Fussell J C, Kelly F J
School of Biochemical and Physiological Sciences, University of Southampton, U.K.
Biochem J. 1991 Jan 1;273(Pt 1)(Pt 1):93-7. doi: 10.1042/bj2730093.
Dexamethasone (2.5 mg/day per kg) treatment of young growing rats resulted in reduced food intake and rapidly inhibited whole-body and lung growth. Although the reduction in food intake partially explained the decrease in whole-body growth, it did not influence lung growth. After 24 h of dexamethasone treatment, ribosomal efficiency in the lung was reduced 44%, producing a 38% decrease in the rate of pulmonary protein synthesis. Extending dexamethasone treatment to 5 days resulted in decreases in both ribosomal efficiency (35%) and capacity (28%), explaining the 53% reduction in lung protein synthesis at this time. After both the acute and chronic steroid regimes, the decreased rates of pulmonary protein synthesis were accompanied by a loss of polyribosomes and an elevated ribosomal monomer pool, indicating that dexamethasone blocked translation at the site of peptide-chain initiation.
地塞米松(每千克体重2.5毫克/天)对幼年生长大鼠进行治疗,导致食物摄入量减少,并迅速抑制全身和肺部生长。尽管食物摄入量的减少部分解释了全身生长的下降,但它并未影响肺部生长。地塞米松治疗24小时后,肺部核糖体效率降低了44%,导致肺蛋白合成速率下降38%。将地塞米松治疗延长至5天,导致核糖体效率(35%)和容量(28%)均下降,解释了此时肺蛋白合成减少53%的原因。在急性和慢性类固醇治疗方案之后,肺蛋白合成速率的降低伴随着多核糖体的损失和核糖体单体池的升高,表明地塞米松在肽链起始位点阻断了翻译。