Hugo-Martínez, Nora V Butta, Elena Monzón, María-José Recio, Manel Giner, Antonio López-Farré
It has been extensively demonstrated that NO binding to heme group of cytochrome C oxidase inhibiting its activity, which has been associated with apoptosis [54–56]. In our experiments, PLPs generated from ASA-incubated megakaryocytes showed higher NOS3 levels than those newly PLPs formed from Meg-01 cells without ASA. Moreover, the presence of the L-arginine antagonist, L-NAME, in A23187-stimulated PLPs generated from ASA-incubated Meg-01 cells, significantly reduced caspase-3 activity. Taken together, these results suggested that NO may at least partially be involved in the higher apoptotic sensitivity of PLPs generated from ASA-incubated Meg-01 cells. Future studies are warranted to study more to study more depth and detail the possible involvement of the NO-dependent pathway in the apoptotic ability of the newly PLPs generated from ASA-incubated megakaryocytes.