Dietary vitamin E and pulmonary biochemical responses of rats to cigarette smoking

Chow, Ching K.; Chen, L.H.; Thacker, Richard R.; Griffith, R.B.

doi:10.1016/0013-9351(84)90070-7

Cited by 35 publications

(9 citation statements)

References 28 publications

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“…It is known that the gas and tar phases of tobacco smoke contain many reactive oxidizing species, 39 and both animal 40 and human 41 studies have shown that exposure to cigarette smoke has a deleterious effect on antioxidant status. Thus, the enhanced free-radical load of smokers, especially when combined with a low antioxidant intake, will result in an increased peroxidation of essential fatty acids and will consequently reduce the availability of these fatty acids.…”

Section: Discussionmentioning

confidence: 99%

Plasma essential fatty acids, cigarette smoking, and dietary antioxidants in peripheral arterial disease. A population-based case-control study.

Leng

Horrobin

Fowkes

et al. 1994

Arterioscler Thromb

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The aim of this study was to determine the levels of plasma fatty acids in patients with peripheral arterial disease and in control subjects and to identify whether any risks of disease related to these differences were influenced by smoking and antioxidant intake. A random sample of 1592 men and women aged 55 to 74 years was selected from the general population (the Edinburgh Artery Study), from which 153 cases of peripheral arterial disease were identified by the presence of intermittent claudication and low ankle systolic pressures at rest and during reactive hyperemia; these were matched by age and sex to 153 control subjects with no evidence of cardiovascular disease. In 113 case and 122 control subjects, fatty acid levels were measured in three plasma fractions (triglyceride, cholesteryl ester, and phospholipid), and smoking habits and dietary antioxidant intake were determined by questionnaire. Arachidonic acid, eicosapentaenoic acid, docosahexaenoic acid, and docosapentaenoic acid (DPA/ T he main dietary essential fatty acids are linoleic acid (18:2 n-6) and a-linolenic acid (18:3 n-3), both found mainly in vegetable oils. Within the body, these parent essential fatty acids are metabolized by a series of reactions to form arachidonic acid and eicosapentaenoic acid (EPA), which are further metabolized to prostacyclins and thromboxanes (Figure), substances known to exert opposing physiological effects on the cardiovascular system. An important rate-limiting step in the metabolism of linoleic acid and a-linolenic acid is the initial desaturation reaction, where the two parent fatty acids compete for the A-6-desaturase enzyme. This step may also be inhibited by several factors associated with cardiovascular disease, such as high cholesterol levels, catecholamines, high saturated-fat intake, and aging.1 It is therefore possible for some individuals to be effectively lacking in essential fatty acid metabolites, despite an adequate dietary intake of linoleic and a-linolenic acids.

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Section: Discussionmentioning

confidence: 99%

Plasma essential fatty acids, cigarette smoking, and dietary antioxidants in peripheral arterial disease. A population-based case-control study.

Leng

Horrobin

Fowkes

et al. 1994

Arterioscler Thromb

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“…Gupta et al (1988) reported that the subchronic exposure of Wistar rats to cigarette smoke resulted in a increase in lung G S H level without altering the activity of antioxidant enzymes such as GPXase, catalase and SOD. On the contrary, short-term exposure o f Sprague D a w l e y rats for less than 7 days to cigarette smoke caused the increase of the levels of both G P X a s e and G S H in the lungs (Chow et al 1984). H o w -ever, Bilimoria and Ecobichon (1992) found GSH level to be decreased by acute exposure in the same strain of animal.…”

Section: Discussionmentioning

confidence: 96%

Effect of subchronic administration of antioxidants against cigarette smoke exposure in rats

et al. 1993

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Effects of subchronic administration of antioxidants against pulmonary damage mediated by cigarette smoke were investigated in rats. Rats were continuously received ascorbic acid, N-acetylcysteine and ginseng extract together drinking water from day 25 after birth. After 30 days of antioxidant supplementation, rats were exposed to cigarette smoke generated from six cigarettes (11 mg tar) for 20 min per day throughout 30 days, and then several biochemical markers related to the redox status in vivo were analyzed in the respiratory system. The cigarette smoke induced mild histological changes in trachea and lungs. The activity of superoxide dismutase (SOD) in the lung was significantly increased, and catalase and glutathione peroxidase activities were increased less than SOD, but total sulfhydryl compounds (Total-SH) content was decreased by cigarette smoking. In spite of the increase in activities of antioxidant enzymes, the inhibitory capacity of lung preparations on in vitro lipid peroxidation using ox brain homogenates was decreased and the change in the capacity was not related to the changes of these intracellular enzymes activities, but with the content of Total-SH. On the other hand, the content of thiobarbituric acid reactive substances and the ratio of elastase to anti-protease in the lung homogenates were significantly increased. Supplementation of antioxidants, however, effectively attenuated all of such alterations induced by cigarette smoke. These results indicate that although cigarette smoking induces antioxidant enzymes in the lung as a self defense mechanism, it seems to be not sufficient to protect the pulmonary system, and that chronic antioxidant feeding could be effective to reduce pulmonary damage induced by free radicals.

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“…A vitamin E-deficient diet caused a 90-fold depletion of α-tocopherol in lung tissues and resulted in a significant decline of other antioxidants (GSH, ascorbate) as well as accumulation of lipid peroxidation products (Shvedova et al, 2007) and led to higher mortality levels (Chow et al, 1984) in animal models.…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, antioxidant agents such as vitamin C (Panda, Chattopadhyay, Ghosh, Chattopadhyay, & Chatterjee, 1999) or vitamin E (Chow, Chen, Thacker, & Griffith, 1984) could be used to prevent this toxicity.…”

Section: Introductionmentioning

confidence: 99%

Development of α-Tocopherol Acetate Nanoparticles: Influence of Preparative Processes

Anais

Razzouq

Carvalho

et al. 2009

Drug Development and Industrial Pharmacy

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We studied different methods of preparing α-tocopherol acetate (ATA) nanoparticles, which are to be used in targeting the lungs as aerosols in order to prevent cigarette smoke toxicity. Poly-(lactide) nanoparticles were prepared using nanoprecipitation and solvent evaporation techniques, which produced, respectively, too small and too large nanoparticles to be aerosolized. The emulsification-diffusion method produced 2 months stable nanoparticles with a size between (500-700 nm). Increasing ATA concentration (1-7 mg/mL) induced a decrease in the association rate (97-93%) and in the adsorbed ATA rate (7-4.5%), which was associated with variations of Zeta potentials (−27.5 to −24.3 mV) and decrease in polymeric wall thickness and density.

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Dietary vitamin E and pulmonary biochemical responses of rats to cigarette smoking

Cited by 35 publications

References 28 publications

Plasma essential fatty acids, cigarette smoking, and dietary antioxidants in peripheral arterial disease. A population-based case-control study.

Plasma essential fatty acids, cigarette smoking, and dietary antioxidants in peripheral arterial disease. A population-based case-control study.

Effect of subchronic administration of antioxidants against cigarette smoke exposure in rats

Development of α-Tocopherol Acetate Nanoparticles: Influence of Preparative Processes

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