Ascorbic Acid and Lung Development

Epidemiological studies have shown the elfect of smoking in reducing ascorbic acid levels in blood (Pelletier, 1970). Exposure to ozone and nitrogen dioxide also reduces blood ascorbic acid content. Unusually low amounts of ascorbate in milk of lactating women smokers have also been reported (Kallner et aL, 1981). This is attributed to the increased need for reducing agents imposed by chemical oxidants contained in tobacco smoke and some metabolic properties of nicotine (Bucca et al., 1989). This explains why the daily intake of ascorbic acid of at least 140 mg is required for smokers to reach a body pool of ascorbic acid comparable to that of nonsmokers, for whom a daily intake of about 100 mg is sufficient (Kallner et aL, 1981). 

Apart from inhibiting glycolysis, maternal nicotine exposure also induces swelling of endothelial cells in lungs of suckling rats (Figs. 2 and 3). Ruptured type 

FIGURE 2. A scanning electron micrograph illustrating membrane blebs (arrows) on the alveolar surface of neonatal rat lung. 

I pneumocytes and blood-air barriers often occur (Maritz et al., 1994). On the other hand, ascorbic acid supplementation during pregnancy prevents the inhibition of glycolysis in the neonatal lung (Maritz, 1987, 1993). This implies that ascorbic acid can prevent these cells from damage related to the inhibition of glycolysis. 

FIGURE 3. A transmission electron micrograph of a section of an alveolar septum of lung tissue of a rat pup exposed to nicotine via the placenta and mother s milk. Swelling of the endothelial cell (asterisks) of the blood-air barrier occurs. Note the focal degeneration of the endothelial cell cytoplasm (star). The blood-air barrier is composed of the endothelial cell (asterisks), type I cell (double arrowheads), and the basement membrane between these cells. Swollen mitochondria can be seen in the interstitial cells (arrowheads). Collagen fibers also occur (arrows), cap = capillary. 

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