Ascorbic acid requirements for smokers: analysis of a population survey

Schectman, Gordon; Byrd, James C.; Hoffmann, Ray

doi:10.1093/ajcn/53.6.1466

Cited by 117 publications

(46 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This is in line with previous studies demonstrating that long-term exposure to SHS decreases plasma ascorbic acid in both active and passive smokers. 7,12 Furthermore, in vitro data exposing human plasma to CS suggest that ascorbic acid is the first antioxidant to be consumed.…”

Section: Discussionmentioning

confidence: 99%

“…11 Therefore, this could be one factor leading to the high incidence of CHD in smokers, who also have decreased plasma levels of certain antioxidants. 12 However, only fractional and, to some extent, controversial evidence concerning the connection between CS and lipid peroxidation has been reported so far from studies conducted with active smokers or under in vitro conditions. [13][14][15] To understand the pathogenesis underlining the connection between CHD and passive smoking, we assessed the acute effect of passive smoking on LDL metabolism.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein

1998

View full text Add to dashboard Cite

Background-According to the American Heart Association, passive smoking is an important risk factor for coronary heart disease (CHD), but the mechanisms underlying this association are not fully understood. We studied the acute effect of passive smoking on the factors that influence the development of CHD: the antioxidant defense of human serum, the extent of lipid peroxidation, and the accumulation of LDL cholesterol in cultured human macrophages, the precursors of foam cells in atherosclerotic lesions. Methods and Results-Blood samples were collected during 2 ordinary working days from healthy, nonsmoking subjects (nϭ10) before and after (up to 5.5 hours) spending half an hour in a smoke-free area (day 1) or in a room for smokers (day 2). Passive smoking caused an acute decrease (1.5 hours after exposure) in serum ascorbic acid (PϽ.001) and in serum antioxidant defense (PϽ.001), a decreased capacity of LDL to resist oxidation (PϽ.01), and the appearance of increased amounts of lipid peroxidation end products in serum (PϽ.01). Finally, LDL isolated from subjects after passive smoking was taken up by cultured macrophages at an increased rate (PϽ.05). Conclusions-Exposure of nonsmoking subjects to secondhand smoke breaks down the serum antioxidant defense, leading to accelerated lipid peroxidation, LDL modification, and accumulation of LDL cholesterol in human macrophages. These data provide the pathophysiological background for the recent epidemiological evidence about the increased CHD risk among passive smokers. (Circulation. 1998;97:2012-2016.)

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein

1998

View full text Add to dashboard Cite

show abstract

“…The inverse relationship between smoking and plasma vitamin C levels is well reported, even for passive smoking. 20 Schectman et al 21 suggested that smokers need more vitamin C to reach the same plasma levels as non-smokers. Vegetables and fruits serve as primary contributors to total vitamin C intake, 22 whereas dietary supplements of vitamin C and other antioxidants have failed to demonstrate consistent therapeutic benefits, 23 therefore grapefruit was choosen to influence vitamin C status.…”

Section: Plasma Vitamin C Levelsmentioning

confidence: 99%

Grapefruit consumption improves vitamin C status in periodontitis patients

2005

View full text Add to dashboard Cite

“…These results demonstrate the protective effect of dietary ascorbate against oxidative damage to human sperm DNA. This protective effect may be especially relevant to about one third of the male population who have low ascorbate levels because of poor diets or smoking (139,143,144). Their progeny may be at a higher risk for birth defects and childhood cancer.…”

Section: Progression and Clonal Instabilitymentioning

confidence: 99%

DNA lesions, inducible DNA repair, and cell division: three key factors in mutagenesis and carcinogenesis.

Ames

Shigenaga

Gold

1993

Environ Health Perspect

268

155

View full text Add to dashboard Cite

DNA lesions that escape repair have a certain probability of giving rise to mutations when the cell divides. Endogenous DNA damage is high: 106 oxidative lesions are present per rat cell. An exogenous mutagen produces an increment in lesions over the background rate of endogenous lesions. The effectiveness of a particular lesion depends on whether it is excised by a DNA repair system and the probability that it gives rise to a mutation when the cell divides. When the cell divides, an unrepaired DNA lesion has a certain probability of giving rise to a mutation. Thus, an important factor in the mutagenic effect of an exogenous agent whether it is genotoxic or non-genotoxic, is the increment it causes over the background cell division rate (mitogenesis) in cells that appear to matter most in cancer, the stem cells, which are not on their way to being discarded. Increasing their cell division rate increases mutation and therefore cancer. There is little cancer from nondividing cells. Endogenous cell division rates can be influenced by hormone levels, decreased by calorie restriction, or increased by high doses of chemicals. If both the rate of DNA lesions and cell division are increased, then there will be a multiplicative effect on mutagenesis (and carcinogenesis), for example, by high doses of a mutagen that also increases mitogenesis through cell killing. The defense system against reactive electrophilic mutagens, such as the glutathione transferases, are also almost all inducible and buffer cells against increments in active forms of chemicals that can cause DNA lesions. A variety of DNA repair defense systems, almost all inducible, buffer the cell against any increment in DNA lesions. Therefore, the effect of a particular chemical insult depends on the level of each defense, which in turn depends on the past history of exposure. Exogenous agents can influence the induction and effectiveness of these defenses. Defenses can be partially disabled by lack of particular micronutrients in the diet (e.g., antioxidants). Four endogenous processes leading to significant DNA damage are oxidation (1-3), methylation, deamination, and depurination (2). The importance of these processes is supported by the existence of specific DNA repair glycosylases for oxidative, methylated, and deaminated adducts and a repair system for apurinic sites that are produced by spontaneous depurination (3). Endogenous DNA Damage and MutagenesisDNA damage produced by oxidation appears to be the most significant endogenous damage (4). We estimate that the DNA hits per cell per day from endogenous oxidants are normally 105 in the rat and 104 in the human (5-7). These oxidative lesions are effectively but not perfectly repaired; the normal steady-state level of oxidative DNA lesions is about 106 per cell in the young rat and about twice this in the old rat (6,8). Oxidants are produced as byproducts of mitochondrial electron transport, various oxygen-utilizing enzyme system, peroxisomes, and other processes associated with normal aerobic metabolism...

show abstract

Ascorbic acid requirements for smokers: analysis of a population survey

Cited by 117 publications

References 21 publications

Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein

Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein

Grapefruit consumption improves vitamin C status in periodontitis patients

DNA lesions, inducible DNA repair, and cell division: three key factors in mutagenesis and carcinogenesis.

Contact Info

Product

Resources

About