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Reactive Oxygen Metabolites and Iron in Toxic Acute Renal Failure
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Karl A. Nath, Norishi Ueda, Patrick D. Walker, Sudhir V. Shah
We recently examined the effect of enzymatically generated hydrogen peroxide on LLC-PK1 cells, a renal tubular epithelial cell line.50 Exposure of LLC-PK1 cells to glucose and glucose oxidase (which generates hydrogen peroxide) resulted in cytotoxicity (as measured by trypan blue exclusion) which was dose dependent and increased linearly over time. Catalase (which decomposes hydrogen peroxide) completely prevented the cytotoxicity, confirming that the toxicity was due to hydrogen peroxide production. In order to assess whether the hydrogen peroxide toxicity was a direct effect or mediated by other toxic oxygen metabolites, several scavengers of ROMs and iron chelators were used. Superoxide dismutase (a scavenger of superoxide) had no effect. In contrast, deferoxamine, an iron chelator, as well as two other metal chelators (dihydroxybenzoic acid and 1,10-phenanthroline) provided marked protection. Taken together, these data indicate that in addition to direct cytotoxicity of hydrogen peroxide, iron plays a critical role in hydrogen peroxide-mediated cytotoxicity to LLC-PK1 cells.
The Use of Brain Slices in the Study of Free Radical Actions
Published in Avital Schurr, Benjamin M. Rigor, BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
Numerous protective systems are normally present to minimize the availability of these reactive compounds. Superoxide dismutase catalyzes the conversion of superoxide to hydrogen peroxide. Various forms of the enzyme are localized within mitochondria, in the cytoplasm as well as in the extracellular space.11,12 Catalase and glutathione peroxidase break down hydrogen peroxide. Catalase, found in peroxisomes in peripheral tissue, is limited in the brain. Glutathione peroxidase, working in concert with glutathione reductase, is distributed throughout the brain and is the primary mechanism for removal of hydrogen peroxide.3,4 In addition to these enzyme systems, tissue contains a number of antioxidant compounds such as ascorbic acid, uric acid, glutathione, and vitamin E that scavenge free radicals and limit their toxicity.3
Bronchopulmonary Dysplasia
Published in Lourdes R. Laraya-Cuasay, Walter T. Hughes, Interstitial Lung Diseases in Children, 2019
R. Boynton Bruce, T. Allen Merritt
Oxygen toxicity appears to be mediated through the action of oxidizing radicals released by phagocytes such as neutrophils and pulmonary alveolar macrophages. When phagocytes are exposed to certain stimuli they reduce molecular oxygen (O2) to superoxide anion (O−2) in a NADPH-dependent reaction catalyzed by the plasma membrane-bound enzyme, pyridine nucleotide oxidase.2 Superoxide has been implicated in the initiation of lipid peroxidation, the oxidation of thiol groups, and the oxidation of purines and pyrimidines.3 However, most superoxide reacts rapidly with itself to produce molecular oxygen and hydrogen peroxide in a reaction catalyzed by superoxide dismutase. Superoxide is not only cytotoxic itself, but also can react with hydrogen peroxide to produce hydroxyl radicals (OH·).2 Thus, superoxide dismutase is thought to be a major protective mechanism against oxygen toxicity. The survival time of rats exposed to 100% oxygen increased from 70 to 118 hr when liposomes containing superoxide dismutase and catalase were injected intravenously before and during exposure.4
D-ribose-L-cysteine exhibits neuroprotective activity through inhibition of oxido-behavioral dysfunctions and modulated activities of neurotransmitters in the cerebellum of Juvenile mice exposed to ethanol
Published in Drug and Chemical Toxicology, 2023
Damilare Adedayo Adekomi, Olamide Janet Olajide, Omowumi Oyeronke Adewale, Akeem Ayodeji Okesina, John Olabode Fatoki, Benedict Abiola Falana, Temidayo Daniel Adeniyi, Adebiyi Aderinola Adegoke, Waliu Adetunji Ojo, Sheriffdeen Oluwabusayo Alabi
Superoxide dismutase is an antioxidant enzyme that catalyzes the conversion of anion superoxide to oxygen and hydrogen peroxide. The reduction of SOD activity in the brain induced by ethanol in this study may be due to the generation of excessive anion, which causes this enzyme to become inactivated. The administration of DRLC provided a better protective effect against ethanol-induced cerebellar damage and this may be due to the high amount of cysteine present in DRLC. Increased SOD and GPx activities observed in this study may correlate to the fact that the high antioxidant activities in DRLC induced endogenous antioxidants thus reduced the free radical activity (Emokpae et al. 2020a). In addition, an increase in the antioxidant activity can be described as an adaptive response to excessive ROS (Haorah et al. 2008). DRLC was sufficient to subdue the ROS generated by the ethanol exposure.
Synergistic hepatoprotective effects of ω-3 and ω-6 fatty acids from Indian flax and sesame seed oils against CCl4-induced oxidative stress-mediated liver damage in rats
Published in Drug and Chemical Toxicology, 2022
Sunil Chikkalakshmipura Gurumallu, Tareq Aqeel, Ashwini Bhaskar, Kannan Chandramohan, Rajesha Javaraiah
Superoxide dismutase is an effective antioxidant enzyme. Administration of CCl4 causes increased production of free radicals, which reduces SOD activity. As shown in Table 4, SOD levels in both the liver and kidneys were significantly reduced (p < 0.001) in CCl4 treated rats. Oral gavage of FSO and SSO individually treated groups exhibited a significant rise in SOD activity in a dose-dependent manner, whereas, the combined treatment of FSO and SSO at 43 + 292 and 86 + 584 mg/kg b.w showed the highest increase in the activity that is almost equal to silymarin treated and control groups in liver and kidney homogenates in a dose-dependent manner. Pretreatment with FSO and SSO alone (p < 0.01), and also in their combined form markedly elevated the activities of SOD in the liver (p < 0.001). An appreciable increase was observed in the activities of SOD of kidney homogenates of FSO (p < 0.05) and SSO alone treated groups also apart from the group of combined treatment (p < 0.01). Silymarin showed significant increase in SOD activity (p < 0.001) at 25 mg/kg b.w.
Continuous positive airway pressure affects mitochondrial function and exhaled PGC1-α levels in obstructive sleep apnea
Published in Experimental Lung Research, 2021
Ching-Chi Lin, Wei-Ji Chen, Yi-Kun Sun, Chung-Hsin Chiu, Mei-Wei Lin, I-Shiang Tzeng
The impact of intermittent hypoxia on systemic oxidative stress, inflammation, and the correlation between systemic inflammation or oxidative stress and the severity of OSA remain controversial. Subjects with OSA show a positive correlation between plasma thiobarbituric acid reactive substances (markers of lipid peroxidation) and C-reactive protein.21 Subjects with OSA and high AHI have a higher oxidative status compared to subjects with OSA and low AHI.21 In contrast, increased blood levels of superoxide dismutase (an anti-oxidant) were observed. However, the blood level of malondialdehyde (blood marker of oxidative stress) did not change significantly and urinary isoprostanes in subjects with severe to moderate OSA decreased after the termination of CPAP for 2 weeks.22,23 In this study, we found no differences in the blood ratio of Mt/N DNA and plasma protein concentration of PGC1-α between subjects with OSA and controls before CPAP treatment. The blood ratio of Mt/N DNA and plasma protein levels of PGC1-α in subjects with OSA did not differ before and after CPAP. There is no evidence to show that OSA increases systemic mitochondrial dysfunction and CPAP treatment can improve systemic mitochondrial dysfunction. However, we consider that it is still necessary to conduct a large-scale randomized controlled trial to evaluate whether OSA increases systemic mitochondrial dysfunction or not.