Detection of catalase in rat heart mitochondria.

Radí, Rafael; Turrens, Julio F.; Chang, Leslie; Bush, Ken; Crapo, James D.; Freeman, Bruce Α.

doi:10.1016/s0021-9258(18)54740-2

Cited by 468 publications

(50 citation statements)

References 22 publications

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“…Although the main physiological role of Cta1 seems to be the removal of hydrogen peroxide produced by fatty acid β‐oxidation, this isoform is also present in yeast mitochondria [Petrova et al, ]. This result confirmed previous studies in mammals, where catalase activity in rat heart mitochondria was identified as a key antioxidant defense mechanism for myocardial tissue [Radi et al, ]. By scavenging hydrogen peroxide in mitochondria, Cta1 plays a crucial role in the oxidative stress response.…”

supporting

confidence: 87%

Oxidative Stress and Amyloid Toxicity: Insights From Yeast

França

Lima

Eleuthério

2017

J of Cellular Biochemistry

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Alzheimer's disease is the most common neurodegenerative disorder. One of the factors that promotes neurodegeneration is the accumulation of senile plaques formed by Aβ peptide. In this paper, it was analyzed that if oxidative stress is cause or consequence of amyloid cascade and the role of antioxidant defense system in this process, using S. cerevisiae (with a multicopy plasmid containing the Aβ1-42 sequence) as experimental model. Cells grown on glycerol were more tolerant than when grown on glucose, strengthening the role of the antioxidant defense system against Aβ accumulation. Antioxidant defense deficiency did not change the pattern of amyloid aggregation. On the other hand, the presence of Aβ increased the level of intracellular oxidation and induced the activity of catalase, superoxide dismutase, and aconitase. Peroxissomal catalase deficient cells (Δcta1), were more sensitive to Aβ toxicity than the wild type strain, while mitochondrial superoxide dismutase (Sod2) deficient cells displayed the highest frequency of petites. Besides, Aβ alters the oxygen consumption and the activity of complex III and IV. Taken together, our results point out that the Aβ toxicity mechanism involves an oxidative stress induction by increasing ROS production into the mitochondria, where Cta1 and Sod2 play a crucial role in the regulation of the redox balance. J. Cell. Biochem. 118: 1442-1452, 2017. © 2016 Wiley Periodicals, Inc.

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supporting

confidence: 87%

Oxidative Stress and Amyloid Toxicity: Insights From Yeast

França

Lima

Eleuthério

2017

J of Cellular Biochemistry

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“…Mitochondrial localization of catalase in rat cardiomyocytes has been reported only in one study (Radi et al 1991). In contrast, it has long been known that cata-lase is localized in peroxisomes of cardiomyocytes Fahimi 1974,1975;Hicks and Fahimi 1977;Fahimi et al 1979;Yokoda and Asayama 1992).…”

Section: Discussionmentioning

confidence: 96%

“…It has been known that catalase is localized in peroxisomes of cardiomyocytes Fahimi 1974,1975;Hicks and Fahimi 1977;Fahimi et al 1979;Yokoda and Asayama 1992). Interestingly, a study by Radi et al (1991) has shown that catalase is localized in mitochondrial matrix of rat cardiomyocytes by biochemical and immunocytochemical methods. However, there were no other studies to support this observation.…”

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confidence: 98%

Cellular and Subcellular Localization of Catalase in the Heart of Transgenic Mice

Zhou

Kang

2000

J Histochem Cytochem.

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Previous studies have described a cardiac-specific, catalase-overexpressing transgenic mouse model that was used to study myocardial oxidative injury. This study was undertaken to demonstrate cellular and subcellular localization of catalase in the hearts of transgenic mice. By the light microscopic immunoperoxidase method, we found that the overexpressed catalase was exclusively localized in cardiomyocytes. The ratios of immunoreactive cardiomyocytes in the heart were quite different among three transgenic lines examined but agreed with the elevated levels of catalase activity. In the cardiac blood vessels, positive cells were found in the walls of pulmonary veins and the vena cava, which consist of cardiomyocytes, but not in the pulmonary arteries, aorta, or cardiac valves. The electron microscopic immunogold method revealed that the elevated catalase was in sarcoplasm, nucleus, and peroxisomes, but not in mitochondria. In contrast to these distributions, catalase in the non-transgenic cardiomyocytes was in peroxisomes only. In addition, the number and size of peroxisomes in the transgenic cardiomyocytes were markedly increased, but no other ultrastructural changes were observed in comparison with those of non-transgenic mice. These results demonstrated that the elevated catalase in transgenic mouse heart is localized in cardiomyocytes and is distributed to peroxisomal and extraperoxisomal, but not mitochondrial, compartments.

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“…CAT is an antioxidant enzyme present in almost all aerobic organisms and is considered the detoxification-completing step initiated by SOD. It is primarily located in the peroxisomes and absent in the mitochondria of almost all tissues (except in the heart) (21,140). The main function of CAT is to catalyze the degradation/reduction of H 2 O 2 to H 2 O and molecular oxygen.…”

Section: Sod Cat and Gpxmentioning

confidence: 99%

Oxidative stress pathways in pancreatic β-cells and insulin-sensitive cells and tissues: importance to cell metabolism, function, and dysfunction

Newsholme

Keane

Carlessi

et al. 2019

American Journal of Physiology-Cell Physiology

161

112

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It is now accepted that nutrient abundance in the blood, especially glucose, leads to the generation of reactive oxygen species (ROS), ultimately leading to increased oxidative stress in a variety of tissues. In the absence of an appropriate compensatory response from antioxidant mechanisms, the cell, or indeed the tissue, becomes overwhelmed by oxidative stress, leading to the activation of intracellular stress-associated pathways. Activation of the same or similar pathways also appears to play a role in mediating insulin resistance, impaired insulin secretion, and late diabetic complications. The ability of antioxidants to protect against the oxidative stress induced by hyperglycemia and elevated free fatty acid (FFA) levels in vitro suggests a causative role of oxidative stress in mediating the latter clinical conditions. In this review, we describe common biochemical processes associated with oxidative stress driven by hyperglycemia and/or elevated FFA and the resulting clinical outcomes: β-cell dysfunction and peripheral tissue insulin resistance.

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Detection of catalase in rat heart mitochondria.

Cited by 468 publications

References 22 publications

Oxidative Stress and Amyloid Toxicity: Insights From Yeast

Oxidative Stress and Amyloid Toxicity: Insights From Yeast

Cellular and Subcellular Localization of Catalase in the Heart of Transgenic Mice

Oxidative stress pathways in pancreatic β-cells and insulin-sensitive cells and tissues: importance to cell metabolism, function, and dysfunction

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