CASTRATION PROLONGS TOLERANCE OF YOUNG MALE-RATS TO PULMONARY O-2 TOXICITY
CASTRATION PROLONGS TOLERANCE OF YOUNG MALE-RATS TO PULMONARY O-2 TOXICITY
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DOI:
10.1152/ajpregu.1984.247.3.r475
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发表时间:
1984-01-01
影响因子:
--
通讯作者:
FRANK, L
中科院分区:
文献类型:
--
作者:
NERIISHI, K;FRANK, L
The hypothesis that the normal loss of tolerance of neonatal rats to prolonged hyperoxic exposure at around 1 mo. of age might be related to the marked increase in sex hormones occurring around this period was tested. Male rats castrated at 20 days of age demonstrated significantly increased survival in > 95% O2 compared with sham-operated rats when exposed to high O2 at various ages > 45 days [castrated, 115 of 166 (69%) vs. sham, 59 of 156 (38%) (P < 0.001)]. Testosterone replacement led to survival rates comparable with sham-operated rats [30 of 87 (34%)]. No such protective effect was observed in female rats [survival: ovariectomy, 16 of 33 (48%) vs. sham, 14 of 28 (50%)]. The improved survival in the older castrated males was not associated with an increase in lung antioxidant enzymes, which is normally seen in O2-tolerant neonatal rats. Castration did result in marked morphological lung changes, including significantly enlarged lung volumes (4.54 .+-. 0.72 vs. 3.76 .+-. 0.29 ml/100 g) and terminal air spaces [mean linear intercept (LM) = 51.6 .+-. 5.0 vs. 46.3 .+-. 4.1 .mu.m (P < 0.001)]. Testosterone replacement also prevented these morphological changes. The altered lung growth may be related to the influence of other endocrine imbalances after castration and may be an important factor in the relative O2 tolerance of the castrated male rats beyond the neonatal period.