Explore chapters and articles related to this topic
Deaths Due to Asphyxiant Gases
Published in Sudhir K. Gupta, Forensic Pathology of Asphyxial Deaths, 2022
Chronic symptoms are said to be occurred probably as a result of direct action on cytochrome oxidase and perhaps other oxidative systems and an effective reduction in oxygen availability.9 After resolution of symptoms of acute poisoning or long-term slow exposure to toxic level, leads to neuropsychiatric sequelae which are seen within 3–240 days (frequently within first month). Delayed impairment may begin subtly with changes in behavior or cognitive ability, personality and be more apparent with severe dementia, psychosis, Parkinsonism or gait disturbances.12
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
Myoclonic epilepsy and ragged red fiber (MERRF) disease
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
Pathologic examination reveals, in addition to the characteristic myopathy with ragged red fibers (Figure 51.8), widespread neurodegeneration in the dentatorubral and pallidal systems, cerebral cortex, cerebellum, pons, and spinal cord [20, 36–39]. Staining of the muscle for cytochrome oxidase activity may show profound deficiency [10].
The vitamin B12 analog cobinamide ameliorates azide toxicity in cells, Drosophila melanogaster, and mice
Published in Clinical Toxicology, 2023
John Tat, Stephen C. Chang, Cole D. Link, Suelen Razo-Lopez, Michael J. Ingerto, Behdod Katebian, Adriano Chan, Hema Kalyanaraman, Renate B. Pilz, Gerry R. Boss
Symptoms occur within minutes of azide exposure, ranging from dizziness, nausea, vomiting, and restlessness at low doses, to seizures, hypotension, metabolic acidosis, coma, and respiratory failure at high doses. Like carbon monoxide, cyanide, hydrogen sulfide, and methyl mercaptan, azide inhibits cytochrome c oxidase in complex IV of the mitochondrial electron transport chain, reducing adenosine triphosphate (ATP) production [16–19]. This results in a compensatory increase in glycolysis with attendant metabolic acidosis. Inhibiting complex IV also increases mitochondrial electron leakage, thereby increasing superoxide anion (O2·-) generation. Consistent with this mechanism, brain, lung, and heart tissues taken from azide-poisoned rats showed significant increases in malondialdehyde concentrations, a marker of lipid peroxidation [20]. Through a poorly understood mechanism, azide appears to be converted to nitric oxide (NO) [21–23], which likely underlies the profound hypotension that can occur in azide-poisoned victims.
Cytochrome c injection induced embryo loss
Published in Drug and Chemical Toxicology, 2021
Tonghui Xu, Qiuhong Yang, Banqin Wang, Wenfu Wang, Jingxin Li, Yuyan Ma, Xiaolin Gao
Cytochrome c plays an important role in electron transfer between cytochrome c oxidase and reductase (Margalit and Schejter 1973). Normally, cytochrome c resides between the inner and outer mitochondrial membrane. At present, cytochrome c has been used as first-aid in the clinic for organs which are lacking oxygen. However, intriguingly based on more recent evidence, injection of cytochrome C has been shown to result in selective suicide of dendritic cells (DCs) (Lin et al.2008) and failure of self-tolerance (Qiu et al.2009). It is widely believed that decidual antigen-presenting cells (APCs), especially DCs, are critical for fetomaternal tolerance (Blois et al.2004, Blois et al.2007). In vivo DCs depletion affects implantation and early placental development in mice (Krey et al.2008). Cross talk between DCs and natural killer cells at the feto-maternal interface is also believed to be pivotal for pregnancy (Laskarin et al.2007). As a failure of self-tolerance result, recurrent spontaneous abortion (RSA) occurs in pregnant women. This type of abortion has been related to a shift in the T helper 2 (Th2) cell response of normal pregnancy to a Th1 response, where cytokines such as interferon-γ (INF-γ) and tumor necrosis factor-α (TNF‐α) can destroy trophoblasts (Raghupathy 1997). Therefore, we hypothesized that transient ablation of decidual DCs by cytochrome c injection may result in failed fetomaternal tolerance induction and Th1/Th2 imbalances, triggering embryo loss and abortion.
Can isosorbide dinitrate oral spray serve as an immediate bridging therapy for a mass cyanide poisoning?
Published in Clinical Toxicology, 2021
Ophir Lavon, Gary A. Rockwood, Arik Eisenkraft
The potential mechanism of antidotal action of ISDN is not totally clear. It is evident that ISDN is not a methemoglobin former; its administration does not result in any significant rise in methemoglobin levels, either in swine, rabbits or humans [2,6–8,14]. ISDN in the body is rapidly reduced to nitric oxide (NO) through a NO synthase-independent pathway [15]. It was previously shown that NO carries antidotal properties against cyanide, specifically in the mitochondrial electron transport chain. NO competes with cyanide for binding to cytochrome C oxidase [15,16]. Both direct or non-direct (through sodium nitrite) NO administration mitigated the inhibition of cytochrome C oxidase by cyanide [16–18]. In addition, NO is neuroprotective mainly by reducing hyperactivity of NMDA receptors in the brain [7,19–21]. This may prevent or counteract the effects of cyanide on the central nervous system, clinically expressed as coma, seizures and respiratory depression.