Ascorbic acid in bronchoalveolar wash

Skoza, L; Snyder, Arthur; Kikkawa, Yutaka

doi:10.1007/bf02713848

Cited by 41 publications

(18 citation statements)

References 21 publications

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“…The ability to increase levels of this cellular antioxidant may protect epithelium in situations where inflammation and subsequent increases in ROS are likely (37). Increases in Mn-SOD would more likely be protective in situations where endogenous ROS pose more of a threat than exogenous ROS, such as hyperoxia (38,39 (40)(41)(42). Airway submucosal gland secretions also contain antioxidants; in human secretions uric acid is especially important (43).…”

Section: Nonenzymatic Antioxidant Defensesmentioning

confidence: 99%

Interactions of Oxygen Radicals with Airway Epithelium

Wright¹,

Cohn²,

Li³

et al. 1994

Environmental Health Perspectives

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Reactive oxygen species (ROS) have been implicated in the pathogenesis of numerous disease processes. Epithelial cells lining the respiratory airways are uniquely vulnerable regarding potential for oxidative damage due to their potential for exposure to both endogenous (e.g., mitochondrial respiration, phagocytic respiratory burst, cellular oxidases) and exogenous (e.g., air pollutants, xenobiotics, catalase negative organisms) oxidants. Airway epithelial cells use several nonenzymatic and enzymatic antioxidant mechanisms to protect against oxidative insult. Nonenzymatic defenses include certain vitamins and low molecular weight compounds such as thiols. The enzymes superoxide dismutase, catalase, and glutatione peroxidase are major sources of antioxidant protection. Other materials associated with airway epithelium such as mucus, epithelial lining fluid, and even the basement membrane/extracellular matrix may have protective actions as well. When the normal balance between oxidants and antioxidants is upset, oxidant stress ensues and subsequent epithelial cell alterations or damage may be a critical component in the pathogenesis of several respiratory diseases. Oxidant stress may profoundly alter lung physiology including pulmonary function (e.g., forced expiratory volumes, flow rates, and maximal inspiratory capacity), mucociliary activity, and airway reactivity. ROS may induce airway inflammation; the inflammatory process may serve as an additional source of ROS in airways and provoke the pathophysiologic responses described. On a more fundamental level, cellular mechanisms in the pathogenesis of ROS may involve activation of intracellular signaling enzymes including phospholipases and protein kinases stimulating the release of inflammatory lipids and cytokines. Respiratory epithelium may be intimately involved in defense against, and pathophysiologic changes invoked by, ROS. -Environ Health Perspect 1 02(Suppl 1 0): 85-90 (1994)

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Section: Nonenzymatic Antioxidant Defensesmentioning

confidence: 99%

Interactions of Oxygen Radicals with Airway Epithelium

Wright¹,

Cohn²,

Li³

et al. 1994

Environmental Health Perspectives

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“…Cigarette smoke contains several free radicals including highly reactive nitrogen oxides, and these radicals cause widespread biologic damage in lung. It has been suggested that ant±oxidants including GSH play a pivotal role in preventing inflammatory responses caused by cigarette smoke [2,14,32]. Although acute exposure to cigarette smoke perturbs GSH synthesis and/or GSH metabolism in animals and humans [15,19,22,30], it is not clear whether chronic exposure to cigarette smoke causes changes in GSH metabolism in vivo.…”

Section: Discussionmentioning

confidence: 93%

Effect of age on alteration of glutathione metabolism following chronic cigarette smoke inhalation in mice

Teramoto

Uejima

Teramoto

et al. 1996

Lung

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Cigarette smoke is the most common oxidant stress in daily life and may affect the antioxidant capacity in humans and animals. The antioxidant functions may play an important role in preventing age-related disorders. However, influences of chronic cigarette smoke on the antioxidant capacity of visceral organs have not been investigated in the age. Senescene-accelerated mice (SAM) are good models for studying physiologic and/or pathologic aging. A senescene-prone strain, SAMP2, shows characteristics of premature aging. The senescence-resistant strain, SAMR1, exhibits relatively normal aging. In this study we examined the effects of chronic cigarette smoke exposure on the glutathione (GSH) metabolism of visceral organs in the two strains of mice that were 6 and 18 months old. After a 4-week cigarette or air exposure, total GSH and oxidized GSH (GSSG) in the organs were examined. In the young (6-month-old) mice, exposure to cigarette smoke caused a significant decrease of GSH in liver, blood, and lung of SAMP2 but not in those of SAMR1. In the aged (18-month-old) mice reduced GSH with a marked increase of GSSG were found in liver of both strains of SAM following cigarette smoke exposure. The baseline values of GSH and the GSSG/GSH ratio after air exposure were slightly changed with age, and the values after exposure to cigarette smoke were changed markedly with advancing age. These results indicate that GSH metabolism may be impaired by chronic cigarette smoke exposure in mice and that aged mice are more susceptible to cigarette smoke than young mice.

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“…However, the problems in concentrating glutathione, a low molecular weight species that is rapidly oxidized when removed from tissues (58) Because of the large dilution of ELF caused by the use of saline to perform the bronchoalveolar lavage, ELF molecules were concentrated by pressure filtration, and thus only molecules with a molecular mass > 10 kD were analyzed. However, smaller antioxidant molecules such as vitamins A, C, and E are also present in biological fluids (62)(63)(64)(65). Vitamin A acts predominantly as a quencher of singlet oxygen (62), and vitamin E is thought to function mainly by interacting with lipid peroxy free radicals (RO2) and stopping the cyclic chain reaction of lipid peroxidation (63,65).…”

Section: Discussionmentioning

confidence: 99%

Antioxidant macromolecules in the epithelial lining fluid of the normal human lower respiratory tract.

Cantin¹,

Fells²,

Hubbard³

et al. 1990

J. Clin. Invest.

124

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We hypothesized that the alveolar structures may contain extracellular macromolecules with antioxidant properties to defend against oxidants. To evaluate this 51Cr-labeled human lung fibroblasts (HFL-1) and cat lung epithelial cells (AKD) were exposed to a H202-generating system and alveolar epithelial lining fluid (ELF) from healthy nonsmokers was tested for its ability to protect the lung cells from H202-mediated injury. The Invest. 1990. 86:962-971.)

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Ascorbic acid in bronchoalveolar wash

Cited by 41 publications

References 21 publications

Interactions of Oxygen Radicals with Airway Epithelium

Interactions of Oxygen Radicals with Airway Epithelium

Effect of age on alteration of glutathione metabolism following chronic cigarette smoke inhalation in mice

Antioxidant macromolecules in the epithelial lining fluid of the normal human lower respiratory tract.

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