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Query: UNIPROT:P04040 (
Catalase
)
3,577
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The
nicotinamide adenine dinucleotide phosphate oxidase
complex (Nox) is a major source of non-mitochondrial reactive oxygen species in cells. Nox contains both membrane (Cytb(558)) and cytosolic (p40(phox), p47(phox), p67(phox) and Rac) components. Nox has been submitted to a combination of oxygen free radicals produced by irradiation and to hydrogen peroxide. Irradiation of a single component with high doses led to partial inactivation; however, the irradiation of the whole system during its assembly phase with lower doses (2-10 Gy) led either to activation (2.7 Gy) or to strong inactivation if irradiation took place during the first minute of the assembly. Incubation of the membrane fractions or of p67(phox) with H(2)O(2) led to fast inactivation.
Catalase
protected weakly p67(phox) from H(2)O(2). Conversely, incubation of the membrane fractions with catalase led to over-activation of the system.
...
PMID:Modulation of the activity of the NADPH oxidase system by reactive oxygen species: influence of catalase. 2118 38
Chronic granulomatous disease (CGD) is a primary immunodeficiency caused by defects of
nicotinamide adenine dinucleotide phosphate oxidase
.
Catalase
-positive bacteria and fungi are phagocytosed, but persist within phagocytes, resulting in granulomatous inflammation. Although allogeneic hematopoietic stem cell transplantation (HSCT) is a curative treatment for CGD, HSCT sometimes leads to fatal outcomes related to the exacerbation of persistent infectious or post-infectious inflammatory diseases, particularly in adolescent and young adult patients with a history of recurrent infections and/or multiple granulomas in organs. Here, we present the case of a young adult with X-linked CGD in whom multiple lesions were found in lungs and lymph nodes on both computed tomography and positron emission tomography (PET) scans before allogeneic HSCT, but all the lesions disappeared only on PET scan 5 months after HSCT. Monitoring the activity of multiple pre-existing lesions with PET scan may be beneficial to adolescent and young adult CGD-patients undergoing allogeneic HSCT.
...
PMID:Dramatic Improvement in the Multifocal Positron Emission Tomography Findings of a Young Adult with Chronic Granulomatous Disease Following Allogeneic Hematopoietic Stem Cell Transplantation. 2536 70
Obesity is regarded as an abnormal expansion and excessive accumulation of fat mass in white adipose tissue. The involvement of oxidative stress in the development of obesity is still unclear. Although mainly present in peroxisomes, catalase scavenges intracellular H
2
O
2
at toxic levels. Therefore, we used catalase-knockout (CKO) mice to elucidate the involvement of excessive H
2
O
2
in the development of obesity. CKO mice with C57BL/6J background gained more weight with higher body fat mass with age than age-matched wild-type (WT) mice fed with either chow or high-fat diets. This phenomenon was attenuated by concomitant treatment with the antioxidants, melatonin or N-acetyl cysteine. Moreover, CKO mouse embryonic fibroblasts (MEFs) appeared to differentiate to adipocytes more easily than WT MEFs, showing increased H
2
O
2
concentrations. Using 3T3-L1-derived adipocytes transfected with catalase-small interfering RNA, we confirmed that a more prominent lipogenesis occurred in catalase-deficient cells than in WT cells.
Catalase
-deficient adipocytes presented increased
nicotinamide adenine dinucleotide phosphate oxidase
4 (NOX4) expression but decreased adenosine monophosphate-activated protein kinase (AMPK) expression. Treatment with a NOX4 inhibitor or AMPK activator rescued the propensity for obesity of CKO mice. These findings suggest that excessive H
2
O
2
and related oxidative stress increase body fat mass via both adipogenesis and lipogenesis. Manipulating NOX4 and AMPK in white adipocytes may be a therapeutic tool against obesity augmented by oxidative stress.
...
PMID:Oxidative stress resulting from the removal of endogenous catalase induces obesity by promoting hyperplasia and hypertrophy of white adipocytes. 3308 Apr 38
