Poschet J F, Hammond S M, Fairclough P D
Department of Gastroenterology, Medical School of St. Bartholomew's Hospital, University of London, London, UK.
Biochim Biophys Acta. 1996 Jan 31;1278(2):233-40. doi: 10.1016/0005-2736(95)00226-x.
Uptake of penicillin-G has been studied in rabbit intestinal brush-border membrane vesicles (BBMV). Penicillin-G was transported into the lumen of BBMV via an H+-dependent, Na+-independent uptake system. This was a saturable carrier-mediated process, which adhered to Michaelis-Menten kinetics, having a pH optimum of 4.5 and resulting in a net-negative charge transfer. Vmax was 59 nmol penicillin-G (mg protein)-1 (30s)-1 and Km 22.7 mM. Ampicillin, penicillin-V, cefadroxil, cephalexin, cephalothin, cephradine, L-carnosine, glycyl-L-alanine, glycyl-L-tyrosine and glycylglycylglycine inhibited the uptake of penicillin-G. However, glycylsarcosine stimulated uptake by 92%. Countertransport experiments suggested that this effect took place at the active site of the transporter. Penicillin-G uptake appeared to be mediated via a common transport system shared by penicillins, cephalosporins and peptides.
已在兔肠刷状缘膜囊泡（BBMV）中研究了青霉素G的摄取情况。青霉素G通过一种H⁺依赖性、Na⁺非依赖性摄取系统转运至BBMV内腔。这是一个可饱和的载体介导过程，符合米氏动力学，最适pH为4.5，导致净负电荷转移。Vmax为59 nmol青霉素G（mg蛋白）⁻¹（30秒）⁻¹，Km为22.7 mM。氨苄西林、青霉素V、头孢羟氨苄、头孢氨苄、头孢噻吩、头孢拉定、L-肌肽、甘氨酰-L-丙氨酸、甘氨酰-L-酪氨酸和甘氨酰甘氨酰甘氨酸抑制青霉素G的摄取。然而，甘氨酰肌氨酸使摄取增加了92%。反向转运实验表明，这种效应发生在转运体的活性位点。青霉素G的摄取似乎是通过青霉素、头孢菌素和肽类共享的共同转运系统介导的。
