Enzyme Catalytic Activities in Chronic Obstructive Pulmonary Disease

Čepelak, Ivana; Dodig, Slavica; Romić, Dominik; Ruljančić, Nedjeljka; Popović‐Grle, Sanja; Malić, Ana

doi:10.1016/j.arcmed.2006.01.004

Cited by 20 publications

(19 citation statements)

References 38 publications

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“…There is no evidence to suggest that either the system Nm amino acid transporter or glutaminase activity are adversely affected in this patient group. However, it is plausible that intramuscular alanine aminotransferase activity is reduced in COPD since this has been shown in the sera of COPD as compared to healthy controls (Cepelak et al, 2006). Though unlikely, it is possible therefore that glutamine ingestion did not result in TCAi pool expansion as previously observed in controls (Bruce et al, 2001) since we were unable to experimentally confirm this.…”

contrasting

confidence: 48%

No effect of glutamine ingestion on indices of oxidative metabolism in stable COPD

Marwood

Jack

Patel

et al. 2011

Respiratory Physiology & Neurobiology

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contrasting

confidence: 48%

No effect of glutamine ingestion on indices of oxidative metabolism in stable COPD

Marwood

Jack

Patel

et al. 2011

Respiratory Physiology & Neurobiology

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“…The significantly elevated LDH activity (Table I) seen in COPD was probably associated with chronic hypoxia and thus a higher supply of lactate posing as this enzyme's substrate, as suggested earlier (24). In other words, this rise in LDH activity might be at-tributed to the facilitated lactate oxidation to pyruvate, which could be subsequently used in the tricarbon acid cycle for energy production.…”

Section: Gst and Ldh Activity And Aat Concentrationmentioning

confidence: 64%

GSTP1, GSTM1 and GSTT1 genetic polymorphisms and total serum GST concentration in stable male COPD

Žuntar¹,

Petlevski²,

Dodig³

et al. 2014

Acta Pharmaceutica

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Chronic obstructive pulmonary disease (COPD) is a common preventable and treatable disease characterized by persistent airflow limitation, which is usually progressive and associated with an enhanced chronic inflammatory response to noxious particles or gases in the airways and the lung. COPD is a leading cause of morbidity and mortality worldwide and is more prevalent in smokers, in those over 60 years of age and in men more than in women (1).Cigarette smoking is the best-studied COPD risk factor (2), but not all people with the same smoking history will develop COPD, due to differences in genetic predisposition to the disease. The best documented genetic risk factor is deficiency of alpha-1- The aim of this study was to test the hypothesis that glutathione-S-transferase (GST) genotypes were associated with COPD. GSTP1, GSTM1 and GSTT1 genotypes were determined by DNA methods and GST activity spectrophotometrically in older male Caucasian Croats (non--smokers, ex-smokers, and smokers) with stable COPD (n = 30) and sex/age matched controls (n = 60). The distribution of GSTP1 genotypes and alleles in controls vs. COPD showed a statistical difference (p < 0.05). The odds ratio of CC/CT+TT (wild type GSTP1 exon 6 vs. joint heterozygous and mutant homozygous GSTP1 exon 6) was 10.000 and statistically different (p = 0.002). In this study, the GSTP1 mutant genotype of exon 5 (GG), as well as GSTP1 mutant and heterozygous genotypes of exon 6 (TT and CT), were suggested to be genetic contributors to COPD susceptibility. Null GSTM1, null GSTT1 and joint GSTM1/GSTT1 null genotypes were not disease associated. Serum GST was not associated with GST genotypes and COPD or smoking history in our study subjects. Conclusions drawn from the study should be further supported and clarified by studies with larger sample sizes.

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“…The peripheral blood and the urine could monitor the systemic effects of COPD such as inflammation, oxidative stress, nutritional abnormalities, elastin or collagen degradation etc [4,6]. Bronchial biopsies and bronchoalveolar lavage (BAL) provide valuable information of inflammatory cells and mediators, but are invasive, so their repeated measurements have to be very limited.…”

Section: Introductionmentioning

confidence: 99%

“…Oxidative stress (1) of cigarette smoke in "susceptible" smokers activates adaptive immunity (2), predisposing dendritic cells (3) to clonal expansion of CD4+ and especially of cytotoxic CD8+ cells (4), and inducing epithelial cell death by perforin (5). Activated macrophages release proteases (6) or neutrophil chemoatractants, together with the release of oxidants (7) resulting in subsequent parenchymal lung damage (8). concurrent therapies, and how they relate to other disease measurements, such as FEV1 decline, exacerbation frequency, and mortality [4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

“…The latest definition of COPD according to ATS/ERS Task Force is that COPD is a preventable and treatable disease state characterised by an abnormal inflammatory response of the lungs to noxious particles and gases, caused primarily by cigarette smoking [2]. Although COPD affects the lungs, it also produces significant systemic consequences such as systemic inflammation, oxidative stress, activation of inflammatory cells (neutrophils and lymphocytes), nutritional abnormalities and weight loss, abnormal amino acid metabolism, skeletal muscle dysfunction, muscle mass wasting, osteoskeletal effects, cardiovascular and nervous system effects [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

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Biomarkers in COPD

Tzortzaki¹,

Lambiri²,

Vlachaki³

et al. 2007

CMC

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Chronic Obstructive Pulmonary Disease is characterized by an abnormal inflammatory response of the lungs to noxious particles and gases, caused primarily by cigarette smoking. Although COPD affects the lung, it also produces significant systemic consequences. Inflammation, proteases-antiproteases imbalance, oxidative stress, tissue damage and tissue repair, apoptosis and several genes seem to be involved in the pathogenesis of the disease. The cellular and molecular events underlying COPD pathogenesis are driven by multifunctional molecules including enzymes, cytokines, chemokines, growth factors, lipid mediators and their respective receptors. A large number of biomarkers evaluated in COPD, showed a high degree of redundancy. Nevertheless, current understanding of the pathobiology of COPD suggests a number of biomarkers as potential candidates. The development of relevant markers of lung damage, pulmonary inflammation, and systemic disease will be essential to our further understanding of the natural history of COPD and the discovery of new, effective treatments for its progression. This review summarizes recent findings, on potential pulmonary biomarkers in the induced sputum, the exhaled air condensate, the peripheral blood, the urine, the bronchoalveolar lavage fluid, and in selective cases, in bronchial biopsies.

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Enzyme Catalytic Activities in Chronic Obstructive Pulmonary Disease

Cited by 20 publications

References 38 publications

No effect of glutamine ingestion on indices of oxidative metabolism in stable COPD

No effect of glutamine ingestion on indices of oxidative metabolism in stable COPD

GSTP1, GSTM1 and GSTT1 genetic polymorphisms and total serum GST concentration in stable male COPD

Biomarkers in COPD

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