Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04040 (Catalase)
 3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxidative stress is a hallmark of asthma, and increased levels of oxidants are considered markers of the inflammatory process. Most studies to date addressing the role of oxidants in the etiology of asthma were based on the therapeutic administration of low m.w. antioxidants or antioxidant mimetic compounds. To directly address the function of endogenous hydrogen peroxide in the pathophysiology of allergic airway disease, we comparatively evaluated mice systemically overexpressing catalase, a major antioxidant enzyme that detoxifies hydrogen peroxide, and C57BL/6 strain matched controls in the OVA model of allergic airways disease. Catalase transgenic mice had 8-fold increases in catalase activity in lung tissue, and had lowered DCF oxidation in tracheal epithelial cells, compared with C57BL/6 controls. Despite these differences, both strains showed similar increases in OVA-specific IgE, IgG1, and IgG2a levels, comparable airway and tissue inflammation, and identical increases in procollagen 1 mRNA expression, following sensitization and challenge with OVA. Unexpectedly, mRNA expression of MUC5AC and CLCA3 genes were enhanced in catalase transgenic mice, compared with C57BL/6 mice subjected to Ag. Furthermore, when compared with control mice, catalase overexpression increased airway hyperresponsiveness to methacholine both in naive mice as well as in response to Ag. In contrast to the prevailing notion that hydrogen peroxide is positively associated with the etiology of allergic airways disease, the current findings suggest that endogenous hydrogen peroxide serves a role in suppressing both mucus production and airway hyperresponsiveness.
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PMID:Catalase overexpression fails to attenuate allergic airways disease in the mouse. 1733 80

inhalation of benzene vapours promote various and dangerous health problems. Fuel station workers are most susceptible to benzene inhalation toxicity. Samples were collected twice, at beginning of the study and 6 months later from 40 fuel station workers from different egyptian governorates and 10 control healthy volunteers. Fuel station workers were sub divided into four groups according to years working in the station. All of them are exposed to benzene vapours and exhausts during their duties, their work shifts were 8 hrs./day. Results indicated that; benzene vapours exposure induced significant increasing in serum Lead and Cadmium and Myeloperoxidase (MPO) enzyme activity levels. This goes with marked immunologic changes presented by decreases in immunoglobulins; IgA and IgG, along with increases in levels of IgM and IgE. Also, Malondialdehyde (MDA) levels were significantly increased. Meanwhile, reduction in some other biochemical parameters including; Copper, Zinc and Iron micronutrients, as well as; Superoxide Dismutase (SOD), Catalase (CAT) enzyme levels and Glutathione (GSH) content. Hence, the study inferred that prolonged benzene inhalation can lead to biochemical and immune disorders, probably through potentiating oxidative stress and inflammation pathways.
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PMID:Biochemical study on occupational inhalation of benzene vapours in petrol station. 3100 48