Karabelnik D, Zbinden G
Arch Toxicol. 1976 Jun 8;35(3):163-74. doi: 10.1007/BF00293563.
The effects of 3 lipidosis-inducing drugs on the incorporation and turnover of palmitic acid-1-14C in lung phospholipids was studied. In rats treated with 1 dose of chlorphentermine or RMI 10.393, the incorporation of palmitate-1-14C into most lung phospholipid fractions was moderately decreased, but markedly lowered after 1 dose of Ro 4-4318. Eight doses of chlorphentermine and RMI 10.393 strongly inhibited the incorporation of palmitate-1-14C into lung phospholipids, whereas with 8 doses of Ro 4-4318 the incorporation was highly increased. Thirty hours after the last of 3 injections of the labeled palmitic acid the turnover of most lung phospholipids was considerably lower in chlorphentermine- and RMI 10.393-treated rats than in controls. Ro 4-4318, however, induced a highly increased turnover of most phospholipids. After 54 h, this effect had practically disappeared. Our studies showed that phospholipid storage after treatment with chlorphentermine and RMI 10.393 is mainly due to decreased degradation of phospholipids, whereas increased synthesis accounts for the effect of Ro 4-4318.
研究了3种致脂质性药物对棕榈酸-1-¹⁴C掺入肺磷脂及其周转的影响。在用一剂氯苯丁胺或RMI 10.393处理的大鼠中,棕榈酸-1-¹⁴C掺入大多数肺磷脂组分的量中度降低,但在用一剂Ro 4-4318处理后显著降低。八剂氯苯丁胺和RMI 10.393强烈抑制棕榈酸-1-¹⁴C掺入肺磷脂,而八剂Ro 4-4318则使掺入量高度增加。在最后一次注射标记的棕榈酸30小时后,氯苯丁胺和RMI 10.393处理的大鼠中大多数肺磷脂的周转比对照组低得多。然而,Ro 4-4318诱导大多数磷脂的周转高度增加。54小时后,这种效应实际上消失了。我们的研究表明,氯苯丁胺和RMI 10.393处理后磷脂储存主要是由于磷脂降解减少,而Ro 4-4318的作用是由于合成增加。