Oxidative Metabolism of Alveolar Macrophages from Young Asymptomatic Cigarette Smokers

Hoidal, John R.; Fox, Richard B.; LeMarbre, P.A.; Takiff, Howard; Repine, John E.

doi:10.1378/chest.77.2_supplement.270

Cited by 35 publications

(37 citation statements)

References 10 publications

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“…This damage can lead to malignant transformation of cells [26]. Lung cancer is the result of exposure to carcinogens such as oxidants contained in cigarette smoke [11,12]. Elevated LPO was proven in the lung malignant cells in present study, as a consequence of GSH depletion.…”

Section: Discussionsupporting

confidence: 49%

“…Since free radical stress has been implicated in malignancy [11,12], clinical trials of antioxidants are required to establish the efficacy of antioxidant therapy in the management of cancer. Therefore, the present study was designed based on the fact that NAC is a glutathione precursor and the hypothesis that combined factors, instead of a single agent, may be more beneficial against malignancy.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

N-Acetyl Cysteine in Combination with Vitamin C Enhances the Antioxidant Status of a Lung Carcinoma Cell Line in Vitro.

Vanisree

Ramamurthy

Shyamaladevi

1999

J. Clin. Biochem. Nutr.

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Section: Discussionsupporting

confidence: 49%

Section: Discussionmentioning

confidence: 99%

N-Acetyl Cysteine in Combination with Vitamin C Enhances the Antioxidant Status of a Lung Carcinoma Cell Line in Vitro.

Vanisree

Ramamurthy

Shyamaladevi

1999

J. Clin. Biochem. Nutr.

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“…For DNA binding studie used RAM. These cells are targ rette smoke damage (19)(20)(21)(22)(23)(24)(25)(26)(27) ai isolated as a homogeneous cell (28) from the lavage of rat lung modified the alkaline elution Kohn et al (14) so that it retains only double-stranded RAM on polycarbonate filters. method, we are able to isolate intact cells that have been expo and show that the tar radical l DNA in these cells.…”

Section: Discussionmentioning

confidence: 99%

Aqueous extracts of cigarette tar containing the tar free radical cause DNA nicks in mammalian cells.

Stone

Bermúdez

Pryor

1994

Environ Health Perspect

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The ability of aqueous extracts of cigarette tar to nick DNA was investigated using viable mammalian cells. Tar extracts contain a radical with a stable electron spin resonance (ESR) signal at g = 2.0036 characteristic of a semiquinone. The association of the tar component that carries the ESR signal with DNA was demonstrated using viable rat alveolar macrophages. The formation of single-strand DNA breaks caused by cigarette tar extracts in viable rat thymocytes follows saturation kinetics, indicating a tar component associates with DNA and then nicks it. These studies support our hypothesis that tar components that contain the cigarette tar radical can enter cells, associate with, and then nick DNA. -Environ Health Perspect 102(Suppl 10): 173-178 (1994)

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“…ROS can promote muscle proteolysis, inhibit muscle-specific protein expression, and increase muscle cell apoptosis (Barreiro et al 2005). Cigarette smoke is an extremely concentrated source of ROS and reactive nitrogen species, and the inflammatory response to smoke potentially augments oxidative stress (Hoidal et al 1981, Ludwig and Hoidal 1982, Bridges et al 1985, MacNee 2005a. Animal models also develop increased protein synthesis by lipid peroxidation products, such as 4-hydroxynonenal, and depletion of antioxidant substances, such as superoxide dismutase, catalase, ascorbic acid and glutathione (McCusker and Hoidal 1990, Churg and Cherukupalli 1993, Cavarra et al 2001, Aoshiba et al 2003a).…”

Section: Elastase Vs Smoke-induced Emphysemamentioning

confidence: 99%

Elastase-induced pulmonary emphysema: insights from experimental models

Antunes

Rocco

2011

An. Acad. Bras. Ciênc.

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Several distinct stimuli can be used to reproduce histological and functional features of human emphysema, a leading cause of disability and death. Since cigarette smoke is the main cause of emphysema in humans, experimental researches have attempted to reproduce this situation. However, this is an expensive and cumbersome method of emphysema induction, and simpler, more efficacious alternatives have been sought. Among these approaches, elastolytic enzymes have been widely used to reproduce some characteristics of human cigarette smoke-induced disease, such as: augmentation of airspaces, inflammatory cell influx into the lungs, and systemic inflammation. Nevertheless, the use of elastase-induced emphysema models is still controversial, since the disease pathways involved in elastase induction may differ from those occurring in smoke-induced emphysema. This indicates that the choice of an emphysema model may impact the results of new therapies or drugs being tested. The aim of this review is to compare the mechanisms of disease induction in smoke and elastase emphysema models, to describe the differences among various elastase models, and to establish the advantages and disadvantages of elastase-induced emphysema models. More studies are required to shed light on the mechanisms of elastase-induced emphysema.

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Oxidative Metabolism of Alveolar Macrophages from Young Asymptomatic Cigarette Smokers

Cited by 35 publications

References 10 publications

N-Acetyl Cysteine in Combination with Vitamin C Enhances the Antioxidant Status of a Lung Carcinoma Cell Line in Vitro.

N-Acetyl Cysteine in Combination with Vitamin C Enhances the Antioxidant Status of a Lung Carcinoma Cell Line in Vitro.

Aqueous extracts of cigarette tar containing the tar free radical cause DNA nicks in mammalian cells.

Elastase-induced pulmonary emphysema: insights from experimental models

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