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Am J Respir Cell Mol Biol. 2003 Sep;29(3):331-43. Epub 2003 Apr 17.
Variability of antioxidant-related gene expression in the airway epithelium of cigarette smokers.

Hackett NR, Heguy A, Harvey BG, O'Connor TP, Luettich K, Flieder DB, Kaplan R, Crystal RG.

Department of Genetic Medicine, Weill Medical College of Cornell University, 515 East 71st Street, Suite 1000, New York, New York 10021. geneticmedicined.cornell.edu

Cigarette smoking is the major risk factor for developing chronic bronchitis, yet only 15-20% of smokers develop this disorder. Because oxidants are the major mechanism of smoking-induced airway damage, we hypothesized that smoking is associated with upregulation of various antioxidant-related genes in the airway epithelium, but the magnitude of the response shows high inter-individual variability. Microarray analysis was used to assess levels of expression of 44 antioxidant-related genes in four categories (catalase/superoxide dismutase family; glutathione metabolism; redox balance; and pentose phosphate cycle) in bronchoscopy-obtained airway epithelium of matched cohorts (13 current smokers, 9 nonsmokers), none of whom had lung disease. There was minimal variation in gene expression levels within the same individual (right versus left lung or over time), but significant upregulation of 16/44 antioxidant-related genes in smoker epithelium compared with nonsmokers. Subgroups of smokers were identified with clusters of expression levels of antioxidant-related genes. We propose that the antioxidant-related genes demonstrating the most variability in the level of expression in smokers may be useful genetic markers in epidemiologic studies assessing susceptibility to smoking-induced chronic bronchitis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12702543&dopt=Abstract [PubMed - in process]

Pediatr Pulmonol. 2001 Feb;31(2):126-32.
Predicted maximal oxygen uptake in normal Hong Kong Chinese schoolchildren and those with respiratory diseases.

Wong TW, Yu TS, Wang XR, Robinson P.

Department of Community and Family Medicine, Chinese University of Hong Kong, Hong Kong, China. twwonuhk.edu.hk

To assess the maximum oxygen uptake (V'O2 max) of Hong Kong Chinese children and to explore its association with respiratory illnesses, we conducted the Multistage Fitness Test (MFT), a 20-m shuttle run test, in 1,427 schoolchildren aged between 8-12 years. Information on respiratory symptoms in the previous year, cumulative respiratory illnesses, and habitual physical activities were collected. Spirometry was carried out to derive forced expiratory volume in 1 sec (FEV1). The V'O2max was 30.3 mL x kg( - 1) x min( - 1) for boys, and 28.6-mL x kg( - 1) x min( - 1) for girls; these values were low by Western standards. V'O2max was significantly reduced in children with asthma ( - 1.3 mL x kg( - 1) x min( - 1)) and bronchitis ( - 0.7.mL x kg( - 1) x min( - 1)) when adjusted for other covariates. A significant decrease in FEV1 was also observed in these children. The correlation between V'O2max and FEV1 was significant but weak. Habitual physical activity was an independent predictor of V'O2max, but not of FEV1. The low V'O2 max in Hong Kong children may be explained in part by ethnic differences and possibly a low level of physical activity.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11180688&dopt=Abstract

J Pharm Pharmacol. 2000 Nov;52(11):1411-6.
Protective effect of erdosteine against hypochlorous acid-induced acute lung injury and lipopolysaccharide-induced neutrophilic lung inflammation in mice.

Hayashi K, Hosoe H, Kaise T, Ohmori K.

Drug Development Research Laboratories, Pharmaceutical Research Institute, Kyowa Hakko Kogyo Co., Ltd, Shizuoka, Japan.

The effect of erdosteine, a mucoactive drug, on hypochlorous acid (HOCl)-induced lung injury, and the lipopolysaccharide (LPS)-induced increase in tumour necrosis factor-alpha (TNF-alpha) production and neutrophil recruitment into the airway, was investigated. Male BALB/c mice were orally administered erdosteine (3-100 mgkg(-1)), ambroxol hydrochloride (ambroxol) (3-30 mgkg(-1)), S-carboxymethyl-L-cysteine (S-CMC) (100-600 mgkg(-1)) or prednisolone (10 mgkg(-1)), 1 h before intratracheal injection of HOCl or LPS. In the HOCl-injected mice, erdosteine markedly suppressed increases in the ratios of lung wet weight to bodyweight and lung dry weight to bodyweight, whereas the other mucoactive drugs ambroxol and S-CMC had little effect. Erdosteine also inhibited the LPS-induced neutrophil influx, although it did not affect the increased level of TNF-alpha in the bronchoalveolar lavage fluid. The results suggest that attenuation of reactive oxygen species and neutrophil recruitment is involved in the clinical efficacy of erdosteine in the treatment of chronic bronchitis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11186250&dopt=Abstract

Rev Fac Cien Med Univ Nac Cordoba. 2000;57(1):95-107.
[Relationship between lung cancer and aflatoxin B1]

[Article in Spanish]

Georggiett OC, Muino JC, Montrull H, Brizuela N, Avalos S, Gomez RM.

Catedra de Cirugia II-UA Cirugia H. Misericordia Fac. Cs. Medicas U.N.C.

The relationship between aflatoxins and liver cancer is well established. In addition the inhalation exposure to carcinogen aflatoxin B1 (AFB 1) is considerable. Genotoxic chemical is known to react with DNA either directly or after metabolic activation to form adducts, a step thought to be relevant with respect to chemical carcinogenesis. The presence and the amount of specific DNA adducts provide a good indication of chemical exposure and genetic damage resulting the exposure to carcinogens and account for same of factors affecting individual susceptibility to cancer. Analysis of DNA adducts requires that the sensitivity of the methods to be sufficient high to allow detection of about 1 adduct/109 normal nucleotides. Most suitable method is based in physiochemical technique such as HPLC. Because circumstantial epidemiological evidence suggests that AFB1 inhalation may cause primary lung cancer. We investigate AFB1 by HPLC in three different tobacco sources, and in 39 patients with compatible lung cancer or chronic bronchitis. The patients were divided by clinical manifestations in lung cancer (n: 25) and chronic bronchitis (n: 14). Twenty-three of 25 patients presented epidermoid lung cancer within smoking habit, and 2 of 25 presented adenocarcinoma without smoking habit. In chronic bronchitis group 12 of 14 cases presented smoking habit. The control PBS liquid was negative to AFB1; the different tobacco sources, a) Virginia of Jujuy, b) Brasilero and c) black of Salta presented AFB1 positive determinations respectively. The bronchial tissues obtained by lung biopsies presented positive AFB1 in lung epidermoid cancer at 0.68 +/- 0.82 mg/L. The adenocarcinoma presented AFB1 negative determinations. In chronic bronchitis patients with smoking habit (n: 12) presented AFB1 positive with a level less than the epidermoid lung cancer group, 0.21 +/- 0.109 mg/L, p < .025.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11188861&dopt=Abstract

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