To examine the role of immaturity in the free radical-mediated rate of
lipid peroxidation in premature infants, we studied 27 infants [gesta
tional age, 27.1 (SD 2.4) wk; birth weight, 970 (SD 330) g]. Ethane an
d pentane were quantitated in expired air during the first 18 d of lif
e. During the first 2 postnatal d ethane [24.1 (SEM 7.8) pmol x kg(-1)
x min(-1)] and pentane [24.2 (SEM 4.1) pmol x kg(-1) x min-1] were st
able but increased during d 5 to maxima of 79.1 (15.8) pmol x kg(-1) x
min(-1) and 62.1 (8.1) pmol x kg(-1) x min(-1), respectively. Maximum
ethane and pentane correlated with gestational age (r = -0.42, p = 0.
03 and r -0.52, p = 0.005, respectively) and birth weight (r = -0.38,
p = 0.05 and r = -0.59, p = 0.001, respectively). Infants with high ma
ximum expired ethane and pentane (exceeding 40 pmol x kg(-1) x min(-1)
) had higher odds of dying or having bronchopulmonary dysplasia than t
hose with low ethane and pentane (odds ratio, 6.5; 95% confidence inte
rval, 1.1 to 38.5; p < 0.05 for ethane and odds ratio, 5.6; 95% confid
ence interval, 1.1 to 29.3;p < 0.05 for pentane). We conclude that deg
ree of prematurity is the single most important factor explaining free
radical-mediated lipid peroxidation in premature infants. A therapeut
ic intervention to limit the effects of free radicals should be starte
d during the Ist postnatal d in premature infants to be effective.