Van der Zee J, Dubbelman T M, Van Steveninck J
Sylvius Laboratories, Department of Medical Biochemistry, Leiden, The Netherlands.
Biochem J. 1987 Jul 1;245(1):301-4. doi: 10.1042/bj2450301.
Exposure of murine L929 fibroblasts to ozone caused inactivation of the energy-coupled transport systems for 2-aminoisobutyric acid and Rb+. Ozone induced an increase of the apparent Km for 2-aminoisobutyric acid transport, with a constant Vmax, indicating impairment of the carrier function, rather than a decrease in the number of transport sites. The uptake rate of 2-deoxy-D-glucose, on the other hand, increased after exposure of the cells to ozone. This was caused by an increased Vmax. of facilitated diffusion, without increased after ozone exposure. Together with the K+ leakage described previously, this reflects ozone-induced impairment of the barrier function of the membrane.
将鼠源L929成纤维细胞暴露于臭氧中会导致2-氨基异丁酸和Rb⁺的能量偶联转运系统失活。臭氧使2-氨基异丁酸转运的表观Km增加,而Vmax恒定,这表明载体功能受损,而非转运位点数量减少。另一方面,细胞暴露于臭氧后,2-脱氧-D-葡萄糖的摄取速率增加。这是由易化扩散的Vmax增加所致,臭氧暴露后其数量并未增加。连同之前描述的K⁺泄漏,这反映了臭氧诱导的细胞膜屏障功能受损。