Las. Brown et al., ASCORBATE DEFICIENCY AND OXIDATIVE STRESS IN THE ALVEOLAR TYPE-II CELL, American journal of physiology. Lung cellular and molecular physiology, 17(4), 1997, pp. 782-788
The objective of this study was to determine the impact of limited asc
orbate (Asc) availability on type II cell sensitivity to oxidant stres
s. Guinea pigs were fed diets with or without Asc for 18 days, and typ
e II cells were isolated. Although lung Asc was decreased by 90% in de
ficient animals (scorbutic), type II cell Asc was decreased by 50%. Up
on treatment with 250 mu M H2O2, the necrotic injury was twofold great
er in scorbutic cells compared with control cells. With 100 mu M H2O2
treatment, apoptotic injury was twofold greater in scorbutic cells com
pared with control cells. Although there was less necrotic injury in c
ells exposed to 95% O-2, the scorbutic cells were more sensitive than
control cells. Ase pretreatment protected against necrosis and apoptos
is. The Asc analog isoascorbate provided partial protection and sugges
ted that part of the protection was not chemical detoxification but wa
s Asc specific. We conclude that limited Asc availability resulted in
a functional type II cell but a cell more sensitive to oxidant-induced
injury.